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New CAR T-cell therapy eliminates MM and tumor propagating cells without fratricide in lab study

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Researchers have developed chimeric antigen receptor (CAR) T cells expressing a fully human antibody against CD229, a surface antigen that shows universal and strong tumor expression in patients with multiple myeloma (MM). These cells proved to be active in vitro and in vivo against MM plasma cells, memory B cells, and MM-propagating cells, according to a report in Nature Communications.

Wikimedia Commons/KGH/Creative Commons License

This research is important because most MM patients eventually succumb to the disease and previously developed CAR T cells targeting B-cell maturation antigen (BCMA) on MM cells have shown high-response rates but limited durability.

Previous research showed that CD229/LY9 is a potential target for CAR T-cell therapy in MM because of its strong and homogeneous expression on the bulk of tumor cells, as well as chemotherapy-resistant myeloma progenitors; its absence from most normal cells; and dependence of MM cells on CD229 for their survival, according to Sabarinath V. Radhakrishnan, MD, of the University of Utah, Salt Lake City, and colleagues.

Using primary CD138+ tumor cells from three patients with plasma cell leukemia, a highly aggressive form of MM, which all showed high expression of CD229, the researchers found that CD229 CAR T cells exhibited high cytotoxic activity against these cells. In addition, when assessing two MM cell lines, U-266 and RPMI-8226, expressing different levels of CD229, they found that CD229 CAR T cells efficiently killed both cell lines in vitro.

“We do not observe fratricide during CD229 CAR T-cell production, as CD229 is downregulated in T cells during activation. In addition, while CD229 CAR T cells target normal CD229high T cells, they spare functional CD229neg/low T cells. These findings indicate that CD229 CAR T cells may be an effective treatment for patients with MM,” the authors concluded.

The study was funded by several nongovernmental organizations and the National Cancer Institute. Three of the authors are inventors on PCT application US2017/42840 “Antibodies and CAR T Cells for the Treatment of Multiple Myeloma” describing the therapeutic use of CD229 CAR T cells.

SOURCE: Radhakrishnan SV et al. Nat Commun. 2020 Feb 7;11(1):798. doi: 10.1038/s41467-020-14619-z.

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Researchers have developed chimeric antigen receptor (CAR) T cells expressing a fully human antibody against CD229, a surface antigen that shows universal and strong tumor expression in patients with multiple myeloma (MM). These cells proved to be active in vitro and in vivo against MM plasma cells, memory B cells, and MM-propagating cells, according to a report in Nature Communications.

Wikimedia Commons/KGH/Creative Commons License

This research is important because most MM patients eventually succumb to the disease and previously developed CAR T cells targeting B-cell maturation antigen (BCMA) on MM cells have shown high-response rates but limited durability.

Previous research showed that CD229/LY9 is a potential target for CAR T-cell therapy in MM because of its strong and homogeneous expression on the bulk of tumor cells, as well as chemotherapy-resistant myeloma progenitors; its absence from most normal cells; and dependence of MM cells on CD229 for their survival, according to Sabarinath V. Radhakrishnan, MD, of the University of Utah, Salt Lake City, and colleagues.

Using primary CD138+ tumor cells from three patients with plasma cell leukemia, a highly aggressive form of MM, which all showed high expression of CD229, the researchers found that CD229 CAR T cells exhibited high cytotoxic activity against these cells. In addition, when assessing two MM cell lines, U-266 and RPMI-8226, expressing different levels of CD229, they found that CD229 CAR T cells efficiently killed both cell lines in vitro.

“We do not observe fratricide during CD229 CAR T-cell production, as CD229 is downregulated in T cells during activation. In addition, while CD229 CAR T cells target normal CD229high T cells, they spare functional CD229neg/low T cells. These findings indicate that CD229 CAR T cells may be an effective treatment for patients with MM,” the authors concluded.

The study was funded by several nongovernmental organizations and the National Cancer Institute. Three of the authors are inventors on PCT application US2017/42840 “Antibodies and CAR T Cells for the Treatment of Multiple Myeloma” describing the therapeutic use of CD229 CAR T cells.

SOURCE: Radhakrishnan SV et al. Nat Commun. 2020 Feb 7;11(1):798. doi: 10.1038/s41467-020-14619-z.

Researchers have developed chimeric antigen receptor (CAR) T cells expressing a fully human antibody against CD229, a surface antigen that shows universal and strong tumor expression in patients with multiple myeloma (MM). These cells proved to be active in vitro and in vivo against MM plasma cells, memory B cells, and MM-propagating cells, according to a report in Nature Communications.

Wikimedia Commons/KGH/Creative Commons License

This research is important because most MM patients eventually succumb to the disease and previously developed CAR T cells targeting B-cell maturation antigen (BCMA) on MM cells have shown high-response rates but limited durability.

Previous research showed that CD229/LY9 is a potential target for CAR T-cell therapy in MM because of its strong and homogeneous expression on the bulk of tumor cells, as well as chemotherapy-resistant myeloma progenitors; its absence from most normal cells; and dependence of MM cells on CD229 for their survival, according to Sabarinath V. Radhakrishnan, MD, of the University of Utah, Salt Lake City, and colleagues.

Using primary CD138+ tumor cells from three patients with plasma cell leukemia, a highly aggressive form of MM, which all showed high expression of CD229, the researchers found that CD229 CAR T cells exhibited high cytotoxic activity against these cells. In addition, when assessing two MM cell lines, U-266 and RPMI-8226, expressing different levels of CD229, they found that CD229 CAR T cells efficiently killed both cell lines in vitro.

“We do not observe fratricide during CD229 CAR T-cell production, as CD229 is downregulated in T cells during activation. In addition, while CD229 CAR T cells target normal CD229high T cells, they spare functional CD229neg/low T cells. These findings indicate that CD229 CAR T cells may be an effective treatment for patients with MM,” the authors concluded.

The study was funded by several nongovernmental organizations and the National Cancer Institute. Three of the authors are inventors on PCT application US2017/42840 “Antibodies and CAR T Cells for the Treatment of Multiple Myeloma” describing the therapeutic use of CD229 CAR T cells.

SOURCE: Radhakrishnan SV et al. Nat Commun. 2020 Feb 7;11(1):798. doi: 10.1038/s41467-020-14619-z.

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Gene therapy appears effective in bladder cancer patients with few options

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A novel gene therapy may expand treatment options for non–muscle invasive bladder cancer that does not respond to Bacillus Calmette-Guerin (BCG), new research suggests.

Susan London/MDedge News
Dr. Stephen A. Boorjian

The therapy, nadofaragene firadenovec, is a recombinant adenovirus that is instilled into the bladder and delivers the human interferon alpha-2b gene, leading to expression of the immune cytokine.

At 3 months, nadofaragene firadenovec had produced a complete response in 53.4% of patients with carcinoma in situ (CIS), and the rate of high-grade recurrence-free survival was 59.6% in all patients. Although most patients (70.1%) experienced adverse events in this trial, few had serious events (1.9%).

Stephen A. Boorjian, MD, of the Mayo Clinic in Rochester, Minn., presented these results at the 2020 Genitourinary Cancers Symposium, sponsored by the American Society for Clinical Oncology, ASTRO, and the Society of Urologic Oncology.

“The optimal management for patients with BCG-unresponsive non–muscle invasive bladder cancer remains to be established,” Dr. Boorjian said. “National and organizational guidelines recommend radical cystectomy in this setting, but we have to acknowledge that many of our patients will be either unwilling or unfit to undergo what is often a highly morbid operation.”

Dr. Boorjian and coinvestigators tested nadofaragene firadenovec in 107 patients with CIS, with or without high-grade Ta or T1 papillary disease, as well as 50 patients with high-grade Ta or T1 papillary disease only.

All patients received nadofaragene firadenovec once every 3 months for up four doses, with additional dosing at the investigator’s discretion. Although the trial was designated as phase 3, it did not have the typical randomized comparative design.

“The challenge in the BCG-unresponsive disease state is that, historically, there has been no validated good comparator to use here; there’s no standard of care for these patients,” Dr. Boorjian explained, noting that the design was chosen after discussion with the Food and Drug Administration.
 

Efficacy

The complete response rate among CIS patients at any time after instillation, the trial’s primary objective, was 53.4%. All of these responses occurred after a single dose of nadofaragene firadenovec. Responses were considered durable, as 45.5% of CIS patients who had a complete response at 3 months still had a complete response at 12 months.

The rate of high-grade recurrence-free survival at 3 months was 59.6% in the overall population, 53.4% in patients with CIS, and 72.9% in patients with papillary disease. At 12 months, the rate of high-grade recurrence-free survival was 30.5%, 24.3%, and 43.8%, respectively.

The rate of high-grade recurrence without muscle invasive bladder cancer was 71.8% in the CIS group and 52.1% in the papillary group. The rate of progression to muscle invasive bladder cancer or more advanced disease was 4.9% and 6.3%, respectively. The overall 2-year rate of cystectomy-free survival was 64%, and there were no bladder cancer deaths.
 

Safety

Nadofaragene firadenovec was considered safe and well tolerated. The most common study drug–related adverse events were irritative voiding symptoms, such as discharge, bladder spasm, micturition urgency, and hematuria.

Although 70.1% of patients experienced a local or systemic adverse event related to the study drug or procedure, few experienced serious adverse events (1.9%), grade 3 adverse events (3.8%), or treatment-emergent adverse events leading to discontinuation (1.9%). The serious adverse events were sepsis, syncope, and hematuria.
 

Next steps

“Nadofaragene firadenovec represents a promising option for patients with BCG-unresponsive [non–muscle invasive bladder cancer],” Dr. Boorjian said. “What we want to see going forward is durability of response, cystectomy-free survival, and metastasis-free and cancer-specific survival. Those are the harder endpoints that, as these data mature, we will want to see so that we are able to counsel our patients accordingly.”

Susan London/MDedge News
Dr. Guru Sonpavde

The FDA recently approved pembrolizumab for this patient population, noted session cochair Guru Sonpavde, MD, of the Dana-Farber Cancer Institute in Boston.

“But nadofaragene firadenovec is much less toxic, it is given intravesically, and it’s only given once every 3 months,” he said. “The outcomes at the 1-year point look similar in terms of the durable complete response rate. So we hope that this therapy will be able to get to the clinic, but we have to wait for the FDA to decide.”

It remains to be seen how nadofaragene firadenovec compares with other emerging therapies for high-risk BCG-unresponsive non–muscle invasive bladder cancer, including pembrolizumab and potentially intravesical oportuzumab monatox (a targeted immunotoxin) and intravesical combination BCG and superagonist interleukin-15 (ALT-803), according to Dr. Boorjian.

“A unique feature of the trial I presented was that the results were validated by a mandatory 12-month study biopsy, which has not been the case in other trials,” he pointed out. “So this separates it a little bit when you are looking at pathologic response rates and high-grade recurrence–free rates. They are based on pathologic confirmation.”

Evaluators will ultimately compare these therapies on safety, efficacy, ease of administration, delivery schedule, and cost, Dr. Boorjian said. “At this stage, it’s very difficult to start to say which agent is going to be placed where in our management paradigm. We have to go step by step: Do the trial that we did, show our data, put it out for review, and then allow the community to engage in a discussion about which agent, and why, for which patient.”

This trial was funded by FKD Therapies Oy. Dr. Boorjian disclosed relationships with Ferring and Sanofi. Dr. Sonpavde disclosed relationships with many companies.

SOURCE: Boorjian SA et al. GUCS 2020, Abstract 442.

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A novel gene therapy may expand treatment options for non–muscle invasive bladder cancer that does not respond to Bacillus Calmette-Guerin (BCG), new research suggests.

Susan London/MDedge News
Dr. Stephen A. Boorjian

The therapy, nadofaragene firadenovec, is a recombinant adenovirus that is instilled into the bladder and delivers the human interferon alpha-2b gene, leading to expression of the immune cytokine.

At 3 months, nadofaragene firadenovec had produced a complete response in 53.4% of patients with carcinoma in situ (CIS), and the rate of high-grade recurrence-free survival was 59.6% in all patients. Although most patients (70.1%) experienced adverse events in this trial, few had serious events (1.9%).

Stephen A. Boorjian, MD, of the Mayo Clinic in Rochester, Minn., presented these results at the 2020 Genitourinary Cancers Symposium, sponsored by the American Society for Clinical Oncology, ASTRO, and the Society of Urologic Oncology.

“The optimal management for patients with BCG-unresponsive non–muscle invasive bladder cancer remains to be established,” Dr. Boorjian said. “National and organizational guidelines recommend radical cystectomy in this setting, but we have to acknowledge that many of our patients will be either unwilling or unfit to undergo what is often a highly morbid operation.”

Dr. Boorjian and coinvestigators tested nadofaragene firadenovec in 107 patients with CIS, with or without high-grade Ta or T1 papillary disease, as well as 50 patients with high-grade Ta or T1 papillary disease only.

All patients received nadofaragene firadenovec once every 3 months for up four doses, with additional dosing at the investigator’s discretion. Although the trial was designated as phase 3, it did not have the typical randomized comparative design.

“The challenge in the BCG-unresponsive disease state is that, historically, there has been no validated good comparator to use here; there’s no standard of care for these patients,” Dr. Boorjian explained, noting that the design was chosen after discussion with the Food and Drug Administration.
 

Efficacy

The complete response rate among CIS patients at any time after instillation, the trial’s primary objective, was 53.4%. All of these responses occurred after a single dose of nadofaragene firadenovec. Responses were considered durable, as 45.5% of CIS patients who had a complete response at 3 months still had a complete response at 12 months.

The rate of high-grade recurrence-free survival at 3 months was 59.6% in the overall population, 53.4% in patients with CIS, and 72.9% in patients with papillary disease. At 12 months, the rate of high-grade recurrence-free survival was 30.5%, 24.3%, and 43.8%, respectively.

The rate of high-grade recurrence without muscle invasive bladder cancer was 71.8% in the CIS group and 52.1% in the papillary group. The rate of progression to muscle invasive bladder cancer or more advanced disease was 4.9% and 6.3%, respectively. The overall 2-year rate of cystectomy-free survival was 64%, and there were no bladder cancer deaths.
 

Safety

Nadofaragene firadenovec was considered safe and well tolerated. The most common study drug–related adverse events were irritative voiding symptoms, such as discharge, bladder spasm, micturition urgency, and hematuria.

Although 70.1% of patients experienced a local or systemic adverse event related to the study drug or procedure, few experienced serious adverse events (1.9%), grade 3 adverse events (3.8%), or treatment-emergent adverse events leading to discontinuation (1.9%). The serious adverse events were sepsis, syncope, and hematuria.
 

Next steps

“Nadofaragene firadenovec represents a promising option for patients with BCG-unresponsive [non–muscle invasive bladder cancer],” Dr. Boorjian said. “What we want to see going forward is durability of response, cystectomy-free survival, and metastasis-free and cancer-specific survival. Those are the harder endpoints that, as these data mature, we will want to see so that we are able to counsel our patients accordingly.”

Susan London/MDedge News
Dr. Guru Sonpavde

The FDA recently approved pembrolizumab for this patient population, noted session cochair Guru Sonpavde, MD, of the Dana-Farber Cancer Institute in Boston.

“But nadofaragene firadenovec is much less toxic, it is given intravesically, and it’s only given once every 3 months,” he said. “The outcomes at the 1-year point look similar in terms of the durable complete response rate. So we hope that this therapy will be able to get to the clinic, but we have to wait for the FDA to decide.”

It remains to be seen how nadofaragene firadenovec compares with other emerging therapies for high-risk BCG-unresponsive non–muscle invasive bladder cancer, including pembrolizumab and potentially intravesical oportuzumab monatox (a targeted immunotoxin) and intravesical combination BCG and superagonist interleukin-15 (ALT-803), according to Dr. Boorjian.

“A unique feature of the trial I presented was that the results were validated by a mandatory 12-month study biopsy, which has not been the case in other trials,” he pointed out. “So this separates it a little bit when you are looking at pathologic response rates and high-grade recurrence–free rates. They are based on pathologic confirmation.”

Evaluators will ultimately compare these therapies on safety, efficacy, ease of administration, delivery schedule, and cost, Dr. Boorjian said. “At this stage, it’s very difficult to start to say which agent is going to be placed where in our management paradigm. We have to go step by step: Do the trial that we did, show our data, put it out for review, and then allow the community to engage in a discussion about which agent, and why, for which patient.”

This trial was funded by FKD Therapies Oy. Dr. Boorjian disclosed relationships with Ferring and Sanofi. Dr. Sonpavde disclosed relationships with many companies.

SOURCE: Boorjian SA et al. GUCS 2020, Abstract 442.

A novel gene therapy may expand treatment options for non–muscle invasive bladder cancer that does not respond to Bacillus Calmette-Guerin (BCG), new research suggests.

Susan London/MDedge News
Dr. Stephen A. Boorjian

The therapy, nadofaragene firadenovec, is a recombinant adenovirus that is instilled into the bladder and delivers the human interferon alpha-2b gene, leading to expression of the immune cytokine.

At 3 months, nadofaragene firadenovec had produced a complete response in 53.4% of patients with carcinoma in situ (CIS), and the rate of high-grade recurrence-free survival was 59.6% in all patients. Although most patients (70.1%) experienced adverse events in this trial, few had serious events (1.9%).

Stephen A. Boorjian, MD, of the Mayo Clinic in Rochester, Minn., presented these results at the 2020 Genitourinary Cancers Symposium, sponsored by the American Society for Clinical Oncology, ASTRO, and the Society of Urologic Oncology.

“The optimal management for patients with BCG-unresponsive non–muscle invasive bladder cancer remains to be established,” Dr. Boorjian said. “National and organizational guidelines recommend radical cystectomy in this setting, but we have to acknowledge that many of our patients will be either unwilling or unfit to undergo what is often a highly morbid operation.”

Dr. Boorjian and coinvestigators tested nadofaragene firadenovec in 107 patients with CIS, with or without high-grade Ta or T1 papillary disease, as well as 50 patients with high-grade Ta or T1 papillary disease only.

All patients received nadofaragene firadenovec once every 3 months for up four doses, with additional dosing at the investigator’s discretion. Although the trial was designated as phase 3, it did not have the typical randomized comparative design.

“The challenge in the BCG-unresponsive disease state is that, historically, there has been no validated good comparator to use here; there’s no standard of care for these patients,” Dr. Boorjian explained, noting that the design was chosen after discussion with the Food and Drug Administration.
 

Efficacy

The complete response rate among CIS patients at any time after instillation, the trial’s primary objective, was 53.4%. All of these responses occurred after a single dose of nadofaragene firadenovec. Responses were considered durable, as 45.5% of CIS patients who had a complete response at 3 months still had a complete response at 12 months.

The rate of high-grade recurrence-free survival at 3 months was 59.6% in the overall population, 53.4% in patients with CIS, and 72.9% in patients with papillary disease. At 12 months, the rate of high-grade recurrence-free survival was 30.5%, 24.3%, and 43.8%, respectively.

The rate of high-grade recurrence without muscle invasive bladder cancer was 71.8% in the CIS group and 52.1% in the papillary group. The rate of progression to muscle invasive bladder cancer or more advanced disease was 4.9% and 6.3%, respectively. The overall 2-year rate of cystectomy-free survival was 64%, and there were no bladder cancer deaths.
 

Safety

Nadofaragene firadenovec was considered safe and well tolerated. The most common study drug–related adverse events were irritative voiding symptoms, such as discharge, bladder spasm, micturition urgency, and hematuria.

Although 70.1% of patients experienced a local or systemic adverse event related to the study drug or procedure, few experienced serious adverse events (1.9%), grade 3 adverse events (3.8%), or treatment-emergent adverse events leading to discontinuation (1.9%). The serious adverse events were sepsis, syncope, and hematuria.
 

Next steps

“Nadofaragene firadenovec represents a promising option for patients with BCG-unresponsive [non–muscle invasive bladder cancer],” Dr. Boorjian said. “What we want to see going forward is durability of response, cystectomy-free survival, and metastasis-free and cancer-specific survival. Those are the harder endpoints that, as these data mature, we will want to see so that we are able to counsel our patients accordingly.”

Susan London/MDedge News
Dr. Guru Sonpavde

The FDA recently approved pembrolizumab for this patient population, noted session cochair Guru Sonpavde, MD, of the Dana-Farber Cancer Institute in Boston.

“But nadofaragene firadenovec is much less toxic, it is given intravesically, and it’s only given once every 3 months,” he said. “The outcomes at the 1-year point look similar in terms of the durable complete response rate. So we hope that this therapy will be able to get to the clinic, but we have to wait for the FDA to decide.”

It remains to be seen how nadofaragene firadenovec compares with other emerging therapies for high-risk BCG-unresponsive non–muscle invasive bladder cancer, including pembrolizumab and potentially intravesical oportuzumab monatox (a targeted immunotoxin) and intravesical combination BCG and superagonist interleukin-15 (ALT-803), according to Dr. Boorjian.

“A unique feature of the trial I presented was that the results were validated by a mandatory 12-month study biopsy, which has not been the case in other trials,” he pointed out. “So this separates it a little bit when you are looking at pathologic response rates and high-grade recurrence–free rates. They are based on pathologic confirmation.”

Evaluators will ultimately compare these therapies on safety, efficacy, ease of administration, delivery schedule, and cost, Dr. Boorjian said. “At this stage, it’s very difficult to start to say which agent is going to be placed where in our management paradigm. We have to go step by step: Do the trial that we did, show our data, put it out for review, and then allow the community to engage in a discussion about which agent, and why, for which patient.”

This trial was funded by FKD Therapies Oy. Dr. Boorjian disclosed relationships with Ferring and Sanofi. Dr. Sonpavde disclosed relationships with many companies.

SOURCE: Boorjian SA et al. GUCS 2020, Abstract 442.

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Should routine colon cancer screening start at 45, not 50?

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SAN FRANCISCO – For years, 50 years old has been the age at which screening for colorectal cancer (CRC) began in the United States, but recently, one group lowered the starting age to 45 years.

pixologicstudio/Thinkstock

This move by the American Cancer Society in 2018 was made in reaction to reports of an increase in the incidence of CRC in younger adults.

However, other groups have stayed with the benchmark 50 years. This includes the U.S. Preventive Services Task Force and the National Comprehensive Cancer Network.

Should the age be lowered in view of the mounting reports of an increase in CRC in younger adults? Experts argued both for and against the move here at the 2020 Gastrointestinal Cancers Symposium.

“We’re having this debate because the health of more than 20 million Americans is in the balance,” commented David Weinberg, MD, MSc, chairman of the department of medicine at Fox Chase Cancer Center in Philadelphia. “This is not just an academic discussion.” If the screening age shifts to 5 years earlier, the impact nationally would be about 30,000 colorectal cancers and 11,000 deaths averted.

“It will take about 11 million additional colonoscopies ... and the overall bill would be $10 billion. That’s not a small number, but if the country has the resources and we want to do this, I would say we can,” argued Uri Ladabaum, MD, director of the gastrointestinal cancer prevention program and the clinical chief of the division of gastroenterology and hepatology at Stanford (Calif.) University.

Lower the age

Dr. Ladabaum argued in favor of lowering the age to 45 years to start screening. “In life, 60 may be the new 40, but for colorectal cancer screening, 45 is definitely the new 50,” he said. Anticipating arguments against such a move, he focused on several points.

First, the magnitude of the problem is certainly not small, he noted, pointing to a 2017 study showing that colorectal cancer rates have increased by 1%-2.4% annually since the mid-1980s in persons aged 20-39 years and by 0.5%-1.3% since the mid-1990s in adults aged 40-54 years (J Natl Cancer Inst. 2017;109:djw322). Rectal cancer incidence has been increasing even more rapidly, at a rate of about 3.2% annually during 1974-2013 in adults aged 20-29 years.

Overall, people who were born around 1990 and later have double the risk of colon cancer (incidence rate ratio, 2.40) and quadruple the risk of rectal cancer (IRR, 4.32) as compared with those born circa 1950.

“Thus, 45- to 49-year-olds are beginning to look like yesterday’s 50- to 54-year-olds used to be,” said Dr. Ladabaum.

One issue that has been raised is lead-time bias, with the burning question: Are the cancers found in adults in their 40s simply the same ones that would have eventually been detected in their 50s? Dr. Ladabaum argued that they are not, referencing a 2019 study showing that among persons aged 40 through 49 years, the disease was diagnosed at later stages (JAMA. 2019;321:1933-4).

For those aged 40- 49 years, there was a significant increase in incidence during 1995-2015. The proportion of distant cancers increased significantly (from 21.7% to 26.6%; P less than .001), and the authors of the study had noted that this increase of 4.9% could not be explained by a decrease in unstaged cases. “In the early ’90s and mid-’90s, we began to see an increase in all stages,” Dr. Ladabaum noted. “And the most important thing here is the distant cancers over time. They’ve gone up.” If the only explanation was lead time bias in people aged 40- 49 years, then a person screened and diagnosed with cancer at age 48 would have earlier-stage disease than if it had been found at age 51. “So is this all lead-time bias?” he said. “I think the answer is no.”

Next, Dr. Ladabaum tackled the issue of whether benefit/risk ratio of CRC screening is different among younger vs. older adults. This is difficult to tease out, he suggested, as the data are sparse and there were no controlled studies to date to address that. One study from Taiwan, which looked at the outcomes of fecal immunochemical testing (FIT), showed that in different age groups, the hazard ratio for detecting cancer in those with positive results is higher in younger people vs. older ones (J Clin Gastroenterol. 2016 Oct;50[9]:761-8).

“Indirect evidence shows that if we do a FIT test and it’s positive, it probably means something,” he said. “But is there something magical that at age 50 and older – that it becomes a screenable disease, and through age 49 it’s not screenable? I would say no. Biology is not like this.”

Finally, is it cost effective to start earlier? In a modeling projection published last summer by Dr. Ladabaum and colleagues, starting at 45 years would avert about four colorectal cancers and two colorectal cancer deaths per 1,000 people, and the cohort would gain approximately 14 quality-adjusted life years (Gastroenterology. 2019;157:137-48).

“The incremental cost per quality-adjusted life year gained is highly acceptable,” said Dr. Ladabaum. “This is well within the range of what’s considered cost-effective in the United States – under $35,000 for colonoscopy, and under $8,000 for fecal immunochemical tests.”

Therefore, the answer is yes, it is cost effective, he concluded.

 

 

Not so fast ...

Arguing the case against a lowering of the starting age, Dr. Weinberg agreed with Dr. Ladabaum that colon cancer risk for younger people is rising.

That risk has increased from 5.9/100,000 to 7.2/100,000, which is a relative increase of 22%, he noted.

“That is what newspapers will want to put on their headlines to sensationalize it – that the risk of colon cancer for young people is up by over 20%,” said Dr. Weinberg. “But that represents an absolute risk of just 1.3 more people/100,000. Put in some context, 99.9% of people in their 40s will not develop colon cancer.”

This observation was not to “make light of the remainder,” he emphasized, but “the overwhelming majority are not going to get this disease at this age,” he noted.

“It’s also not entirely clear that starting screening at 45 is the right answer,” he added.

“Taken to a somewhat ridiculous extreme,” he continued, “why not start at 40? You’ll catch more people that way, but no one is advocating that.”

A better understanding of the factors contributing to the increased CRC incidence seen in younger adults is very important, he argued, and he suggested that some of it may occur because of screening, along with factors such as obesity, diabetes, and childhood exposures.

Modeling has been done to calculate the risk and benefit of early screening, but while useful for decision making, models are “usually wrong and sit near the bottom of the evidence hierarchy.”

“Models help inform decisions, but they don’t define the standard of care,” Dr. Weinberg said. “No one would vaccinate a population based on a model.”

Dr. Weinberg also emphasized that the new recommendation from the American Cancer Society to start screening at age 45 years is qualified. This means that while “clear evidence of benefit exists,” so does uncertainty about whether “the benefits really outweigh the harms.”

The current evidence for reducing the screening age is not yet clear, he believes, and he questioned the premise that age should be the only criteria for cancer stratification.

Dr. Weinberg cited one study that looked at early-onset colon cancer (ages 18-49 years) and compared it with two groups: patients diagnosed at 50 years and older and matched controls (Clin Gastroenterol Hepatol. 2019;S1542-3565[19]31108-5). Besides age, the study authors identified several nonmodifiable risk factors that were associated with early-onset disease, including sex, race, history of inflammatory bowel disease (IBD), and family history of colorectal cancer.

“Being male was a risk factor and having a family history increased your risk by three times,” said Dr. Weinberg. “And I would note that this study had removed people, at least as best one can, who were known to have syndromic risks of early-onset colon cancer (such as familial adenomatous polyposis.”

Earlier screening (by age 40 years) should already be taking place in people with such syndromes, he commented, as well as those with a known family history and IBD. “Those recommendations were there before the ACS, and we don’t necessarily need another one,” he added.

To make things a little more confusing, a second recent study, using National Cancer Data Base data from 2004 to 2015, identified another set of factors associated with colon cancer in younger adults (Cancer. 2019 Nov 1;125:3828-35). This study showed diagnosis younger than 50 years rose only in non-Hispanic white men, in Hispanic and non-Hispanic white women, and in those living in urban vs. rural areas.

“But it gets more interesting,” Dr. Weinberg pointed out. “Risk increased over time for people in the highest zip code income quartile and those with private insurance, and risk was lower for people with Medicaid and no insurance at all,” he noted. “Well, that smacks of access to me,” he commented.

Another issue is the possibility of lead-time bias. During 1975-2015, incidence rose over time, according to Surveillance, Epidemiology, and End Results data (J Natl Cancer Inst. 2017 Aug;109:djw322). Screening of persons younger than age 49 years also more than doubled, from a low level in 2000 of about 6% to more than 15% by 2010. As screening increases, the incidence increases, Dr. Weinberg pointed out. “But mortality doesn’t change. And despite what Dr. Ladabaum said a moment ago about lead-time bias, that is textbook lead-time bias in any epidemiology study.”

Finally, it is essential to carefully weigh the benefit against the risk, Dr. Weinberg said.

A core principle of population screening is to create more future health benefits than harms, and if the screening age is lowered, several million additional colonoscopies will be performed.

Colonoscopy reduces the colorectal cancer mortality risk by about 75%, and the incidence of the disease is 7.2/100,000 in the younger age group. But colonoscopy-specific mortality – just having the test – is associated with a death rate of 7/100,000,” Dr. Weinberg pointed out. “Let’s not forget that there is a risk associated with this procedure.” (Gastrointest Endosc. 2011 Oct;74:745-52).

Dr. Weinberg emphasized that everyone wants to reduce the burden of cancer, and models are helpful for that purpose. “They’re obviously thought provoking, but they’re not adequate to drive change without additional evidence of clinical and cost-effectiveness,” he said. “These are important questions that need better data.”

He added that without changing the current screening protocol, “we could certainly emphasize more than ever the impact of family history and IBD on colon cancer risk and colon cancer prevention.”

“And certainly, there’s plenty of evidence that patients with a known family history of colon cancer are not getting screened at the right age or with the right frequency,” Dr. Weinberg concluded. “We can do better. All of us can do better.”

Dr. Weinberg has disclosed relationships with Fujifilm and Exact Sciences. Dr. Ladabaum has disclosed relationships with Lean Medical, Universal Dx, Clinical Genomics, Medtronic, Modus GI, and Quorum Consulting.
 

This article first appeared on Medscape.com.

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SAN FRANCISCO – For years, 50 years old has been the age at which screening for colorectal cancer (CRC) began in the United States, but recently, one group lowered the starting age to 45 years.

pixologicstudio/Thinkstock

This move by the American Cancer Society in 2018 was made in reaction to reports of an increase in the incidence of CRC in younger adults.

However, other groups have stayed with the benchmark 50 years. This includes the U.S. Preventive Services Task Force and the National Comprehensive Cancer Network.

Should the age be lowered in view of the mounting reports of an increase in CRC in younger adults? Experts argued both for and against the move here at the 2020 Gastrointestinal Cancers Symposium.

“We’re having this debate because the health of more than 20 million Americans is in the balance,” commented David Weinberg, MD, MSc, chairman of the department of medicine at Fox Chase Cancer Center in Philadelphia. “This is not just an academic discussion.” If the screening age shifts to 5 years earlier, the impact nationally would be about 30,000 colorectal cancers and 11,000 deaths averted.

“It will take about 11 million additional colonoscopies ... and the overall bill would be $10 billion. That’s not a small number, but if the country has the resources and we want to do this, I would say we can,” argued Uri Ladabaum, MD, director of the gastrointestinal cancer prevention program and the clinical chief of the division of gastroenterology and hepatology at Stanford (Calif.) University.

Lower the age

Dr. Ladabaum argued in favor of lowering the age to 45 years to start screening. “In life, 60 may be the new 40, but for colorectal cancer screening, 45 is definitely the new 50,” he said. Anticipating arguments against such a move, he focused on several points.

First, the magnitude of the problem is certainly not small, he noted, pointing to a 2017 study showing that colorectal cancer rates have increased by 1%-2.4% annually since the mid-1980s in persons aged 20-39 years and by 0.5%-1.3% since the mid-1990s in adults aged 40-54 years (J Natl Cancer Inst. 2017;109:djw322). Rectal cancer incidence has been increasing even more rapidly, at a rate of about 3.2% annually during 1974-2013 in adults aged 20-29 years.

Overall, people who were born around 1990 and later have double the risk of colon cancer (incidence rate ratio, 2.40) and quadruple the risk of rectal cancer (IRR, 4.32) as compared with those born circa 1950.

“Thus, 45- to 49-year-olds are beginning to look like yesterday’s 50- to 54-year-olds used to be,” said Dr. Ladabaum.

One issue that has been raised is lead-time bias, with the burning question: Are the cancers found in adults in their 40s simply the same ones that would have eventually been detected in their 50s? Dr. Ladabaum argued that they are not, referencing a 2019 study showing that among persons aged 40 through 49 years, the disease was diagnosed at later stages (JAMA. 2019;321:1933-4).

For those aged 40- 49 years, there was a significant increase in incidence during 1995-2015. The proportion of distant cancers increased significantly (from 21.7% to 26.6%; P less than .001), and the authors of the study had noted that this increase of 4.9% could not be explained by a decrease in unstaged cases. “In the early ’90s and mid-’90s, we began to see an increase in all stages,” Dr. Ladabaum noted. “And the most important thing here is the distant cancers over time. They’ve gone up.” If the only explanation was lead time bias in people aged 40- 49 years, then a person screened and diagnosed with cancer at age 48 would have earlier-stage disease than if it had been found at age 51. “So is this all lead-time bias?” he said. “I think the answer is no.”

Next, Dr. Ladabaum tackled the issue of whether benefit/risk ratio of CRC screening is different among younger vs. older adults. This is difficult to tease out, he suggested, as the data are sparse and there were no controlled studies to date to address that. One study from Taiwan, which looked at the outcomes of fecal immunochemical testing (FIT), showed that in different age groups, the hazard ratio for detecting cancer in those with positive results is higher in younger people vs. older ones (J Clin Gastroenterol. 2016 Oct;50[9]:761-8).

“Indirect evidence shows that if we do a FIT test and it’s positive, it probably means something,” he said. “But is there something magical that at age 50 and older – that it becomes a screenable disease, and through age 49 it’s not screenable? I would say no. Biology is not like this.”

Finally, is it cost effective to start earlier? In a modeling projection published last summer by Dr. Ladabaum and colleagues, starting at 45 years would avert about four colorectal cancers and two colorectal cancer deaths per 1,000 people, and the cohort would gain approximately 14 quality-adjusted life years (Gastroenterology. 2019;157:137-48).

“The incremental cost per quality-adjusted life year gained is highly acceptable,” said Dr. Ladabaum. “This is well within the range of what’s considered cost-effective in the United States – under $35,000 for colonoscopy, and under $8,000 for fecal immunochemical tests.”

Therefore, the answer is yes, it is cost effective, he concluded.

 

 

Not so fast ...

Arguing the case against a lowering of the starting age, Dr. Weinberg agreed with Dr. Ladabaum that colon cancer risk for younger people is rising.

That risk has increased from 5.9/100,000 to 7.2/100,000, which is a relative increase of 22%, he noted.

“That is what newspapers will want to put on their headlines to sensationalize it – that the risk of colon cancer for young people is up by over 20%,” said Dr. Weinberg. “But that represents an absolute risk of just 1.3 more people/100,000. Put in some context, 99.9% of people in their 40s will not develop colon cancer.”

This observation was not to “make light of the remainder,” he emphasized, but “the overwhelming majority are not going to get this disease at this age,” he noted.

“It’s also not entirely clear that starting screening at 45 is the right answer,” he added.

“Taken to a somewhat ridiculous extreme,” he continued, “why not start at 40? You’ll catch more people that way, but no one is advocating that.”

A better understanding of the factors contributing to the increased CRC incidence seen in younger adults is very important, he argued, and he suggested that some of it may occur because of screening, along with factors such as obesity, diabetes, and childhood exposures.

Modeling has been done to calculate the risk and benefit of early screening, but while useful for decision making, models are “usually wrong and sit near the bottom of the evidence hierarchy.”

“Models help inform decisions, but they don’t define the standard of care,” Dr. Weinberg said. “No one would vaccinate a population based on a model.”

Dr. Weinberg also emphasized that the new recommendation from the American Cancer Society to start screening at age 45 years is qualified. This means that while “clear evidence of benefit exists,” so does uncertainty about whether “the benefits really outweigh the harms.”

The current evidence for reducing the screening age is not yet clear, he believes, and he questioned the premise that age should be the only criteria for cancer stratification.

Dr. Weinberg cited one study that looked at early-onset colon cancer (ages 18-49 years) and compared it with two groups: patients diagnosed at 50 years and older and matched controls (Clin Gastroenterol Hepatol. 2019;S1542-3565[19]31108-5). Besides age, the study authors identified several nonmodifiable risk factors that were associated with early-onset disease, including sex, race, history of inflammatory bowel disease (IBD), and family history of colorectal cancer.

“Being male was a risk factor and having a family history increased your risk by three times,” said Dr. Weinberg. “And I would note that this study had removed people, at least as best one can, who were known to have syndromic risks of early-onset colon cancer (such as familial adenomatous polyposis.”

Earlier screening (by age 40 years) should already be taking place in people with such syndromes, he commented, as well as those with a known family history and IBD. “Those recommendations were there before the ACS, and we don’t necessarily need another one,” he added.

To make things a little more confusing, a second recent study, using National Cancer Data Base data from 2004 to 2015, identified another set of factors associated with colon cancer in younger adults (Cancer. 2019 Nov 1;125:3828-35). This study showed diagnosis younger than 50 years rose only in non-Hispanic white men, in Hispanic and non-Hispanic white women, and in those living in urban vs. rural areas.

“But it gets more interesting,” Dr. Weinberg pointed out. “Risk increased over time for people in the highest zip code income quartile and those with private insurance, and risk was lower for people with Medicaid and no insurance at all,” he noted. “Well, that smacks of access to me,” he commented.

Another issue is the possibility of lead-time bias. During 1975-2015, incidence rose over time, according to Surveillance, Epidemiology, and End Results data (J Natl Cancer Inst. 2017 Aug;109:djw322). Screening of persons younger than age 49 years also more than doubled, from a low level in 2000 of about 6% to more than 15% by 2010. As screening increases, the incidence increases, Dr. Weinberg pointed out. “But mortality doesn’t change. And despite what Dr. Ladabaum said a moment ago about lead-time bias, that is textbook lead-time bias in any epidemiology study.”

Finally, it is essential to carefully weigh the benefit against the risk, Dr. Weinberg said.

A core principle of population screening is to create more future health benefits than harms, and if the screening age is lowered, several million additional colonoscopies will be performed.

Colonoscopy reduces the colorectal cancer mortality risk by about 75%, and the incidence of the disease is 7.2/100,000 in the younger age group. But colonoscopy-specific mortality – just having the test – is associated with a death rate of 7/100,000,” Dr. Weinberg pointed out. “Let’s not forget that there is a risk associated with this procedure.” (Gastrointest Endosc. 2011 Oct;74:745-52).

Dr. Weinberg emphasized that everyone wants to reduce the burden of cancer, and models are helpful for that purpose. “They’re obviously thought provoking, but they’re not adequate to drive change without additional evidence of clinical and cost-effectiveness,” he said. “These are important questions that need better data.”

He added that without changing the current screening protocol, “we could certainly emphasize more than ever the impact of family history and IBD on colon cancer risk and colon cancer prevention.”

“And certainly, there’s plenty of evidence that patients with a known family history of colon cancer are not getting screened at the right age or with the right frequency,” Dr. Weinberg concluded. “We can do better. All of us can do better.”

Dr. Weinberg has disclosed relationships with Fujifilm and Exact Sciences. Dr. Ladabaum has disclosed relationships with Lean Medical, Universal Dx, Clinical Genomics, Medtronic, Modus GI, and Quorum Consulting.
 

This article first appeared on Medscape.com.

SAN FRANCISCO – For years, 50 years old has been the age at which screening for colorectal cancer (CRC) began in the United States, but recently, one group lowered the starting age to 45 years.

pixologicstudio/Thinkstock

This move by the American Cancer Society in 2018 was made in reaction to reports of an increase in the incidence of CRC in younger adults.

However, other groups have stayed with the benchmark 50 years. This includes the U.S. Preventive Services Task Force and the National Comprehensive Cancer Network.

Should the age be lowered in view of the mounting reports of an increase in CRC in younger adults? Experts argued both for and against the move here at the 2020 Gastrointestinal Cancers Symposium.

“We’re having this debate because the health of more than 20 million Americans is in the balance,” commented David Weinberg, MD, MSc, chairman of the department of medicine at Fox Chase Cancer Center in Philadelphia. “This is not just an academic discussion.” If the screening age shifts to 5 years earlier, the impact nationally would be about 30,000 colorectal cancers and 11,000 deaths averted.

“It will take about 11 million additional colonoscopies ... and the overall bill would be $10 billion. That’s not a small number, but if the country has the resources and we want to do this, I would say we can,” argued Uri Ladabaum, MD, director of the gastrointestinal cancer prevention program and the clinical chief of the division of gastroenterology and hepatology at Stanford (Calif.) University.

Lower the age

Dr. Ladabaum argued in favor of lowering the age to 45 years to start screening. “In life, 60 may be the new 40, but for colorectal cancer screening, 45 is definitely the new 50,” he said. Anticipating arguments against such a move, he focused on several points.

First, the magnitude of the problem is certainly not small, he noted, pointing to a 2017 study showing that colorectal cancer rates have increased by 1%-2.4% annually since the mid-1980s in persons aged 20-39 years and by 0.5%-1.3% since the mid-1990s in adults aged 40-54 years (J Natl Cancer Inst. 2017;109:djw322). Rectal cancer incidence has been increasing even more rapidly, at a rate of about 3.2% annually during 1974-2013 in adults aged 20-29 years.

Overall, people who were born around 1990 and later have double the risk of colon cancer (incidence rate ratio, 2.40) and quadruple the risk of rectal cancer (IRR, 4.32) as compared with those born circa 1950.

“Thus, 45- to 49-year-olds are beginning to look like yesterday’s 50- to 54-year-olds used to be,” said Dr. Ladabaum.

One issue that has been raised is lead-time bias, with the burning question: Are the cancers found in adults in their 40s simply the same ones that would have eventually been detected in their 50s? Dr. Ladabaum argued that they are not, referencing a 2019 study showing that among persons aged 40 through 49 years, the disease was diagnosed at later stages (JAMA. 2019;321:1933-4).

For those aged 40- 49 years, there was a significant increase in incidence during 1995-2015. The proportion of distant cancers increased significantly (from 21.7% to 26.6%; P less than .001), and the authors of the study had noted that this increase of 4.9% could not be explained by a decrease in unstaged cases. “In the early ’90s and mid-’90s, we began to see an increase in all stages,” Dr. Ladabaum noted. “And the most important thing here is the distant cancers over time. They’ve gone up.” If the only explanation was lead time bias in people aged 40- 49 years, then a person screened and diagnosed with cancer at age 48 would have earlier-stage disease than if it had been found at age 51. “So is this all lead-time bias?” he said. “I think the answer is no.”

Next, Dr. Ladabaum tackled the issue of whether benefit/risk ratio of CRC screening is different among younger vs. older adults. This is difficult to tease out, he suggested, as the data are sparse and there were no controlled studies to date to address that. One study from Taiwan, which looked at the outcomes of fecal immunochemical testing (FIT), showed that in different age groups, the hazard ratio for detecting cancer in those with positive results is higher in younger people vs. older ones (J Clin Gastroenterol. 2016 Oct;50[9]:761-8).

“Indirect evidence shows that if we do a FIT test and it’s positive, it probably means something,” he said. “But is there something magical that at age 50 and older – that it becomes a screenable disease, and through age 49 it’s not screenable? I would say no. Biology is not like this.”

Finally, is it cost effective to start earlier? In a modeling projection published last summer by Dr. Ladabaum and colleagues, starting at 45 years would avert about four colorectal cancers and two colorectal cancer deaths per 1,000 people, and the cohort would gain approximately 14 quality-adjusted life years (Gastroenterology. 2019;157:137-48).

“The incremental cost per quality-adjusted life year gained is highly acceptable,” said Dr. Ladabaum. “This is well within the range of what’s considered cost-effective in the United States – under $35,000 for colonoscopy, and under $8,000 for fecal immunochemical tests.”

Therefore, the answer is yes, it is cost effective, he concluded.

 

 

Not so fast ...

Arguing the case against a lowering of the starting age, Dr. Weinberg agreed with Dr. Ladabaum that colon cancer risk for younger people is rising.

That risk has increased from 5.9/100,000 to 7.2/100,000, which is a relative increase of 22%, he noted.

“That is what newspapers will want to put on their headlines to sensationalize it – that the risk of colon cancer for young people is up by over 20%,” said Dr. Weinberg. “But that represents an absolute risk of just 1.3 more people/100,000. Put in some context, 99.9% of people in their 40s will not develop colon cancer.”

This observation was not to “make light of the remainder,” he emphasized, but “the overwhelming majority are not going to get this disease at this age,” he noted.

“It’s also not entirely clear that starting screening at 45 is the right answer,” he added.

“Taken to a somewhat ridiculous extreme,” he continued, “why not start at 40? You’ll catch more people that way, but no one is advocating that.”

A better understanding of the factors contributing to the increased CRC incidence seen in younger adults is very important, he argued, and he suggested that some of it may occur because of screening, along with factors such as obesity, diabetes, and childhood exposures.

Modeling has been done to calculate the risk and benefit of early screening, but while useful for decision making, models are “usually wrong and sit near the bottom of the evidence hierarchy.”

“Models help inform decisions, but they don’t define the standard of care,” Dr. Weinberg said. “No one would vaccinate a population based on a model.”

Dr. Weinberg also emphasized that the new recommendation from the American Cancer Society to start screening at age 45 years is qualified. This means that while “clear evidence of benefit exists,” so does uncertainty about whether “the benefits really outweigh the harms.”

The current evidence for reducing the screening age is not yet clear, he believes, and he questioned the premise that age should be the only criteria for cancer stratification.

Dr. Weinberg cited one study that looked at early-onset colon cancer (ages 18-49 years) and compared it with two groups: patients diagnosed at 50 years and older and matched controls (Clin Gastroenterol Hepatol. 2019;S1542-3565[19]31108-5). Besides age, the study authors identified several nonmodifiable risk factors that were associated with early-onset disease, including sex, race, history of inflammatory bowel disease (IBD), and family history of colorectal cancer.

“Being male was a risk factor and having a family history increased your risk by three times,” said Dr. Weinberg. “And I would note that this study had removed people, at least as best one can, who were known to have syndromic risks of early-onset colon cancer (such as familial adenomatous polyposis.”

Earlier screening (by age 40 years) should already be taking place in people with such syndromes, he commented, as well as those with a known family history and IBD. “Those recommendations were there before the ACS, and we don’t necessarily need another one,” he added.

To make things a little more confusing, a second recent study, using National Cancer Data Base data from 2004 to 2015, identified another set of factors associated with colon cancer in younger adults (Cancer. 2019 Nov 1;125:3828-35). This study showed diagnosis younger than 50 years rose only in non-Hispanic white men, in Hispanic and non-Hispanic white women, and in those living in urban vs. rural areas.

“But it gets more interesting,” Dr. Weinberg pointed out. “Risk increased over time for people in the highest zip code income quartile and those with private insurance, and risk was lower for people with Medicaid and no insurance at all,” he noted. “Well, that smacks of access to me,” he commented.

Another issue is the possibility of lead-time bias. During 1975-2015, incidence rose over time, according to Surveillance, Epidemiology, and End Results data (J Natl Cancer Inst. 2017 Aug;109:djw322). Screening of persons younger than age 49 years also more than doubled, from a low level in 2000 of about 6% to more than 15% by 2010. As screening increases, the incidence increases, Dr. Weinberg pointed out. “But mortality doesn’t change. And despite what Dr. Ladabaum said a moment ago about lead-time bias, that is textbook lead-time bias in any epidemiology study.”

Finally, it is essential to carefully weigh the benefit against the risk, Dr. Weinberg said.

A core principle of population screening is to create more future health benefits than harms, and if the screening age is lowered, several million additional colonoscopies will be performed.

Colonoscopy reduces the colorectal cancer mortality risk by about 75%, and the incidence of the disease is 7.2/100,000 in the younger age group. But colonoscopy-specific mortality – just having the test – is associated with a death rate of 7/100,000,” Dr. Weinberg pointed out. “Let’s not forget that there is a risk associated with this procedure.” (Gastrointest Endosc. 2011 Oct;74:745-52).

Dr. Weinberg emphasized that everyone wants to reduce the burden of cancer, and models are helpful for that purpose. “They’re obviously thought provoking, but they’re not adequate to drive change without additional evidence of clinical and cost-effectiveness,” he said. “These are important questions that need better data.”

He added that without changing the current screening protocol, “we could certainly emphasize more than ever the impact of family history and IBD on colon cancer risk and colon cancer prevention.”

“And certainly, there’s plenty of evidence that patients with a known family history of colon cancer are not getting screened at the right age or with the right frequency,” Dr. Weinberg concluded. “We can do better. All of us can do better.”

Dr. Weinberg has disclosed relationships with Fujifilm and Exact Sciences. Dr. Ladabaum has disclosed relationships with Lean Medical, Universal Dx, Clinical Genomics, Medtronic, Modus GI, and Quorum Consulting.
 

This article first appeared on Medscape.com.

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Seminoma: Risk-adapted strategy could mean less toxic chemo

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SAN FRANCISCOUse of FDG-PET early in the course of chemotherapy can identify men with low-volume seminoma who have highly chemosensitive disease, enabling them to safely skip the standard chemotherapy regimen with its toxicity. This was among key findings of the phase 2 SEMITEP trial reported at the 2020 Genitourinary Cancers Symposium.

Susan London/MDedge News
Dr. Yohann Loriot

Although four cycles of etoposide-cisplatin cure almost all cases of good-prognosis metastatic seminoma (Eur Urol. 2014;65:381-6), long-term cisplatin toxicity in this predominantly young population remains problematic, noted lead investigator Yohann Loriot, MD, PhD, a medical oncologist at Gustave Roussy Institute, Villejuif, France.

In SEMITEP, he and his colleagues tested a risk-adapted strategy among 98 patients with metastatic seminoma who met International Germ Cell Cancer Collaboration Group criteria for good prognosis and had not received any chemotherapy or radiotherapy.

Fully 68.4% had a negative FDG-PET result after two cycles of etoposide-cisplatin and were given only one cycle of carboplatin to complete treatment (based on that drug’s activity in low-volume disease), Dr. Loriot reported. The rest went on to receive an additional two cycles of etoposide-cisplatin, completing the standard regimen.

At 3 years, 9 in 10 patients were alive and free of progression in both the deescalated chemotherapy group and the standard chemotherapy group. The cumulative incidence of peripheral neuropathy, however, was about 10 times higher in the standard chemotherapy group.

“Deescalating chemotherapy based on an early FDG-PET is safe and feasible in metastatic seminoma,” Dr. Loriot said. “This strategy provides shorter treatment, reduces neuropathy, and eliminates need for bleomycin and its associated toxicity. SEMITEP supports the deescalating strategy in metastatic seminoma.”

Ready for prime time?

The SEMITEP trial achieved the main goal of reducing toxicity but had several noteworthy caveats, according to invited discussant Peter Albers, MD, professor and chairman of the department of urology, Heinrich-Heine University Düsseldorf, Germany.

Susan London/MDedge News
Dr. Peter Albers

First, in an “astonishing” feat, FDG-PET was performed and evaluable after just two cycles of chemotherapy, or 3 weeks, when typical practice is to wait until 8 or 10 weeks, he said.

“Second, I really don’t understand why carboplatin was given in an FDG-PET–negative seminoma,” Dr. Albers said. “There is, in my view, no reason to add another chemotherapy agent to this patient population if you really claim this to be a biomarker. Carboplatin is known to be inferior to cisplatin in metastatic seminoma.”

Third, enrolled patients predominantly had low-volume disease, with about two-thirds having clinical stage IIA or IIB. “So this study is not representative for all metastatic seminoma patients,” Dr. Albers cautioned. “But obviously, it gives a good signal, and those patients who had IIC disease in the deescalation arm have shown no recurrences so far.

“This trial is important and obviously accurately done, but to my mind, it’s not yet practice-changing. We need a clear comparison to standard treatment before we introduce FDG-PET as a biomarker in this indication,” he concluded, recommending that, for now, risk-stratified approaches should be limited to clinical trials.

 

 

Study details

Although 72% of patients in SEMITEP had a negative early FDG-PET result, four of them requested standard chemotherapy anyway and were analyzed in that group, Dr. Loriot noted at the symposium, which was sponsored by the American Society of Clinical Oncology, ASTRO, and the Society of Urologic Oncology.

With a median follow-up of 33.9 months, the 36-month rate of progression-free survival was 89.9% in the deescalated chemotherapy group, essentially the same as the 90% in the standard chemotherapy group. There were no deaths during follow-up in either group.

During chemotherapy, the deescalation group had lower rates of grade 3 or 4 nausea and vomiting and ototoxicity, and a higher rate of grade 3 or 4 thrombocytopenia.

At 3 years, the cumulative incidence of any-grade peripheral neuropathy was less than 5% in the deescalated chemotherapy group, compared with about 50% in the standard chemotherapy group (P less than .001). There was also a trend toward a lower incidence of ototoxicity with deescalation.

The trial was funded by Institut National du Cancer (Programme Hospitalier de Recherche Clinique). Dr. Loriot disclosed no relevant conflicts of interest. Dr. Albers disclosed relationships with Sanofi, Roche, and Merck Sharp & Dohme Corp.

SOURCE: Loriot Y et al. GUCS 2020. Abstract 387.

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SAN FRANCISCOUse of FDG-PET early in the course of chemotherapy can identify men with low-volume seminoma who have highly chemosensitive disease, enabling them to safely skip the standard chemotherapy regimen with its toxicity. This was among key findings of the phase 2 SEMITEP trial reported at the 2020 Genitourinary Cancers Symposium.

Susan London/MDedge News
Dr. Yohann Loriot

Although four cycles of etoposide-cisplatin cure almost all cases of good-prognosis metastatic seminoma (Eur Urol. 2014;65:381-6), long-term cisplatin toxicity in this predominantly young population remains problematic, noted lead investigator Yohann Loriot, MD, PhD, a medical oncologist at Gustave Roussy Institute, Villejuif, France.

In SEMITEP, he and his colleagues tested a risk-adapted strategy among 98 patients with metastatic seminoma who met International Germ Cell Cancer Collaboration Group criteria for good prognosis and had not received any chemotherapy or radiotherapy.

Fully 68.4% had a negative FDG-PET result after two cycles of etoposide-cisplatin and were given only one cycle of carboplatin to complete treatment (based on that drug’s activity in low-volume disease), Dr. Loriot reported. The rest went on to receive an additional two cycles of etoposide-cisplatin, completing the standard regimen.

At 3 years, 9 in 10 patients were alive and free of progression in both the deescalated chemotherapy group and the standard chemotherapy group. The cumulative incidence of peripheral neuropathy, however, was about 10 times higher in the standard chemotherapy group.

“Deescalating chemotherapy based on an early FDG-PET is safe and feasible in metastatic seminoma,” Dr. Loriot said. “This strategy provides shorter treatment, reduces neuropathy, and eliminates need for bleomycin and its associated toxicity. SEMITEP supports the deescalating strategy in metastatic seminoma.”

Ready for prime time?

The SEMITEP trial achieved the main goal of reducing toxicity but had several noteworthy caveats, according to invited discussant Peter Albers, MD, professor and chairman of the department of urology, Heinrich-Heine University Düsseldorf, Germany.

Susan London/MDedge News
Dr. Peter Albers

First, in an “astonishing” feat, FDG-PET was performed and evaluable after just two cycles of chemotherapy, or 3 weeks, when typical practice is to wait until 8 or 10 weeks, he said.

“Second, I really don’t understand why carboplatin was given in an FDG-PET–negative seminoma,” Dr. Albers said. “There is, in my view, no reason to add another chemotherapy agent to this patient population if you really claim this to be a biomarker. Carboplatin is known to be inferior to cisplatin in metastatic seminoma.”

Third, enrolled patients predominantly had low-volume disease, with about two-thirds having clinical stage IIA or IIB. “So this study is not representative for all metastatic seminoma patients,” Dr. Albers cautioned. “But obviously, it gives a good signal, and those patients who had IIC disease in the deescalation arm have shown no recurrences so far.

“This trial is important and obviously accurately done, but to my mind, it’s not yet practice-changing. We need a clear comparison to standard treatment before we introduce FDG-PET as a biomarker in this indication,” he concluded, recommending that, for now, risk-stratified approaches should be limited to clinical trials.

 

 

Study details

Although 72% of patients in SEMITEP had a negative early FDG-PET result, four of them requested standard chemotherapy anyway and were analyzed in that group, Dr. Loriot noted at the symposium, which was sponsored by the American Society of Clinical Oncology, ASTRO, and the Society of Urologic Oncology.

With a median follow-up of 33.9 months, the 36-month rate of progression-free survival was 89.9% in the deescalated chemotherapy group, essentially the same as the 90% in the standard chemotherapy group. There were no deaths during follow-up in either group.

During chemotherapy, the deescalation group had lower rates of grade 3 or 4 nausea and vomiting and ototoxicity, and a higher rate of grade 3 or 4 thrombocytopenia.

At 3 years, the cumulative incidence of any-grade peripheral neuropathy was less than 5% in the deescalated chemotherapy group, compared with about 50% in the standard chemotherapy group (P less than .001). There was also a trend toward a lower incidence of ototoxicity with deescalation.

The trial was funded by Institut National du Cancer (Programme Hospitalier de Recherche Clinique). Dr. Loriot disclosed no relevant conflicts of interest. Dr. Albers disclosed relationships with Sanofi, Roche, and Merck Sharp & Dohme Corp.

SOURCE: Loriot Y et al. GUCS 2020. Abstract 387.

SAN FRANCISCOUse of FDG-PET early in the course of chemotherapy can identify men with low-volume seminoma who have highly chemosensitive disease, enabling them to safely skip the standard chemotherapy regimen with its toxicity. This was among key findings of the phase 2 SEMITEP trial reported at the 2020 Genitourinary Cancers Symposium.

Susan London/MDedge News
Dr. Yohann Loriot

Although four cycles of etoposide-cisplatin cure almost all cases of good-prognosis metastatic seminoma (Eur Urol. 2014;65:381-6), long-term cisplatin toxicity in this predominantly young population remains problematic, noted lead investigator Yohann Loriot, MD, PhD, a medical oncologist at Gustave Roussy Institute, Villejuif, France.

In SEMITEP, he and his colleagues tested a risk-adapted strategy among 98 patients with metastatic seminoma who met International Germ Cell Cancer Collaboration Group criteria for good prognosis and had not received any chemotherapy or radiotherapy.

Fully 68.4% had a negative FDG-PET result after two cycles of etoposide-cisplatin and were given only one cycle of carboplatin to complete treatment (based on that drug’s activity in low-volume disease), Dr. Loriot reported. The rest went on to receive an additional two cycles of etoposide-cisplatin, completing the standard regimen.

At 3 years, 9 in 10 patients were alive and free of progression in both the deescalated chemotherapy group and the standard chemotherapy group. The cumulative incidence of peripheral neuropathy, however, was about 10 times higher in the standard chemotherapy group.

“Deescalating chemotherapy based on an early FDG-PET is safe and feasible in metastatic seminoma,” Dr. Loriot said. “This strategy provides shorter treatment, reduces neuropathy, and eliminates need for bleomycin and its associated toxicity. SEMITEP supports the deescalating strategy in metastatic seminoma.”

Ready for prime time?

The SEMITEP trial achieved the main goal of reducing toxicity but had several noteworthy caveats, according to invited discussant Peter Albers, MD, professor and chairman of the department of urology, Heinrich-Heine University Düsseldorf, Germany.

Susan London/MDedge News
Dr. Peter Albers

First, in an “astonishing” feat, FDG-PET was performed and evaluable after just two cycles of chemotherapy, or 3 weeks, when typical practice is to wait until 8 or 10 weeks, he said.

“Second, I really don’t understand why carboplatin was given in an FDG-PET–negative seminoma,” Dr. Albers said. “There is, in my view, no reason to add another chemotherapy agent to this patient population if you really claim this to be a biomarker. Carboplatin is known to be inferior to cisplatin in metastatic seminoma.”

Third, enrolled patients predominantly had low-volume disease, with about two-thirds having clinical stage IIA or IIB. “So this study is not representative for all metastatic seminoma patients,” Dr. Albers cautioned. “But obviously, it gives a good signal, and those patients who had IIC disease in the deescalation arm have shown no recurrences so far.

“This trial is important and obviously accurately done, but to my mind, it’s not yet practice-changing. We need a clear comparison to standard treatment before we introduce FDG-PET as a biomarker in this indication,” he concluded, recommending that, for now, risk-stratified approaches should be limited to clinical trials.

 

 

Study details

Although 72% of patients in SEMITEP had a negative early FDG-PET result, four of them requested standard chemotherapy anyway and were analyzed in that group, Dr. Loriot noted at the symposium, which was sponsored by the American Society of Clinical Oncology, ASTRO, and the Society of Urologic Oncology.

With a median follow-up of 33.9 months, the 36-month rate of progression-free survival was 89.9% in the deescalated chemotherapy group, essentially the same as the 90% in the standard chemotherapy group. There were no deaths during follow-up in either group.

During chemotherapy, the deescalation group had lower rates of grade 3 or 4 nausea and vomiting and ototoxicity, and a higher rate of grade 3 or 4 thrombocytopenia.

At 3 years, the cumulative incidence of any-grade peripheral neuropathy was less than 5% in the deescalated chemotherapy group, compared with about 50% in the standard chemotherapy group (P less than .001). There was also a trend toward a lower incidence of ototoxicity with deescalation.

The trial was funded by Institut National du Cancer (Programme Hospitalier de Recherche Clinique). Dr. Loriot disclosed no relevant conflicts of interest. Dr. Albers disclosed relationships with Sanofi, Roche, and Merck Sharp & Dohme Corp.

SOURCE: Loriot Y et al. GUCS 2020. Abstract 387.

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Psoriasis elevates cancer risk

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Psoriasis patients are at increased risk for several types of cancer, notably lymphoma and keratinocyte cancer, based on data from a systematic review and meta-analysis of more than 2 million patients.

Previous studies have identified an increased overall cancer risk in psoriasis patients, compared with the general population or controls without psoriasis, and both lymphomas and keratinocyte cancers occur more often in psoriasis patients, compared with controls, but additional larger studies have been conducted since the last meta-analysis was published in 2013, wrote Sofie Vaengebjerg, MD, of the University of Copenhagen and colleagues.

To better identify the risk of cancer in psoriasis and psoriatic arthritis patients and to explore the impact of biologics, the researchers reviewed data from 112 studies totaling 2,053,932 patients in a study published in JAMA Dermatology.

Overall, the risk of any cancer was slightly higher in psoriasis patients (risk ratio, 1.21; 95% confidence interval, 1.11-1.33), compared with controls, with a prevalence of 4.78% and an incidence rate of 11.75 per 1,000 person-years. The most common cancer among psoriasis patients was keratinocyte cancer, with a risk ratio of 2.28 (95% CI, 1.73-3.01), a prevalence of 2.55%, and an incidence rate of 4.35 per 1,000 person-years.

Other cancers with significantly elevated risk among psoriasis patients were lymphomas (RR, 1.56; 95% CI, 1.37-1.78), lung cancer (RR, 1.26; 95% CI, 1.13-1.40), and bladder cancer (RR, 1.12; 95% CI, 1.04-1.19).



No increased risk of cancer was noted among psoriasis patients who were treated with biologics. “However, patients receiving biologic agents are selected and the results might be reliant on selection bias, and studies investigating long-term safety of these drugs are still limited,” the researchers wrote.

In addition, psoriatic arthritis was not associated with any overall increase in cancer risk, with the exception of three studies showing an increased risk for breast cancer, the researchers noted. The overall cancer prevalence for psoriatic arthritis patients was 5.74%, with an incidence rate of 6.44 per 1,000 person-years.

The study findings were limited by several factors, including the inconsistencies in study design and characteristics and the small amount of data on biologic agents and psoriatic arthritis, the researchers noted. However, the results were strengthened by the large number of patients, real-world study settings, inclusion of biologics, and analysis of cancer in psoriatic arthritis patients.

“Clinicians treating patients with psoriasis should be aware of this increased risk, especially for lymphomas, as immunogenic treatment might be associated with exacerbations,” and should be aware that more research is needed to assess cancer risk associated with biologics, they concluded.

The study received no outside funding. Lead author Dr. Vaengebjerg had no financial conflicts to disclose. Several coauthors disclosed relationships with multiple companies, including AbbVie, Janssen, Novartis, Eli Lilly, LEO Pharma, UCB, Almirall, and Sanofi.

SOURCE: Vaengebjerg S et al. JAMA Dermatol. 2020 Feb 19. doi:10.1001/jamadermatol.2020.0024.

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Psoriasis patients are at increased risk for several types of cancer, notably lymphoma and keratinocyte cancer, based on data from a systematic review and meta-analysis of more than 2 million patients.

Previous studies have identified an increased overall cancer risk in psoriasis patients, compared with the general population or controls without psoriasis, and both lymphomas and keratinocyte cancers occur more often in psoriasis patients, compared with controls, but additional larger studies have been conducted since the last meta-analysis was published in 2013, wrote Sofie Vaengebjerg, MD, of the University of Copenhagen and colleagues.

To better identify the risk of cancer in psoriasis and psoriatic arthritis patients and to explore the impact of biologics, the researchers reviewed data from 112 studies totaling 2,053,932 patients in a study published in JAMA Dermatology.

Overall, the risk of any cancer was slightly higher in psoriasis patients (risk ratio, 1.21; 95% confidence interval, 1.11-1.33), compared with controls, with a prevalence of 4.78% and an incidence rate of 11.75 per 1,000 person-years. The most common cancer among psoriasis patients was keratinocyte cancer, with a risk ratio of 2.28 (95% CI, 1.73-3.01), a prevalence of 2.55%, and an incidence rate of 4.35 per 1,000 person-years.

Other cancers with significantly elevated risk among psoriasis patients were lymphomas (RR, 1.56; 95% CI, 1.37-1.78), lung cancer (RR, 1.26; 95% CI, 1.13-1.40), and bladder cancer (RR, 1.12; 95% CI, 1.04-1.19).



No increased risk of cancer was noted among psoriasis patients who were treated with biologics. “However, patients receiving biologic agents are selected and the results might be reliant on selection bias, and studies investigating long-term safety of these drugs are still limited,” the researchers wrote.

In addition, psoriatic arthritis was not associated with any overall increase in cancer risk, with the exception of three studies showing an increased risk for breast cancer, the researchers noted. The overall cancer prevalence for psoriatic arthritis patients was 5.74%, with an incidence rate of 6.44 per 1,000 person-years.

The study findings were limited by several factors, including the inconsistencies in study design and characteristics and the small amount of data on biologic agents and psoriatic arthritis, the researchers noted. However, the results were strengthened by the large number of patients, real-world study settings, inclusion of biologics, and analysis of cancer in psoriatic arthritis patients.

“Clinicians treating patients with psoriasis should be aware of this increased risk, especially for lymphomas, as immunogenic treatment might be associated with exacerbations,” and should be aware that more research is needed to assess cancer risk associated with biologics, they concluded.

The study received no outside funding. Lead author Dr. Vaengebjerg had no financial conflicts to disclose. Several coauthors disclosed relationships with multiple companies, including AbbVie, Janssen, Novartis, Eli Lilly, LEO Pharma, UCB, Almirall, and Sanofi.

SOURCE: Vaengebjerg S et al. JAMA Dermatol. 2020 Feb 19. doi:10.1001/jamadermatol.2020.0024.

Psoriasis patients are at increased risk for several types of cancer, notably lymphoma and keratinocyte cancer, based on data from a systematic review and meta-analysis of more than 2 million patients.

Previous studies have identified an increased overall cancer risk in psoriasis patients, compared with the general population or controls without psoriasis, and both lymphomas and keratinocyte cancers occur more often in psoriasis patients, compared with controls, but additional larger studies have been conducted since the last meta-analysis was published in 2013, wrote Sofie Vaengebjerg, MD, of the University of Copenhagen and colleagues.

To better identify the risk of cancer in psoriasis and psoriatic arthritis patients and to explore the impact of biologics, the researchers reviewed data from 112 studies totaling 2,053,932 patients in a study published in JAMA Dermatology.

Overall, the risk of any cancer was slightly higher in psoriasis patients (risk ratio, 1.21; 95% confidence interval, 1.11-1.33), compared with controls, with a prevalence of 4.78% and an incidence rate of 11.75 per 1,000 person-years. The most common cancer among psoriasis patients was keratinocyte cancer, with a risk ratio of 2.28 (95% CI, 1.73-3.01), a prevalence of 2.55%, and an incidence rate of 4.35 per 1,000 person-years.

Other cancers with significantly elevated risk among psoriasis patients were lymphomas (RR, 1.56; 95% CI, 1.37-1.78), lung cancer (RR, 1.26; 95% CI, 1.13-1.40), and bladder cancer (RR, 1.12; 95% CI, 1.04-1.19).



No increased risk of cancer was noted among psoriasis patients who were treated with biologics. “However, patients receiving biologic agents are selected and the results might be reliant on selection bias, and studies investigating long-term safety of these drugs are still limited,” the researchers wrote.

In addition, psoriatic arthritis was not associated with any overall increase in cancer risk, with the exception of three studies showing an increased risk for breast cancer, the researchers noted. The overall cancer prevalence for psoriatic arthritis patients was 5.74%, with an incidence rate of 6.44 per 1,000 person-years.

The study findings were limited by several factors, including the inconsistencies in study design and characteristics and the small amount of data on biologic agents and psoriatic arthritis, the researchers noted. However, the results were strengthened by the large number of patients, real-world study settings, inclusion of biologics, and analysis of cancer in psoriatic arthritis patients.

“Clinicians treating patients with psoriasis should be aware of this increased risk, especially for lymphomas, as immunogenic treatment might be associated with exacerbations,” and should be aware that more research is needed to assess cancer risk associated with biologics, they concluded.

The study received no outside funding. Lead author Dr. Vaengebjerg had no financial conflicts to disclose. Several coauthors disclosed relationships with multiple companies, including AbbVie, Janssen, Novartis, Eli Lilly, LEO Pharma, UCB, Almirall, and Sanofi.

SOURCE: Vaengebjerg S et al. JAMA Dermatol. 2020 Feb 19. doi:10.1001/jamadermatol.2020.0024.

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Number of sexual partners linked to cancer risk

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Mon, 06/08/2020 - 16:30

A higher lifetime number of sexual partners was associated with a greater risk of being diagnosed with cancer in older adults, according to a recent study.

Additionally, among women, having had more lifetime partners was linked to higher odds of reporting a limiting long-standing condition.

Igor Grabovac, MD, of the Medical University of Vienna, and colleagues reported these results in BMJ Sexual & Reproductive Health.

The exploratory analysis included 2,537 men and 3,185 women, aged 50 years and older, who were a part of the English Longitudinal Study of Ageing. The mean age of study subjects was 64 years in men and 65 years in women, and most were either married or cohabitating.

Researchers collected data on sexual history using a self-administered questionnaire, which privately recorded the lifetime number of sexual partners among study participants. Data on other health outcomes, such as limiting long-standing illness and cancer diagnoses, were also self-reported.

Among male participants, 28.5% reported a history of 0-1 lifetime sexual partners, 29.0% had 2-4 partners, 20.2% had 5-9 partners, and 22.2% had 10 or more partners. The respective measures in women were 40.8%, 35.5%, 15.8%, and 7.8%.

Among all participants, a greater number of sexual partners was associated with being single, younger age, and being in the least or greatest brackets of household income.

The researchers found that, compared with having 0-1 sexual partners, a lifetime history of 10 or more sexual partners was associated with a greater risk of reported cancer in both men (odds ratio, 1.69; P = .047) and women (OR, 1.91; P = .038).

In addition, women with a lifetime history of 10 or more sexual partners had greater odds of reporting a limiting long-standing condition (OR, 1.64; P = .007).

“We observed no statistically significant association between number of lifetime sexual partners and self-rated health, CHD [coronary heart disease], or stroke in either sex, or with limiting long-standing illness in men,” the researchers explained.

They acknowledged that a key limitation of the study was the self-reported nature of the data. As a result, further studies are required to establish causality.

“Sexual history may be a relevant clinical indicator for cancer risk in older patients,” they concluded.

No funding sources were reported. The authors reported having no conflicts of interest.
 

SOURCE: Grabovac I et al. BMJ Sex Reprod Health. 2020 Feb 13. doi: 10.1136/bmjsrh-2019-200352.

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A higher lifetime number of sexual partners was associated with a greater risk of being diagnosed with cancer in older adults, according to a recent study.

Additionally, among women, having had more lifetime partners was linked to higher odds of reporting a limiting long-standing condition.

Igor Grabovac, MD, of the Medical University of Vienna, and colleagues reported these results in BMJ Sexual & Reproductive Health.

The exploratory analysis included 2,537 men and 3,185 women, aged 50 years and older, who were a part of the English Longitudinal Study of Ageing. The mean age of study subjects was 64 years in men and 65 years in women, and most were either married or cohabitating.

Researchers collected data on sexual history using a self-administered questionnaire, which privately recorded the lifetime number of sexual partners among study participants. Data on other health outcomes, such as limiting long-standing illness and cancer diagnoses, were also self-reported.

Among male participants, 28.5% reported a history of 0-1 lifetime sexual partners, 29.0% had 2-4 partners, 20.2% had 5-9 partners, and 22.2% had 10 or more partners. The respective measures in women were 40.8%, 35.5%, 15.8%, and 7.8%.

Among all participants, a greater number of sexual partners was associated with being single, younger age, and being in the least or greatest brackets of household income.

The researchers found that, compared with having 0-1 sexual partners, a lifetime history of 10 or more sexual partners was associated with a greater risk of reported cancer in both men (odds ratio, 1.69; P = .047) and women (OR, 1.91; P = .038).

In addition, women with a lifetime history of 10 or more sexual partners had greater odds of reporting a limiting long-standing condition (OR, 1.64; P = .007).

“We observed no statistically significant association between number of lifetime sexual partners and self-rated health, CHD [coronary heart disease], or stroke in either sex, or with limiting long-standing illness in men,” the researchers explained.

They acknowledged that a key limitation of the study was the self-reported nature of the data. As a result, further studies are required to establish causality.

“Sexual history may be a relevant clinical indicator for cancer risk in older patients,” they concluded.

No funding sources were reported. The authors reported having no conflicts of interest.
 

SOURCE: Grabovac I et al. BMJ Sex Reprod Health. 2020 Feb 13. doi: 10.1136/bmjsrh-2019-200352.

A higher lifetime number of sexual partners was associated with a greater risk of being diagnosed with cancer in older adults, according to a recent study.

Additionally, among women, having had more lifetime partners was linked to higher odds of reporting a limiting long-standing condition.

Igor Grabovac, MD, of the Medical University of Vienna, and colleagues reported these results in BMJ Sexual & Reproductive Health.

The exploratory analysis included 2,537 men and 3,185 women, aged 50 years and older, who were a part of the English Longitudinal Study of Ageing. The mean age of study subjects was 64 years in men and 65 years in women, and most were either married or cohabitating.

Researchers collected data on sexual history using a self-administered questionnaire, which privately recorded the lifetime number of sexual partners among study participants. Data on other health outcomes, such as limiting long-standing illness and cancer diagnoses, were also self-reported.

Among male participants, 28.5% reported a history of 0-1 lifetime sexual partners, 29.0% had 2-4 partners, 20.2% had 5-9 partners, and 22.2% had 10 or more partners. The respective measures in women were 40.8%, 35.5%, 15.8%, and 7.8%.

Among all participants, a greater number of sexual partners was associated with being single, younger age, and being in the least or greatest brackets of household income.

The researchers found that, compared with having 0-1 sexual partners, a lifetime history of 10 or more sexual partners was associated with a greater risk of reported cancer in both men (odds ratio, 1.69; P = .047) and women (OR, 1.91; P = .038).

In addition, women with a lifetime history of 10 or more sexual partners had greater odds of reporting a limiting long-standing condition (OR, 1.64; P = .007).

“We observed no statistically significant association between number of lifetime sexual partners and self-rated health, CHD [coronary heart disease], or stroke in either sex, or with limiting long-standing illness in men,” the researchers explained.

They acknowledged that a key limitation of the study was the self-reported nature of the data. As a result, further studies are required to establish causality.

“Sexual history may be a relevant clinical indicator for cancer risk in older patients,” they concluded.

No funding sources were reported. The authors reported having no conflicts of interest.
 

SOURCE: Grabovac I et al. BMJ Sex Reprod Health. 2020 Feb 13. doi: 10.1136/bmjsrh-2019-200352.

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Oncologists are average in terms of happiness, survey suggests

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Mon, 02/24/2020 - 09:03

When it comes to physician happiness both in and outside the workplace, oncologists are about average, according to Medscape’s 2020 Lifestyle, Happiness, and Burnout Report.

Oncologists landed in the middle of the pack among all physicians surveyed for happiness. Rheumatologists were most likely to report being very or extremely happy outside of work (60%) and neurologists were least likely to do so (44%), but about half of oncologists (51%) reported being very/extremely happy outside of work. For happiness at work, dermatologists topped the list (41%), neurologists came in last (18%), and oncologists remained in the middle (29%).

Oncologists were average when it came to burnout as well, matching the rate of overall physicians. Specifically, 32% of oncologists were burned out, 4% were depressed, and 9% were both burned out and depressed.

The most commonly reported factors contributing to burnout among oncologists were an overabundance of bureaucratic tasks (74%), spending too many hours at work (42%), and a lack of respect from colleagues in the workplace (36%).

Exercise was the most commonly reported way oncologists dealt with burnout (51%), followed by talking with family and friends (49%), and isolating themselves from others (38%). In addition, 57% of oncologists took 3-4 weeks’ vacation, compared with 44% of physicians overall; 29% of oncologists took less than 3 weeks’ vacation.

About 18% of oncologists said they had contemplated suicide, and 1% said they’d attempted it; 72% said they’d never had thoughts of suicide. Just under one-quarter of oncologists said they were currently seeking professional help or were planning to seek help for symptoms of depression and/or burnout.

“The survey results are concerning on several levels,” Maurie Markman, MD, of Cancer Treatment Centers of America, Philadelphia, said in an interview.

“First, the data suggest a considerable number of oncologists are simply burned out from the day-to-day bureaucracy (paperwork, etc.) of medical practice, which has absolutely nothing to do with the actual care delivered. This likely impacts the willingness to continue in this role. Second, one must be concerned for the future recruitment of physicians to become clinical oncologists. And finally, one must wonder about the impact of these concerning figures on the quality of care being provided to cancer patients.”

This survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians. Oncologists made up 1% of the survey pool.

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When it comes to physician happiness both in and outside the workplace, oncologists are about average, according to Medscape’s 2020 Lifestyle, Happiness, and Burnout Report.

Oncologists landed in the middle of the pack among all physicians surveyed for happiness. Rheumatologists were most likely to report being very or extremely happy outside of work (60%) and neurologists were least likely to do so (44%), but about half of oncologists (51%) reported being very/extremely happy outside of work. For happiness at work, dermatologists topped the list (41%), neurologists came in last (18%), and oncologists remained in the middle (29%).

Oncologists were average when it came to burnout as well, matching the rate of overall physicians. Specifically, 32% of oncologists were burned out, 4% were depressed, and 9% were both burned out and depressed.

The most commonly reported factors contributing to burnout among oncologists were an overabundance of bureaucratic tasks (74%), spending too many hours at work (42%), and a lack of respect from colleagues in the workplace (36%).

Exercise was the most commonly reported way oncologists dealt with burnout (51%), followed by talking with family and friends (49%), and isolating themselves from others (38%). In addition, 57% of oncologists took 3-4 weeks’ vacation, compared with 44% of physicians overall; 29% of oncologists took less than 3 weeks’ vacation.

About 18% of oncologists said they had contemplated suicide, and 1% said they’d attempted it; 72% said they’d never had thoughts of suicide. Just under one-quarter of oncologists said they were currently seeking professional help or were planning to seek help for symptoms of depression and/or burnout.

“The survey results are concerning on several levels,” Maurie Markman, MD, of Cancer Treatment Centers of America, Philadelphia, said in an interview.

“First, the data suggest a considerable number of oncologists are simply burned out from the day-to-day bureaucracy (paperwork, etc.) of medical practice, which has absolutely nothing to do with the actual care delivered. This likely impacts the willingness to continue in this role. Second, one must be concerned for the future recruitment of physicians to become clinical oncologists. And finally, one must wonder about the impact of these concerning figures on the quality of care being provided to cancer patients.”

This survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians. Oncologists made up 1% of the survey pool.

When it comes to physician happiness both in and outside the workplace, oncologists are about average, according to Medscape’s 2020 Lifestyle, Happiness, and Burnout Report.

Oncologists landed in the middle of the pack among all physicians surveyed for happiness. Rheumatologists were most likely to report being very or extremely happy outside of work (60%) and neurologists were least likely to do so (44%), but about half of oncologists (51%) reported being very/extremely happy outside of work. For happiness at work, dermatologists topped the list (41%), neurologists came in last (18%), and oncologists remained in the middle (29%).

Oncologists were average when it came to burnout as well, matching the rate of overall physicians. Specifically, 32% of oncologists were burned out, 4% were depressed, and 9% were both burned out and depressed.

The most commonly reported factors contributing to burnout among oncologists were an overabundance of bureaucratic tasks (74%), spending too many hours at work (42%), and a lack of respect from colleagues in the workplace (36%).

Exercise was the most commonly reported way oncologists dealt with burnout (51%), followed by talking with family and friends (49%), and isolating themselves from others (38%). In addition, 57% of oncologists took 3-4 weeks’ vacation, compared with 44% of physicians overall; 29% of oncologists took less than 3 weeks’ vacation.

About 18% of oncologists said they had contemplated suicide, and 1% said they’d attempted it; 72% said they’d never had thoughts of suicide. Just under one-quarter of oncologists said they were currently seeking professional help or were planning to seek help for symptoms of depression and/or burnout.

“The survey results are concerning on several levels,” Maurie Markman, MD, of Cancer Treatment Centers of America, Philadelphia, said in an interview.

“First, the data suggest a considerable number of oncologists are simply burned out from the day-to-day bureaucracy (paperwork, etc.) of medical practice, which has absolutely nothing to do with the actual care delivered. This likely impacts the willingness to continue in this role. Second, one must be concerned for the future recruitment of physicians to become clinical oncologists. And finally, one must wonder about the impact of these concerning figures on the quality of care being provided to cancer patients.”

This survey was conducted from June 25 to Sept. 19, 2019, and involved 15,181 physicians. Oncologists made up 1% of the survey pool.

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Shorter time to metastases associated with worse RCC outcomes

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Fri, 02/14/2020 - 09:40

 

Shorter time to metastatic development was associated with shorter time to treatment failure and shorter overall survival in an international review of over 7,000 renal cell carcinoma (RCC) patients treated with first-line tyrosine kinase inhibitors.

“Patients with synchronous disease, compared with patients with metachronous disease, have more adverse prognostic features, significantly shorter TTF [time to treatment failure], and poorer survival. This may help in patient counseling and may be taken into consideration in clinical trial designs in the future, in order to avoid an imbalance between treatment arms,” wrote investigators led by Frede Donskov, MD, a clinical professor at Aarhus (Denmark) University Hospital, in European Urology Oncology.

In the largest study to date to address the impact of timing of metastases on outcomes from tyrosine kinase inhibitor (TKI) treatment, something that’s been unclear until now, Dr. Donskov and associates turned to the International Metastatic Renal Cell Carcinoma Database Consortium (IMDC) to compare outcomes of 3,906 patients with synchronous metastases, meaning metastases within 3 months of initial RCC diagnosis, with 3,480 with metachronous disease, meaning metastases after that point.

They found that more patients with synchronous versus metachronous disease had higher T stage (T1-2, 19% vs. 34%), N1 disease (21% vs. 6%), presence of sarcomatoid differentiation (15.8% vs. 7.9%), Karnofsky performance status less than 80 (25.9% vs. 15.1%), anemia (62.5% vs. 42.3%), elevated neutrophils (18.9% vs. 10.9%), elevated platelets (21.6% vs. 11.4%), bone metastases (40.4% vs. 29.8%); and IMDC poor risk (40.6% vs.11.3%).

Synchronous versus metachronous disease by intervals of more than 3-12 months, more than 1-2 years, more than 2-7 years, and more than 7 years correlated with poor TTF (5.6 months vs. 7.3, 8.0, 10.8, and 13.3 months; P less than .0001) and poor overall survival (median, 16.7 months vs. 23.8, 30.2, 34.8, and 41.7 months; P less than .0001).

On multivariable regressions adjusting for baseline variables, metachronous disease was protective versus synchronous RCC on overall survival and TTF, with a greater protective effect the longer it took for the disease to metastasize.

“Synchronous disease may represent a distinct pathologic and molecular phenotype ... a high proportion of patients with synchronous disease have tumors with punctuated evolution, harboring aggressive disease features, consolidating in worse risk factors, requiring systemic therapy earlier, and having almost half the expected survival after the initiation of targeted therapy, compared with the latest metastatic timing, as shown in our study,” the investigators wrote.

The findings “reflect the underlying aggressive tumor biology. Whether [time to metastasis] impacts outcome to checkpoint immunotherapy is yet to be elucidated,” they added.

Patients were a median of 59 years at diagnosis, and 72.9% were men. None of the synchronous patients had a surgical nephrectomy, compared with 95.4% of metachronous patients; 67.2% of patients in both groups were treated with the TKI sunitinib (Sutent).

The work was funded by the IMDC. The lead investigator reported institutional grants from Ipsen and Pfizer, maker of sunitinib.
 

SOURCE: Donskov F et al. Eur Urol Oncol. 2020 Feb 6. doi: 10.1016/j.euo.2020.01.001.

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Shorter time to metastatic development was associated with shorter time to treatment failure and shorter overall survival in an international review of over 7,000 renal cell carcinoma (RCC) patients treated with first-line tyrosine kinase inhibitors.

“Patients with synchronous disease, compared with patients with metachronous disease, have more adverse prognostic features, significantly shorter TTF [time to treatment failure], and poorer survival. This may help in patient counseling and may be taken into consideration in clinical trial designs in the future, in order to avoid an imbalance between treatment arms,” wrote investigators led by Frede Donskov, MD, a clinical professor at Aarhus (Denmark) University Hospital, in European Urology Oncology.

In the largest study to date to address the impact of timing of metastases on outcomes from tyrosine kinase inhibitor (TKI) treatment, something that’s been unclear until now, Dr. Donskov and associates turned to the International Metastatic Renal Cell Carcinoma Database Consortium (IMDC) to compare outcomes of 3,906 patients with synchronous metastases, meaning metastases within 3 months of initial RCC diagnosis, with 3,480 with metachronous disease, meaning metastases after that point.

They found that more patients with synchronous versus metachronous disease had higher T stage (T1-2, 19% vs. 34%), N1 disease (21% vs. 6%), presence of sarcomatoid differentiation (15.8% vs. 7.9%), Karnofsky performance status less than 80 (25.9% vs. 15.1%), anemia (62.5% vs. 42.3%), elevated neutrophils (18.9% vs. 10.9%), elevated platelets (21.6% vs. 11.4%), bone metastases (40.4% vs. 29.8%); and IMDC poor risk (40.6% vs.11.3%).

Synchronous versus metachronous disease by intervals of more than 3-12 months, more than 1-2 years, more than 2-7 years, and more than 7 years correlated with poor TTF (5.6 months vs. 7.3, 8.0, 10.8, and 13.3 months; P less than .0001) and poor overall survival (median, 16.7 months vs. 23.8, 30.2, 34.8, and 41.7 months; P less than .0001).

On multivariable regressions adjusting for baseline variables, metachronous disease was protective versus synchronous RCC on overall survival and TTF, with a greater protective effect the longer it took for the disease to metastasize.

“Synchronous disease may represent a distinct pathologic and molecular phenotype ... a high proportion of patients with synchronous disease have tumors with punctuated evolution, harboring aggressive disease features, consolidating in worse risk factors, requiring systemic therapy earlier, and having almost half the expected survival after the initiation of targeted therapy, compared with the latest metastatic timing, as shown in our study,” the investigators wrote.

The findings “reflect the underlying aggressive tumor biology. Whether [time to metastasis] impacts outcome to checkpoint immunotherapy is yet to be elucidated,” they added.

Patients were a median of 59 years at diagnosis, and 72.9% were men. None of the synchronous patients had a surgical nephrectomy, compared with 95.4% of metachronous patients; 67.2% of patients in both groups were treated with the TKI sunitinib (Sutent).

The work was funded by the IMDC. The lead investigator reported institutional grants from Ipsen and Pfizer, maker of sunitinib.
 

SOURCE: Donskov F et al. Eur Urol Oncol. 2020 Feb 6. doi: 10.1016/j.euo.2020.01.001.

 

Shorter time to metastatic development was associated with shorter time to treatment failure and shorter overall survival in an international review of over 7,000 renal cell carcinoma (RCC) patients treated with first-line tyrosine kinase inhibitors.

“Patients with synchronous disease, compared with patients with metachronous disease, have more adverse prognostic features, significantly shorter TTF [time to treatment failure], and poorer survival. This may help in patient counseling and may be taken into consideration in clinical trial designs in the future, in order to avoid an imbalance between treatment arms,” wrote investigators led by Frede Donskov, MD, a clinical professor at Aarhus (Denmark) University Hospital, in European Urology Oncology.

In the largest study to date to address the impact of timing of metastases on outcomes from tyrosine kinase inhibitor (TKI) treatment, something that’s been unclear until now, Dr. Donskov and associates turned to the International Metastatic Renal Cell Carcinoma Database Consortium (IMDC) to compare outcomes of 3,906 patients with synchronous metastases, meaning metastases within 3 months of initial RCC diagnosis, with 3,480 with metachronous disease, meaning metastases after that point.

They found that more patients with synchronous versus metachronous disease had higher T stage (T1-2, 19% vs. 34%), N1 disease (21% vs. 6%), presence of sarcomatoid differentiation (15.8% vs. 7.9%), Karnofsky performance status less than 80 (25.9% vs. 15.1%), anemia (62.5% vs. 42.3%), elevated neutrophils (18.9% vs. 10.9%), elevated platelets (21.6% vs. 11.4%), bone metastases (40.4% vs. 29.8%); and IMDC poor risk (40.6% vs.11.3%).

Synchronous versus metachronous disease by intervals of more than 3-12 months, more than 1-2 years, more than 2-7 years, and more than 7 years correlated with poor TTF (5.6 months vs. 7.3, 8.0, 10.8, and 13.3 months; P less than .0001) and poor overall survival (median, 16.7 months vs. 23.8, 30.2, 34.8, and 41.7 months; P less than .0001).

On multivariable regressions adjusting for baseline variables, metachronous disease was protective versus synchronous RCC on overall survival and TTF, with a greater protective effect the longer it took for the disease to metastasize.

“Synchronous disease may represent a distinct pathologic and molecular phenotype ... a high proportion of patients with synchronous disease have tumors with punctuated evolution, harboring aggressive disease features, consolidating in worse risk factors, requiring systemic therapy earlier, and having almost half the expected survival after the initiation of targeted therapy, compared with the latest metastatic timing, as shown in our study,” the investigators wrote.

The findings “reflect the underlying aggressive tumor biology. Whether [time to metastasis] impacts outcome to checkpoint immunotherapy is yet to be elucidated,” they added.

Patients were a median of 59 years at diagnosis, and 72.9% were men. None of the synchronous patients had a surgical nephrectomy, compared with 95.4% of metachronous patients; 67.2% of patients in both groups were treated with the TKI sunitinib (Sutent).

The work was funded by the IMDC. The lead investigator reported institutional grants from Ipsen and Pfizer, maker of sunitinib.
 

SOURCE: Donskov F et al. Eur Urol Oncol. 2020 Feb 6. doi: 10.1016/j.euo.2020.01.001.

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Glaring gap in CV event reporting in pivotal cancer trials

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Thu, 12/15/2022 - 17:38

Clinical trials supporting Food and Drug Adminstration approval of contemporary cancer therapies frequently failed to capture major adverse cardiovascular events (MACE) and, when they did, reported rates 2.6-fold lower than noncancer trials, new research shows.

Overall, 51.3% of trials did not report MACE, with that number reaching 57.6% in trials enrolling patients with baseline cardiovascular disease (CVD).

Nearly 40% of trials did not report any CVD events in follow-up, the authors reported online Feb. 10, 2020, in the Journal of the American College of Cardiology (2020;75:620-8).

“Even in drug classes where there were established or emerging associations with cardiotoxic events, often there were no reported heart events or cardiovascular events across years of follow-up in trials that examined hundreds or even thousands of patients. That was actually pretty surprising,” senior author Daniel Addison, MD, codirector of the cardio-oncology program at the Ohio State University Medical Center, Columbus, said in an interview.

The study was prompted by a series of events that crescendoed when his team was called to the ICU to determine whether a novel targeted agent played a role in the heart decline of a patient with acute myeloid leukemia. “I had a resident ask me a very important question: ‘How do we really know for sure that the trial actually reflects the true risk of heart events?’ to which I told him, ‘it’s difficult to know,’ ” he said.

“I think many of us rely heavily on what we see in the trials, particularly when they make it to the top journals, and quite frankly, we generally take it at face value,” Dr. Addison observed.
 

Lower Rate of Reported Events

The investigators reviewed CV events reported in 97,365 patients (median age, 61 years; 46% female) enrolled in 189 phase 2 and 3 trials supporting FDA approval of 123 anticancer drugs from 1998 to 2018. Biologic, targeted, or immune-based therapies accounted for 72.5% of drug approvals.

Over 148,138 person-years of follow-up (median trial duration, 30 months), there were 1,148 incidents of MACE (375 heart failure, 253 MIs, 180 strokes, 65 atrial fibrillation, 29 coronary revascularizations, and 246 CVD deaths). MACE rates were higher in the intervention group than in the control group (792 vs. 356; P less than .01). Among the 64 trials that excluded patients with baseline CVD, there were 269 incidents of MACE.

To put this finding in context, the researchers examined the reported incidence of MACE among some 6,000 similarly aged participants in the Multi-Ethnic Study of Atherosclerosis (MESA). The overall weighted-average incidence rate was 1,408 per 100,000 person-years among MESA participants, compared with 542 events per 100,000 person-years among oncology trial participants (716 per 100,000 in the intervention arm). This represents a reported-to-expected ratio of 0.38 – a 2.6-fold lower rate of reported events (P less than .001) – and a risk difference of 866.

Further, MACE reporting was lower by a factor of 1.7 among all cancer trial participants irrespective of baseline CVD status (reported-to-expected ratio, 0.56; risk difference, 613; P less than .001).

There was no significant difference in MACE reporting between independent or industry-sponsored trials, the authors report.
 

 

 

No malicious intent

“There are likely some that might lean toward not wanting to attribute blame to a new drug when the drug is in a study, but I really think that the leading factor is lack of awareness,” Dr. Addison said. “I’ve talked with several cancer collaborators around the country who run large clinical trials, and I think often, when an event may be brought to someone’s attention, there is a tendency to just write it off as kind of a generic expected event due to age, or just something that’s not really pertinent to the study. So they don’t really focus on it as much.”

“Closer collaboration between cardiologists and cancer physicians is needed to better determine true cardiac risks among patients treated with these drugs.”

Breast cancer oncologist Marc E. Lippman, MD, of Georgetown University Medical Center and Georgetown Lombardi Comprehensive Cancer Center, Washington, D.C., isn’t convinced a lack of awareness is the culprit.

“I don’t agree with that at all,” he said in an interview. “I think there are very, very clear rules and guidelines these days for adverse-event reporting. I think that’s not a very likely explanation – that it’s not on the radar.”

Part of the problem may be that some of the toxicities, particularly cardiovascular, may not emerge for years, he said. Participant screening for the trials also likely removed patients with high cardiovascular risk. “It’s very understandable to me – I’m not saying it’s good particularly – but I think it’s very understandable that, if you’re trying to develop a drug, the last thing you’d want to have is a lot of toxicity that you might have avoided by just being restrictive in who you let into the study,” Dr. Lippman said.

The underreported CVD events may also reflect the rapidly changing profile of cardiovascular toxicities associated with novel anticancer therapies.

“Providers, both cancer and noncancer, generally put cardiotoxicity in the box of anthracyclines and radiation, but particularly over the last decade, we’ve begun to understand it’s well beyond any one class of drugs,” Dr. Addison said.

“I agree completely,” Dr. Lippman said. For example, “the checkpoint inhibitors are so unbelievably different in terms of their toxicities that many people simply didn’t even know what they were getting into at first.”
 

One size does not fit all

Javid Moslehi, MD, director of the cardio-oncology program at Vanderbilt University, Nashville, Tenn., said echocardiography – recommended to detect changes in left ventricular function in patients exposed to anthracyclines or targeted agents like trastuzumab (Herceptin) – isn’t enough to address today’s cancer therapy–related CVD events.

Courtesy Joe Howell
Dr. Javed Moslehi

“Initial drugs like anthracyclines or Herceptin in cardio-oncology were associated with systolic cardiac dysfunction, whereas the majority of issues we see in the cardio-oncology clinics today are vascular, metabolic, arrhythmogenic, and inflammatory,” he said in an interview. “Echocardiography misses the big and increasingly complex picture.”

His group, for example, has been studying myocarditis associated with immunotherapies, but none of the clinical trials require screening or surveillance for myocarditis with a cardiac biomarker like troponin.

The group also recently identified 303 deaths in patients exposed to ibrutinib, a drug that revolutionized the treatment of several B-cell malignancies but is associated with higher rates of atrial fibrillation, which is also associated with increased bleeding risk. “So there’s a little bit of a double whammy there, given that we often treat atrial fibrillation with anticoagulation and where we can cause complications in patients,” Dr. Moslehi noted.

Although there needs to be closer collaboration between cardiologists and oncologists on individual trials, cardiologists also have to realize that oncology care has become very personalized, he suggested.

“What’s probably relevant for the breast cancer patient may not be relevant for the prostate cancer patient and their respective treatments,” Dr. Moslehi said. “So if we were to say, ‘every person should get an echo,’ that may be less relevant to the prostate cancer patient where treatments can cause vascular and metabolic perturbations or to the patient treated with immunotherapy who may have myocarditis, where many of the echos can be normal. There’s no one-size-fits-all for these things.”

Wearable technologies like smartwatches could play a role in improving the reporting of CVD events with novel therapies but a lot more research needs to be done to validate these tools, Dr. Addison said. “But as we continue on into the 21st century, this is going to expand and may potentially help us,” he added.

In the interim, better standardization is needed of the cardiovascular events reported in oncology trials, particularly the Common Terminology Criteria for Adverse Events (CTCAE), said Dr. Moslehi, who also serves as chair of the American Heart Association’s subcommittee on cardio-oncology.

“Cardiovascular definitions are not exactly uniform and are not consistent with what we in cardiology consider to be important or relevant,” he said. “So I think there needs to be better standardization of these definitions, specifically within the CTCAE, which is what the oncologists use to identify adverse events.”

In a linked editorial (J Am Coll Cardiol. 2020;75:629-31), Dr. Lippman and cardiologist Nanette Bishopric, MD, of the Medstar Heart and Vascular Institute in Washington, D.C., suggested it may also be time to organize a consortium that can carry out “rigorous multicenter clinical investigations to evaluate the cardiotoxicity of emerging cancer treatments,” similar to the Thrombosis in Myocardial Infarction Study Group.

“The success of this consortium in pioneering and targeting multiple generations of drugs for the treatment of MI, involving tens of thousands of patients and thousands of collaborations across multiple national borders, is a model for how to move forward in providing the new hope of cancer cure without the trade-off of years lost to heart disease,” the editorialists concluded.

The study was supported in part by National Institutes of Health grants, including a K12-CA133250 grant to Dr. Addison. Dr. Bishopric reported being on the scientific board of C&C Biopharma. Dr. Lippman reports being on the board of directors of and holding stock in Seattle Genetics. Dr. Moslehi reported having served on advisory boards for Pfizer, Novartis, Bristol-Myers Squibb, Deciphera, Audentes Pharmaceuticals, Nektar, Takeda, Ipsen, Myokardia, AstraZeneca, GlaxoSmithKline, Intrexon, and Regeneron.

This article first appeared on Medscape.com.

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Clinical trials supporting Food and Drug Adminstration approval of contemporary cancer therapies frequently failed to capture major adverse cardiovascular events (MACE) and, when they did, reported rates 2.6-fold lower than noncancer trials, new research shows.

Overall, 51.3% of trials did not report MACE, with that number reaching 57.6% in trials enrolling patients with baseline cardiovascular disease (CVD).

Nearly 40% of trials did not report any CVD events in follow-up, the authors reported online Feb. 10, 2020, in the Journal of the American College of Cardiology (2020;75:620-8).

“Even in drug classes where there were established or emerging associations with cardiotoxic events, often there were no reported heart events or cardiovascular events across years of follow-up in trials that examined hundreds or even thousands of patients. That was actually pretty surprising,” senior author Daniel Addison, MD, codirector of the cardio-oncology program at the Ohio State University Medical Center, Columbus, said in an interview.

The study was prompted by a series of events that crescendoed when his team was called to the ICU to determine whether a novel targeted agent played a role in the heart decline of a patient with acute myeloid leukemia. “I had a resident ask me a very important question: ‘How do we really know for sure that the trial actually reflects the true risk of heart events?’ to which I told him, ‘it’s difficult to know,’ ” he said.

“I think many of us rely heavily on what we see in the trials, particularly when they make it to the top journals, and quite frankly, we generally take it at face value,” Dr. Addison observed.
 

Lower Rate of Reported Events

The investigators reviewed CV events reported in 97,365 patients (median age, 61 years; 46% female) enrolled in 189 phase 2 and 3 trials supporting FDA approval of 123 anticancer drugs from 1998 to 2018. Biologic, targeted, or immune-based therapies accounted for 72.5% of drug approvals.

Over 148,138 person-years of follow-up (median trial duration, 30 months), there were 1,148 incidents of MACE (375 heart failure, 253 MIs, 180 strokes, 65 atrial fibrillation, 29 coronary revascularizations, and 246 CVD deaths). MACE rates were higher in the intervention group than in the control group (792 vs. 356; P less than .01). Among the 64 trials that excluded patients with baseline CVD, there were 269 incidents of MACE.

To put this finding in context, the researchers examined the reported incidence of MACE among some 6,000 similarly aged participants in the Multi-Ethnic Study of Atherosclerosis (MESA). The overall weighted-average incidence rate was 1,408 per 100,000 person-years among MESA participants, compared with 542 events per 100,000 person-years among oncology trial participants (716 per 100,000 in the intervention arm). This represents a reported-to-expected ratio of 0.38 – a 2.6-fold lower rate of reported events (P less than .001) – and a risk difference of 866.

Further, MACE reporting was lower by a factor of 1.7 among all cancer trial participants irrespective of baseline CVD status (reported-to-expected ratio, 0.56; risk difference, 613; P less than .001).

There was no significant difference in MACE reporting between independent or industry-sponsored trials, the authors report.
 

 

 

No malicious intent

“There are likely some that might lean toward not wanting to attribute blame to a new drug when the drug is in a study, but I really think that the leading factor is lack of awareness,” Dr. Addison said. “I’ve talked with several cancer collaborators around the country who run large clinical trials, and I think often, when an event may be brought to someone’s attention, there is a tendency to just write it off as kind of a generic expected event due to age, or just something that’s not really pertinent to the study. So they don’t really focus on it as much.”

“Closer collaboration between cardiologists and cancer physicians is needed to better determine true cardiac risks among patients treated with these drugs.”

Breast cancer oncologist Marc E. Lippman, MD, of Georgetown University Medical Center and Georgetown Lombardi Comprehensive Cancer Center, Washington, D.C., isn’t convinced a lack of awareness is the culprit.

“I don’t agree with that at all,” he said in an interview. “I think there are very, very clear rules and guidelines these days for adverse-event reporting. I think that’s not a very likely explanation – that it’s not on the radar.”

Part of the problem may be that some of the toxicities, particularly cardiovascular, may not emerge for years, he said. Participant screening for the trials also likely removed patients with high cardiovascular risk. “It’s very understandable to me – I’m not saying it’s good particularly – but I think it’s very understandable that, if you’re trying to develop a drug, the last thing you’d want to have is a lot of toxicity that you might have avoided by just being restrictive in who you let into the study,” Dr. Lippman said.

The underreported CVD events may also reflect the rapidly changing profile of cardiovascular toxicities associated with novel anticancer therapies.

“Providers, both cancer and noncancer, generally put cardiotoxicity in the box of anthracyclines and radiation, but particularly over the last decade, we’ve begun to understand it’s well beyond any one class of drugs,” Dr. Addison said.

“I agree completely,” Dr. Lippman said. For example, “the checkpoint inhibitors are so unbelievably different in terms of their toxicities that many people simply didn’t even know what they were getting into at first.”
 

One size does not fit all

Javid Moslehi, MD, director of the cardio-oncology program at Vanderbilt University, Nashville, Tenn., said echocardiography – recommended to detect changes in left ventricular function in patients exposed to anthracyclines or targeted agents like trastuzumab (Herceptin) – isn’t enough to address today’s cancer therapy–related CVD events.

Courtesy Joe Howell
Dr. Javed Moslehi

“Initial drugs like anthracyclines or Herceptin in cardio-oncology were associated with systolic cardiac dysfunction, whereas the majority of issues we see in the cardio-oncology clinics today are vascular, metabolic, arrhythmogenic, and inflammatory,” he said in an interview. “Echocardiography misses the big and increasingly complex picture.”

His group, for example, has been studying myocarditis associated with immunotherapies, but none of the clinical trials require screening or surveillance for myocarditis with a cardiac biomarker like troponin.

The group also recently identified 303 deaths in patients exposed to ibrutinib, a drug that revolutionized the treatment of several B-cell malignancies but is associated with higher rates of atrial fibrillation, which is also associated with increased bleeding risk. “So there’s a little bit of a double whammy there, given that we often treat atrial fibrillation with anticoagulation and where we can cause complications in patients,” Dr. Moslehi noted.

Although there needs to be closer collaboration between cardiologists and oncologists on individual trials, cardiologists also have to realize that oncology care has become very personalized, he suggested.

“What’s probably relevant for the breast cancer patient may not be relevant for the prostate cancer patient and their respective treatments,” Dr. Moslehi said. “So if we were to say, ‘every person should get an echo,’ that may be less relevant to the prostate cancer patient where treatments can cause vascular and metabolic perturbations or to the patient treated with immunotherapy who may have myocarditis, where many of the echos can be normal. There’s no one-size-fits-all for these things.”

Wearable technologies like smartwatches could play a role in improving the reporting of CVD events with novel therapies but a lot more research needs to be done to validate these tools, Dr. Addison said. “But as we continue on into the 21st century, this is going to expand and may potentially help us,” he added.

In the interim, better standardization is needed of the cardiovascular events reported in oncology trials, particularly the Common Terminology Criteria for Adverse Events (CTCAE), said Dr. Moslehi, who also serves as chair of the American Heart Association’s subcommittee on cardio-oncology.

“Cardiovascular definitions are not exactly uniform and are not consistent with what we in cardiology consider to be important or relevant,” he said. “So I think there needs to be better standardization of these definitions, specifically within the CTCAE, which is what the oncologists use to identify adverse events.”

In a linked editorial (J Am Coll Cardiol. 2020;75:629-31), Dr. Lippman and cardiologist Nanette Bishopric, MD, of the Medstar Heart and Vascular Institute in Washington, D.C., suggested it may also be time to organize a consortium that can carry out “rigorous multicenter clinical investigations to evaluate the cardiotoxicity of emerging cancer treatments,” similar to the Thrombosis in Myocardial Infarction Study Group.

“The success of this consortium in pioneering and targeting multiple generations of drugs for the treatment of MI, involving tens of thousands of patients and thousands of collaborations across multiple national borders, is a model for how to move forward in providing the new hope of cancer cure without the trade-off of years lost to heart disease,” the editorialists concluded.

The study was supported in part by National Institutes of Health grants, including a K12-CA133250 grant to Dr. Addison. Dr. Bishopric reported being on the scientific board of C&C Biopharma. Dr. Lippman reports being on the board of directors of and holding stock in Seattle Genetics. Dr. Moslehi reported having served on advisory boards for Pfizer, Novartis, Bristol-Myers Squibb, Deciphera, Audentes Pharmaceuticals, Nektar, Takeda, Ipsen, Myokardia, AstraZeneca, GlaxoSmithKline, Intrexon, and Regeneron.

This article first appeared on Medscape.com.

Clinical trials supporting Food and Drug Adminstration approval of contemporary cancer therapies frequently failed to capture major adverse cardiovascular events (MACE) and, when they did, reported rates 2.6-fold lower than noncancer trials, new research shows.

Overall, 51.3% of trials did not report MACE, with that number reaching 57.6% in trials enrolling patients with baseline cardiovascular disease (CVD).

Nearly 40% of trials did not report any CVD events in follow-up, the authors reported online Feb. 10, 2020, in the Journal of the American College of Cardiology (2020;75:620-8).

“Even in drug classes where there were established or emerging associations with cardiotoxic events, often there were no reported heart events or cardiovascular events across years of follow-up in trials that examined hundreds or even thousands of patients. That was actually pretty surprising,” senior author Daniel Addison, MD, codirector of the cardio-oncology program at the Ohio State University Medical Center, Columbus, said in an interview.

The study was prompted by a series of events that crescendoed when his team was called to the ICU to determine whether a novel targeted agent played a role in the heart decline of a patient with acute myeloid leukemia. “I had a resident ask me a very important question: ‘How do we really know for sure that the trial actually reflects the true risk of heart events?’ to which I told him, ‘it’s difficult to know,’ ” he said.

“I think many of us rely heavily on what we see in the trials, particularly when they make it to the top journals, and quite frankly, we generally take it at face value,” Dr. Addison observed.
 

Lower Rate of Reported Events

The investigators reviewed CV events reported in 97,365 patients (median age, 61 years; 46% female) enrolled in 189 phase 2 and 3 trials supporting FDA approval of 123 anticancer drugs from 1998 to 2018. Biologic, targeted, or immune-based therapies accounted for 72.5% of drug approvals.

Over 148,138 person-years of follow-up (median trial duration, 30 months), there were 1,148 incidents of MACE (375 heart failure, 253 MIs, 180 strokes, 65 atrial fibrillation, 29 coronary revascularizations, and 246 CVD deaths). MACE rates were higher in the intervention group than in the control group (792 vs. 356; P less than .01). Among the 64 trials that excluded patients with baseline CVD, there were 269 incidents of MACE.

To put this finding in context, the researchers examined the reported incidence of MACE among some 6,000 similarly aged participants in the Multi-Ethnic Study of Atherosclerosis (MESA). The overall weighted-average incidence rate was 1,408 per 100,000 person-years among MESA participants, compared with 542 events per 100,000 person-years among oncology trial participants (716 per 100,000 in the intervention arm). This represents a reported-to-expected ratio of 0.38 – a 2.6-fold lower rate of reported events (P less than .001) – and a risk difference of 866.

Further, MACE reporting was lower by a factor of 1.7 among all cancer trial participants irrespective of baseline CVD status (reported-to-expected ratio, 0.56; risk difference, 613; P less than .001).

There was no significant difference in MACE reporting between independent or industry-sponsored trials, the authors report.
 

 

 

No malicious intent

“There are likely some that might lean toward not wanting to attribute blame to a new drug when the drug is in a study, but I really think that the leading factor is lack of awareness,” Dr. Addison said. “I’ve talked with several cancer collaborators around the country who run large clinical trials, and I think often, when an event may be brought to someone’s attention, there is a tendency to just write it off as kind of a generic expected event due to age, or just something that’s not really pertinent to the study. So they don’t really focus on it as much.”

“Closer collaboration between cardiologists and cancer physicians is needed to better determine true cardiac risks among patients treated with these drugs.”

Breast cancer oncologist Marc E. Lippman, MD, of Georgetown University Medical Center and Georgetown Lombardi Comprehensive Cancer Center, Washington, D.C., isn’t convinced a lack of awareness is the culprit.

“I don’t agree with that at all,” he said in an interview. “I think there are very, very clear rules and guidelines these days for adverse-event reporting. I think that’s not a very likely explanation – that it’s not on the radar.”

Part of the problem may be that some of the toxicities, particularly cardiovascular, may not emerge for years, he said. Participant screening for the trials also likely removed patients with high cardiovascular risk. “It’s very understandable to me – I’m not saying it’s good particularly – but I think it’s very understandable that, if you’re trying to develop a drug, the last thing you’d want to have is a lot of toxicity that you might have avoided by just being restrictive in who you let into the study,” Dr. Lippman said.

The underreported CVD events may also reflect the rapidly changing profile of cardiovascular toxicities associated with novel anticancer therapies.

“Providers, both cancer and noncancer, generally put cardiotoxicity in the box of anthracyclines and radiation, but particularly over the last decade, we’ve begun to understand it’s well beyond any one class of drugs,” Dr. Addison said.

“I agree completely,” Dr. Lippman said. For example, “the checkpoint inhibitors are so unbelievably different in terms of their toxicities that many people simply didn’t even know what they were getting into at first.”
 

One size does not fit all

Javid Moslehi, MD, director of the cardio-oncology program at Vanderbilt University, Nashville, Tenn., said echocardiography – recommended to detect changes in left ventricular function in patients exposed to anthracyclines or targeted agents like trastuzumab (Herceptin) – isn’t enough to address today’s cancer therapy–related CVD events.

Courtesy Joe Howell
Dr. Javed Moslehi

“Initial drugs like anthracyclines or Herceptin in cardio-oncology were associated with systolic cardiac dysfunction, whereas the majority of issues we see in the cardio-oncology clinics today are vascular, metabolic, arrhythmogenic, and inflammatory,” he said in an interview. “Echocardiography misses the big and increasingly complex picture.”

His group, for example, has been studying myocarditis associated with immunotherapies, but none of the clinical trials require screening or surveillance for myocarditis with a cardiac biomarker like troponin.

The group also recently identified 303 deaths in patients exposed to ibrutinib, a drug that revolutionized the treatment of several B-cell malignancies but is associated with higher rates of atrial fibrillation, which is also associated with increased bleeding risk. “So there’s a little bit of a double whammy there, given that we often treat atrial fibrillation with anticoagulation and where we can cause complications in patients,” Dr. Moslehi noted.

Although there needs to be closer collaboration between cardiologists and oncologists on individual trials, cardiologists also have to realize that oncology care has become very personalized, he suggested.

“What’s probably relevant for the breast cancer patient may not be relevant for the prostate cancer patient and their respective treatments,” Dr. Moslehi said. “So if we were to say, ‘every person should get an echo,’ that may be less relevant to the prostate cancer patient where treatments can cause vascular and metabolic perturbations or to the patient treated with immunotherapy who may have myocarditis, where many of the echos can be normal. There’s no one-size-fits-all for these things.”

Wearable technologies like smartwatches could play a role in improving the reporting of CVD events with novel therapies but a lot more research needs to be done to validate these tools, Dr. Addison said. “But as we continue on into the 21st century, this is going to expand and may potentially help us,” he added.

In the interim, better standardization is needed of the cardiovascular events reported in oncology trials, particularly the Common Terminology Criteria for Adverse Events (CTCAE), said Dr. Moslehi, who also serves as chair of the American Heart Association’s subcommittee on cardio-oncology.

“Cardiovascular definitions are not exactly uniform and are not consistent with what we in cardiology consider to be important or relevant,” he said. “So I think there needs to be better standardization of these definitions, specifically within the CTCAE, which is what the oncologists use to identify adverse events.”

In a linked editorial (J Am Coll Cardiol. 2020;75:629-31), Dr. Lippman and cardiologist Nanette Bishopric, MD, of the Medstar Heart and Vascular Institute in Washington, D.C., suggested it may also be time to organize a consortium that can carry out “rigorous multicenter clinical investigations to evaluate the cardiotoxicity of emerging cancer treatments,” similar to the Thrombosis in Myocardial Infarction Study Group.

“The success of this consortium in pioneering and targeting multiple generations of drugs for the treatment of MI, involving tens of thousands of patients and thousands of collaborations across multiple national borders, is a model for how to move forward in providing the new hope of cancer cure without the trade-off of years lost to heart disease,” the editorialists concluded.

The study was supported in part by National Institutes of Health grants, including a K12-CA133250 grant to Dr. Addison. Dr. Bishopric reported being on the scientific board of C&C Biopharma. Dr. Lippman reports being on the board of directors of and holding stock in Seattle Genetics. Dr. Moslehi reported having served on advisory boards for Pfizer, Novartis, Bristol-Myers Squibb, Deciphera, Audentes Pharmaceuticals, Nektar, Takeda, Ipsen, Myokardia, AstraZeneca, GlaxoSmithKline, Intrexon, and Regeneron.

This article first appeared on Medscape.com.

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Older NHL survivors show worse cognitive decline

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Mon, 06/08/2020 - 16:30

Older long-term survivors of non-Hodgkin lymphoma (NHL) may have worse cognitive outcomes compared with the noncancer aging population, according to a cross-sectional study.

The findings suggest additional research is needed to better understand cognitive decline in older survivors of NHL.

“The aim of the present study was to examine the difference in cognitive status between a group of long-term older survivors of NHL compared with a group of noncancer controls of the same age,” wrote Domenico La Carpia, MD, of Fondazione ANT Italia Onlus, Florence, Italy, and colleagues.

The researchers conducted a multicenter cross-sectional cohort study involving 63 long-term survivors of NHL and 61 age-matched controls. Their report was published in the Journal of Geriatric Oncology.

Eligible survivors and controls were aged 65 years and older. Among both groups, the mean age of study participants was 74 years, and most survivors were women (58.7%).

While cognitive decline was assessed via standardized neuropsychological testing, the team also evaluated polypharmacy, functional status, and level of multimorbidity in the cohort.

Other clinical data, including the time from complete remission, type of treatment received, and histopathological type of tumor, were collected from patient charts and included in the analysis.

After analysis, the researchers found that NHL survivors had a higher mean number of chronic conditions (3.4 vs. 2.3; P = .003), were receiving more medications (3.4 vs. 2.3; P = .03), and had worse functional status compared with controls.

In addition, survivors had impaired executive functioning compared with control subjects (Trail Making Test B-A, 47.9 vs. 32.1; P = .04), but scores on the Mini Mental State Examination (MMSE) did not differ between the groups.

“A small, statistically significant difference was also observed in verbal memory scores between the two groups,” they reported.

The researchers acknowledged that a key limitation was the cross-sectional nature of the study; hence, causality cannot be inferred from the data.

“Comprehensive geriatric assessment for older cancer survivors is advisable to identify those individuals who are at highest risk of developing disability and to implement tailored early interventions,” they concluded.

No funding sources were reported. The authors reported having no conflicts of interest.

SOURCE: La Carpia D et al. J Geriatr Oncol. 2020 Jan 31. doi: 10.1016/j.jgo.2020.01.007.

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Older long-term survivors of non-Hodgkin lymphoma (NHL) may have worse cognitive outcomes compared with the noncancer aging population, according to a cross-sectional study.

The findings suggest additional research is needed to better understand cognitive decline in older survivors of NHL.

“The aim of the present study was to examine the difference in cognitive status between a group of long-term older survivors of NHL compared with a group of noncancer controls of the same age,” wrote Domenico La Carpia, MD, of Fondazione ANT Italia Onlus, Florence, Italy, and colleagues.

The researchers conducted a multicenter cross-sectional cohort study involving 63 long-term survivors of NHL and 61 age-matched controls. Their report was published in the Journal of Geriatric Oncology.

Eligible survivors and controls were aged 65 years and older. Among both groups, the mean age of study participants was 74 years, and most survivors were women (58.7%).

While cognitive decline was assessed via standardized neuropsychological testing, the team also evaluated polypharmacy, functional status, and level of multimorbidity in the cohort.

Other clinical data, including the time from complete remission, type of treatment received, and histopathological type of tumor, were collected from patient charts and included in the analysis.

After analysis, the researchers found that NHL survivors had a higher mean number of chronic conditions (3.4 vs. 2.3; P = .003), were receiving more medications (3.4 vs. 2.3; P = .03), and had worse functional status compared with controls.

In addition, survivors had impaired executive functioning compared with control subjects (Trail Making Test B-A, 47.9 vs. 32.1; P = .04), but scores on the Mini Mental State Examination (MMSE) did not differ between the groups.

“A small, statistically significant difference was also observed in verbal memory scores between the two groups,” they reported.

The researchers acknowledged that a key limitation was the cross-sectional nature of the study; hence, causality cannot be inferred from the data.

“Comprehensive geriatric assessment for older cancer survivors is advisable to identify those individuals who are at highest risk of developing disability and to implement tailored early interventions,” they concluded.

No funding sources were reported. The authors reported having no conflicts of interest.

SOURCE: La Carpia D et al. J Geriatr Oncol. 2020 Jan 31. doi: 10.1016/j.jgo.2020.01.007.

Older long-term survivors of non-Hodgkin lymphoma (NHL) may have worse cognitive outcomes compared with the noncancer aging population, according to a cross-sectional study.

The findings suggest additional research is needed to better understand cognitive decline in older survivors of NHL.

“The aim of the present study was to examine the difference in cognitive status between a group of long-term older survivors of NHL compared with a group of noncancer controls of the same age,” wrote Domenico La Carpia, MD, of Fondazione ANT Italia Onlus, Florence, Italy, and colleagues.

The researchers conducted a multicenter cross-sectional cohort study involving 63 long-term survivors of NHL and 61 age-matched controls. Their report was published in the Journal of Geriatric Oncology.

Eligible survivors and controls were aged 65 years and older. Among both groups, the mean age of study participants was 74 years, and most survivors were women (58.7%).

While cognitive decline was assessed via standardized neuropsychological testing, the team also evaluated polypharmacy, functional status, and level of multimorbidity in the cohort.

Other clinical data, including the time from complete remission, type of treatment received, and histopathological type of tumor, were collected from patient charts and included in the analysis.

After analysis, the researchers found that NHL survivors had a higher mean number of chronic conditions (3.4 vs. 2.3; P = .003), were receiving more medications (3.4 vs. 2.3; P = .03), and had worse functional status compared with controls.

In addition, survivors had impaired executive functioning compared with control subjects (Trail Making Test B-A, 47.9 vs. 32.1; P = .04), but scores on the Mini Mental State Examination (MMSE) did not differ between the groups.

“A small, statistically significant difference was also observed in verbal memory scores between the two groups,” they reported.

The researchers acknowledged that a key limitation was the cross-sectional nature of the study; hence, causality cannot be inferred from the data.

“Comprehensive geriatric assessment for older cancer survivors is advisable to identify those individuals who are at highest risk of developing disability and to implement tailored early interventions,” they concluded.

No funding sources were reported. The authors reported having no conflicts of interest.

SOURCE: La Carpia D et al. J Geriatr Oncol. 2020 Jan 31. doi: 10.1016/j.jgo.2020.01.007.

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