Breast Cancer ICYMI

Over the past decade, the U.S. Food and Drug Administration has approved new cancer drugs twice as fast as the European Medicines Agency (EMA), often using accelerated pathways, a new analysis shows.

Between 2010 and 2019, the FDA approved almost all oncology therapies ahead of the EMA. Drugs entered the United States market about 8 months (241 days) before European market authorization.

But do quicker review times translate to wins for patients?

“The faster FDA approval process potentially provides earlier access to potentially life-prolonging medications for patients with cancer in the United States,” Ali Raza Khaki, MD, department of oncology, Stanford (Calif.) University School of Medicine, told this news organization. “On the surface, this is a good thing. However, it comes with limitations.”

Earlier drug approval often means greater uncertainty about an agent’s benefit – most notably, whether it will improve a patient’s survival or quality of life. Dr. Khaki pointed to a study published in JAMA Internal Medicine, which found that only 19 of 93 (20%) cancer drugs that had been recently approved through the FDA’s accelerated approval pathway demonstrated an improvement in overall survival.

In the new study, published online in JAMA Network Open, Dr. Khaki and colleagues found that among the 89 cancer drugs approved in the United States and Europe between January 2010 and December 2019, the FDA approved 85 (95%) before European authorization and four (5%) after.

The researchers found that the median FDA review time was half that of the EMA’s (200 vs. 426 days). Furthermore, 64 new drug applications (72%) were submitted to the FDA first, compared with 21 (23%) to the EMA.

Of the drugs approved through an accelerated pathway, three were ultimately pulled from the U.S. market, compared with one in Europe.

“These early drug approvals that later lead to withdrawal expose many more patients to toxicity, including financial toxicity, given the high cost of cancer medications,” Dr. Khaki commented.

In addition, 35 oncology therapies (39%) were approved by the FDA before trial results were published, compared with only eight (9%) by the EMA. Although FDA drug labels contain some information about efficacy and toxicity, scientific publications often have much more, including details about study populations and toxicities.

“Without this information, providers may be limited in their knowledge about patient selection, clinical benefit, and optimal toxicity management,” Dr. Khaki said.

Jeff Allen PhD, president and CEO of the nonprofit Friends of Cancer Research, who wasn’t involved in the study, believes that an FDA approval before publication shouldn’t be “particularly concerning.”

“Peer-reviewed publication is an important component of validating and communicating scientific findings, but the processes and time lines for individual journals can be highly variable,” he said. “I don’t think we would want to see a situation where potential beneficial treatments are held up due to unrelated publication processes.”

The author of an invited commentary in JAMA Network Open had a different take on the study findings.

“A tempting interpretation” of this study is that the FDA is a “superior agency for expedited review times that bring cancer drugs to patients earlier,” Kristina Jenei, BSN, MSc, with the University of British Columbia School of Population and Public Health, writes. In addition, the fact that more drugs were pulled from the market after approval in the United States than in Europe could be interpreted to mean that the system is working as it should.

Although the speed of FDA reviews and the number of subsequent approvals have increased over time, the proportion of cancer drugs that improve survival has declined. In addition, because the FDA’s follow-up of postmarketing studies has been “inconsistent,” a substantial number of cancer drugs that were approved through accelerated pathways have remained on the market for years without confirmation of their benefit.

Although regulatory agencies must balance earlier patient access to novel treatments with evidence that the therapies are effective and safe, “faster review times and approvals are not cause for celebration; better patient outcomes are,” Ms. Jenei writes. “In other words, quality over quantity.”

The study was supported by the National Cancer Institute. Dr. Khaki reported stock ownership from Merck and stock ownership from Sanofi outside the submitted work. Dr. Allen and Ms. Jenei have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Over the past decade, the U.S. Food and Drug Administration has approved new cancer drugs twice as fast as the European Medicines Agency (EMA), often using accelerated pathways, a new analysis shows.

Between 2010 and 2019, the FDA approved almost all oncology therapies ahead of the EMA. Drugs entered the United States market about 8 months (241 days) before European market authorization.

But do quicker review times translate to wins for patients?

“The faster FDA approval process potentially provides earlier access to potentially life-prolonging medications for patients with cancer in the United States,” Ali Raza Khaki, MD, department of oncology, Stanford (Calif.) University School of Medicine, told this news organization. “On the surface, this is a good thing. However, it comes with limitations.”

Earlier drug approval often means greater uncertainty about an agent’s benefit – most notably, whether it will improve a patient’s survival or quality of life. Dr. Khaki pointed to a study published in JAMA Internal Medicine, which found that only 19 of 93 (20%) cancer drugs that had been recently approved through the FDA’s accelerated approval pathway demonstrated an improvement in overall survival.

In the new study, published online in JAMA Network Open, Dr. Khaki and colleagues found that among the 89 cancer drugs approved in the United States and Europe between January 2010 and December 2019, the FDA approved 85 (95%) before European authorization and four (5%) after.

The researchers found that the median FDA review time was half that of the EMA’s (200 vs. 426 days). Furthermore, 64 new drug applications (72%) were submitted to the FDA first, compared with 21 (23%) to the EMA.

Of the drugs approved through an accelerated pathway, three were ultimately pulled from the U.S. market, compared with one in Europe.

“These early drug approvals that later lead to withdrawal expose many more patients to toxicity, including financial toxicity, given the high cost of cancer medications,” Dr. Khaki commented.

In addition, 35 oncology therapies (39%) were approved by the FDA before trial results were published, compared with only eight (9%) by the EMA. Although FDA drug labels contain some information about efficacy and toxicity, scientific publications often have much more, including details about study populations and toxicities.

“Without this information, providers may be limited in their knowledge about patient selection, clinical benefit, and optimal toxicity management,” Dr. Khaki said.

Jeff Allen PhD, president and CEO of the nonprofit Friends of Cancer Research, who wasn’t involved in the study, believes that an FDA approval before publication shouldn’t be “particularly concerning.”

“Peer-reviewed publication is an important component of validating and communicating scientific findings, but the processes and time lines for individual journals can be highly variable,” he said. “I don’t think we would want to see a situation where potential beneficial treatments are held up due to unrelated publication processes.”

The author of an invited commentary in JAMA Network Open had a different take on the study findings.

“A tempting interpretation” of this study is that the FDA is a “superior agency for expedited review times that bring cancer drugs to patients earlier,” Kristina Jenei, BSN, MSc, with the University of British Columbia School of Population and Public Health, writes. In addition, the fact that more drugs were pulled from the market after approval in the United States than in Europe could be interpreted to mean that the system is working as it should.

Although the speed of FDA reviews and the number of subsequent approvals have increased over time, the proportion of cancer drugs that improve survival has declined. In addition, because the FDA’s follow-up of postmarketing studies has been “inconsistent,” a substantial number of cancer drugs that were approved through accelerated pathways have remained on the market for years without confirmation of their benefit.

Although regulatory agencies must balance earlier patient access to novel treatments with evidence that the therapies are effective and safe, “faster review times and approvals are not cause for celebration; better patient outcomes are,” Ms. Jenei writes. “In other words, quality over quantity.”

The study was supported by the National Cancer Institute. Dr. Khaki reported stock ownership from Merck and stock ownership from Sanofi outside the submitted work. Dr. Allen and Ms. Jenei have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Over the past decade, the U.S. Food and Drug Administration has approved new cancer drugs twice as fast as the European Medicines Agency (EMA), often using accelerated pathways, a new analysis shows.

Between 2010 and 2019, the FDA approved almost all oncology therapies ahead of the EMA. Drugs entered the United States market about 8 months (241 days) before European market authorization.

But do quicker review times translate to wins for patients?

“The faster FDA approval process potentially provides earlier access to potentially life-prolonging medications for patients with cancer in the United States,” Ali Raza Khaki, MD, department of oncology, Stanford (Calif.) University School of Medicine, told this news organization. “On the surface, this is a good thing. However, it comes with limitations.”

Earlier drug approval often means greater uncertainty about an agent’s benefit – most notably, whether it will improve a patient’s survival or quality of life. Dr. Khaki pointed to a study published in JAMA Internal Medicine, which found that only 19 of 93 (20%) cancer drugs that had been recently approved through the FDA’s accelerated approval pathway demonstrated an improvement in overall survival.

In the new study, published online in JAMA Network Open, Dr. Khaki and colleagues found that among the 89 cancer drugs approved in the United States and Europe between January 2010 and December 2019, the FDA approved 85 (95%) before European authorization and four (5%) after.

The researchers found that the median FDA review time was half that of the EMA’s (200 vs. 426 days). Furthermore, 64 new drug applications (72%) were submitted to the FDA first, compared with 21 (23%) to the EMA.

Of the drugs approved through an accelerated pathway, three were ultimately pulled from the U.S. market, compared with one in Europe.

“These early drug approvals that later lead to withdrawal expose many more patients to toxicity, including financial toxicity, given the high cost of cancer medications,” Dr. Khaki commented.

In addition, 35 oncology therapies (39%) were approved by the FDA before trial results were published, compared with only eight (9%) by the EMA. Although FDA drug labels contain some information about efficacy and toxicity, scientific publications often have much more, including details about study populations and toxicities.

“Without this information, providers may be limited in their knowledge about patient selection, clinical benefit, and optimal toxicity management,” Dr. Khaki said.

Jeff Allen PhD, president and CEO of the nonprofit Friends of Cancer Research, who wasn’t involved in the study, believes that an FDA approval before publication shouldn’t be “particularly concerning.”

“Peer-reviewed publication is an important component of validating and communicating scientific findings, but the processes and time lines for individual journals can be highly variable,” he said. “I don’t think we would want to see a situation where potential beneficial treatments are held up due to unrelated publication processes.”

The author of an invited commentary in JAMA Network Open had a different take on the study findings.

“A tempting interpretation” of this study is that the FDA is a “superior agency for expedited review times that bring cancer drugs to patients earlier,” Kristina Jenei, BSN, MSc, with the University of British Columbia School of Population and Public Health, writes. In addition, the fact that more drugs were pulled from the market after approval in the United States than in Europe could be interpreted to mean that the system is working as it should.

Although the speed of FDA reviews and the number of subsequent approvals have increased over time, the proportion of cancer drugs that improve survival has declined. In addition, because the FDA’s follow-up of postmarketing studies has been “inconsistent,” a substantial number of cancer drugs that were approved through accelerated pathways have remained on the market for years without confirmation of their benefit.

Although regulatory agencies must balance earlier patient access to novel treatments with evidence that the therapies are effective and safe, “faster review times and approvals are not cause for celebration; better patient outcomes are,” Ms. Jenei writes. “In other words, quality over quantity.”

The study was supported by the National Cancer Institute. Dr. Khaki reported stock ownership from Merck and stock ownership from Sanofi outside the submitted work. Dr. Allen and Ms. Jenei have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

For most of us, the “best” time of day to work out is simple: When we can.

Maybe that’s before or after work. Or when the gym offers free daycare. Or when our favorite instructor teaches our favorite class.

That’s why we call it a “routine.” And if the results are the same, it’s hard to imagine changing it up.

But what if the results aren’t the same?

pojoslaw/Thinkstock

They may not be, according to a new study from a research team at Skidmore College in Saratoga Springs, N.Y. The results of a 12-week exercise program were different for morning versus evening workouts.

Women who worked out in the morning lost more fat, while those who trained in the evening gained more upper-body strength and power. As for men, the performance improvements were similar no matter when they exercised. But those who did so in the evening had a significant drop in blood pressure, among other benefits.

The study is part of a growing body of research showing different results for different times of day among different populations. As it turns out, when you exercise can ultimately have a big effect, not just on strength and fat loss, but also heart health, mood, and quality of sleep.
 

An accidental discovery

The original goal of the Skidmore study was to test a unique fitness program with a group of healthy, fit, and extremely active adults in early middle age.

The program includes four workouts a week, each with a different focus: strength, steady-pace endurance, high-intensity intervals, and flexibility (traditional stretching combined with yoga and Pilates exercises).

But because the group was so large – 27 women and 20 men completed the 3-month program – they had to split them into morning and evening workout groups.

It wasn’t until researchers looked at the results that they saw the differences between morning and evening exercise, says lead author Paul Arciero, PhD.

Dr. Arciero stressed that participants in every group got leaner and stronger. But the women who worked out in the morning got much bigger reductions in body fat and body-fat percentage than the evening group. Meanwhile, women in the evening group got much bigger gains in upper-body strength, power, and muscular endurance than their morning counterparts.

Among the men, the evening group had significantly larger improvements in blood pressure, cholesterol levels, and the percentage of fat they burned for energy, along with a bigger drop in feelings of fatigue.
 

Strategic timing for powerful results

Some of these findings are consistent with previous research. For example, a study published in 2021 showed that the ability to exert high effort and express strength and power peaks in the late afternoon, about the same time that your core body temperature is at its highest point.

On the other hand, you’ll probably perform better in the morning when the activity requires a lot of skill and coordination or depends on strategic decision-making.

The findings apply to both men and women.

Performance aside, exercise timing might offer strong health benefits for men with type 2 diabetes, or at high risk for it.

A study showed that men who exercised between 3 p.m. and 6 p.m. saw dramatic improvements in blood sugar management and insulin sensitivity, compared to a group that worked out between 8 a.m. and 10 a.m.

They also lost more fat during the 12-week program, even though they were doing the exact same workouts.
 

Train consistently, sleep well

When you exercise can affect your sleep quality in many ways, said neuroscientist Jennifer Heisz, PhD, of McMaster University, Hamilton, Ont.

First, she said, “exercise helps you fall asleep faster and sleep deeper at night.” (The only exception is if you exercise so intensely or so close to bedtime that your heart rate is still elevated.)

Second, “exercising at a consistent time every day helps regulate the body’s circadian rhythms.” It doesn’t matter if the exercise is in the morning, evening, or anywhere in between. As long as it’s predictable, it will help you fall asleep and wake up at the same times.

Outdoor exercise is even better, she said. The sun is the most powerful regulator of the circadian clock and works in tandem with physical activity.

Third, exercising at specific times can help you overcome jet lag or adjust to an earlier or later shift at work.

“Exercising at 7 a.m. or between 1 and 4 p.m. helps your circadian clock to ‘fall back’ in time, making it easier to wake up earlier,” Dr. Heisz said. If you need to train your body to wake up later in the morning, try working out between 7 p.m. and 10 p.m.
 

All exercise is good, but the right timing can make it even better

“The best time to exercise is when you can fit it in,” Dr. Arciero said. “You’ve got to choose the time that fits your lifestyle best.”

But context matters, he noted.

“For someone needing to achieve an improvement in their risk for cardiometabolic disease,” his study shows an advantage to working out later in the day, especially for men. If you’re more focused on building upper-body strength and power, you’ll probably get better results from training in the afternoon or evening.

And for fat loss, the Skidmore study shows better results for women who did morning workouts.

And if you’re still not sure? Try sleeping on it – preferably after your workout.

A version of this article first appeared on WebMD.com.

For most of us, the “best” time of day to work out is simple: When we can.

Maybe that’s before or after work. Or when the gym offers free daycare. Or when our favorite instructor teaches our favorite class.

That’s why we call it a “routine.” And if the results are the same, it’s hard to imagine changing it up.

But what if the results aren’t the same?

pojoslaw/Thinkstock

They may not be, according to a new study from a research team at Skidmore College in Saratoga Springs, N.Y. The results of a 12-week exercise program were different for morning versus evening workouts.

Women who worked out in the morning lost more fat, while those who trained in the evening gained more upper-body strength and power. As for men, the performance improvements were similar no matter when they exercised. But those who did so in the evening had a significant drop in blood pressure, among other benefits.

The study is part of a growing body of research showing different results for different times of day among different populations. As it turns out, when you exercise can ultimately have a big effect, not just on strength and fat loss, but also heart health, mood, and quality of sleep.
 

An accidental discovery

The original goal of the Skidmore study was to test a unique fitness program with a group of healthy, fit, and extremely active adults in early middle age.

The program includes four workouts a week, each with a different focus: strength, steady-pace endurance, high-intensity intervals, and flexibility (traditional stretching combined with yoga and Pilates exercises).

But because the group was so large – 27 women and 20 men completed the 3-month program – they had to split them into morning and evening workout groups.

It wasn’t until researchers looked at the results that they saw the differences between morning and evening exercise, says lead author Paul Arciero, PhD.

Dr. Arciero stressed that participants in every group got leaner and stronger. But the women who worked out in the morning got much bigger reductions in body fat and body-fat percentage than the evening group. Meanwhile, women in the evening group got much bigger gains in upper-body strength, power, and muscular endurance than their morning counterparts.

Among the men, the evening group had significantly larger improvements in blood pressure, cholesterol levels, and the percentage of fat they burned for energy, along with a bigger drop in feelings of fatigue.
 

Strategic timing for powerful results

Some of these findings are consistent with previous research. For example, a study published in 2021 showed that the ability to exert high effort and express strength and power peaks in the late afternoon, about the same time that your core body temperature is at its highest point.

On the other hand, you’ll probably perform better in the morning when the activity requires a lot of skill and coordination or depends on strategic decision-making.

The findings apply to both men and women.

Performance aside, exercise timing might offer strong health benefits for men with type 2 diabetes, or at high risk for it.

A study showed that men who exercised between 3 p.m. and 6 p.m. saw dramatic improvements in blood sugar management and insulin sensitivity, compared to a group that worked out between 8 a.m. and 10 a.m.

They also lost more fat during the 12-week program, even though they were doing the exact same workouts.
 

Train consistently, sleep well

When you exercise can affect your sleep quality in many ways, said neuroscientist Jennifer Heisz, PhD, of McMaster University, Hamilton, Ont.

First, she said, “exercise helps you fall asleep faster and sleep deeper at night.” (The only exception is if you exercise so intensely or so close to bedtime that your heart rate is still elevated.)

Second, “exercising at a consistent time every day helps regulate the body’s circadian rhythms.” It doesn’t matter if the exercise is in the morning, evening, or anywhere in between. As long as it’s predictable, it will help you fall asleep and wake up at the same times.

Outdoor exercise is even better, she said. The sun is the most powerful regulator of the circadian clock and works in tandem with physical activity.

Third, exercising at specific times can help you overcome jet lag or adjust to an earlier or later shift at work.

“Exercising at 7 a.m. or between 1 and 4 p.m. helps your circadian clock to ‘fall back’ in time, making it easier to wake up earlier,” Dr. Heisz said. If you need to train your body to wake up later in the morning, try working out between 7 p.m. and 10 p.m.
 

All exercise is good, but the right timing can make it even better

“The best time to exercise is when you can fit it in,” Dr. Arciero said. “You’ve got to choose the time that fits your lifestyle best.”

But context matters, he noted.

“For someone needing to achieve an improvement in their risk for cardiometabolic disease,” his study shows an advantage to working out later in the day, especially for men. If you’re more focused on building upper-body strength and power, you’ll probably get better results from training in the afternoon or evening.

And for fat loss, the Skidmore study shows better results for women who did morning workouts.

And if you’re still not sure? Try sleeping on it – preferably after your workout.

A version of this article first appeared on WebMD.com.

For most of us, the “best” time of day to work out is simple: When we can.

Maybe that’s before or after work. Or when the gym offers free daycare. Or when our favorite instructor teaches our favorite class.

That’s why we call it a “routine.” And if the results are the same, it’s hard to imagine changing it up.

But what if the results aren’t the same?

pojoslaw/Thinkstock

They may not be, according to a new study from a research team at Skidmore College in Saratoga Springs, N.Y. The results of a 12-week exercise program were different for morning versus evening workouts.

Women who worked out in the morning lost more fat, while those who trained in the evening gained more upper-body strength and power. As for men, the performance improvements were similar no matter when they exercised. But those who did so in the evening had a significant drop in blood pressure, among other benefits.

The study is part of a growing body of research showing different results for different times of day among different populations. As it turns out, when you exercise can ultimately have a big effect, not just on strength and fat loss, but also heart health, mood, and quality of sleep.
 

An accidental discovery

The original goal of the Skidmore study was to test a unique fitness program with a group of healthy, fit, and extremely active adults in early middle age.

The program includes four workouts a week, each with a different focus: strength, steady-pace endurance, high-intensity intervals, and flexibility (traditional stretching combined with yoga and Pilates exercises).

But because the group was so large – 27 women and 20 men completed the 3-month program – they had to split them into morning and evening workout groups.

It wasn’t until researchers looked at the results that they saw the differences between morning and evening exercise, says lead author Paul Arciero, PhD.

Dr. Arciero stressed that participants in every group got leaner and stronger. But the women who worked out in the morning got much bigger reductions in body fat and body-fat percentage than the evening group. Meanwhile, women in the evening group got much bigger gains in upper-body strength, power, and muscular endurance than their morning counterparts.

Among the men, the evening group had significantly larger improvements in blood pressure, cholesterol levels, and the percentage of fat they burned for energy, along with a bigger drop in feelings of fatigue.
 

Strategic timing for powerful results

Some of these findings are consistent with previous research. For example, a study published in 2021 showed that the ability to exert high effort and express strength and power peaks in the late afternoon, about the same time that your core body temperature is at its highest point.

On the other hand, you’ll probably perform better in the morning when the activity requires a lot of skill and coordination or depends on strategic decision-making.

The findings apply to both men and women.

Performance aside, exercise timing might offer strong health benefits for men with type 2 diabetes, or at high risk for it.

A study showed that men who exercised between 3 p.m. and 6 p.m. saw dramatic improvements in blood sugar management and insulin sensitivity, compared to a group that worked out between 8 a.m. and 10 a.m.

They also lost more fat during the 12-week program, even though they were doing the exact same workouts.
 

Train consistently, sleep well

When you exercise can affect your sleep quality in many ways, said neuroscientist Jennifer Heisz, PhD, of McMaster University, Hamilton, Ont.

First, she said, “exercise helps you fall asleep faster and sleep deeper at night.” (The only exception is if you exercise so intensely or so close to bedtime that your heart rate is still elevated.)

Second, “exercising at a consistent time every day helps regulate the body’s circadian rhythms.” It doesn’t matter if the exercise is in the morning, evening, or anywhere in between. As long as it’s predictable, it will help you fall asleep and wake up at the same times.

Outdoor exercise is even better, she said. The sun is the most powerful regulator of the circadian clock and works in tandem with physical activity.

Third, exercising at specific times can help you overcome jet lag or adjust to an earlier or later shift at work.

“Exercising at 7 a.m. or between 1 and 4 p.m. helps your circadian clock to ‘fall back’ in time, making it easier to wake up earlier,” Dr. Heisz said. If you need to train your body to wake up later in the morning, try working out between 7 p.m. and 10 p.m.
 

All exercise is good, but the right timing can make it even better

“The best time to exercise is when you can fit it in,” Dr. Arciero said. “You’ve got to choose the time that fits your lifestyle best.”

But context matters, he noted.

“For someone needing to achieve an improvement in their risk for cardiometabolic disease,” his study shows an advantage to working out later in the day, especially for men. If you’re more focused on building upper-body strength and power, you’ll probably get better results from training in the afternoon or evening.

And for fat loss, the Skidmore study shows better results for women who did morning workouts.

And if you’re still not sure? Try sleeping on it – preferably after your workout.

A version of this article first appeared on WebMD.com.

Although breast cancer occurs less frequently in Black women, compared with White women, they have a much higher risk of dying from the disease.

In the United States, age-adjusted breast cancer mortality between 2014 and 2018 was approximately 40% higher among Black women than among non-Hispanic White women.

This mortality gap likely reflects the fact that Black women face substantial barriers to obtaining timely, high-quality medical care, compared with White women, lead author Ismail Jatoi, MD, PhD, University of Texas Health Science Center, San Antonio, and colleagues suggest in a recent opinion piece.

The article was published online  in The New England Journal of Medicine.

When the team examined the statistics for breast cancer mortality, they found a surprise: The mortality gap between races only dates back to 1980.

Prior to 1980, mortality from breast cancer among Black women was slightly lower than White women, Dr. Jatoi and colleagues point out.

That year was a turning point in breast cancer management, as in 1980, both mammography screening and adjuvant endocrine therapy became available.

This was also when the mortality gap between the races started to show up.

It was disparities in access to the two new interventions that precipitated the divergence, as the authors suggest. Why this occurred is fairly self-evident, they comment.

“Black women are more likely than White women to lack health insurance or to have inadequate coverage, which has limited their access to mammography screening and adversely affected therapeutic decisionmaking,” researchers point out.

Moreover, both mammography screening and endocrine therapy primarily benefit patients with hormone receptor (HR)-positive breast cancer, which is equally common in Black and White patients. However, Black women have a 65% higher rate of HR-negative cancers than White women – and HR-negative tumors are often detected during the interval between mammography screening exams as palpable cancers.

Black women also have an 81% higher rate of triple-negative breast cancer, so they have benefited less from mammography screening and adjuvant endocrine therapy, both of which favor the detection and treatment of HR-positive breast cancer, the authors emphasize.

Some have suggested that the excess HR-negative breast cancer in Black women might be explained by hereditary factors. Yet as Dr. Jatoi and colleagues point out, the incidence of HR-negative breast cancer has actually been falling across all races in the United States since 1992.

However, the declines have been slower among Black women, and reductions in its incidence have been smaller among White women living in less affluent regions of the United States compared with White women from more affluent regions.

These patterns suggest that social determinants of health influence not only access to and quality of health care but also the development of HR-negative breast cancers, as the authors observe.

“If all people with breast cancer benefited equally from effective medical interventions, racial differences in mortality for individual tumor subtypes would largely reflect differences in incidence,” Dr. Jatoi and colleagues continue.

Yet the statistics show that the substantial racial disparities in mortality for both HR-positive and HR-negative cancers between Black and White women cannot be explained by differences in the incidence of either tumor alone, they write.

For example, mortality for HR-positive breast cancer is 19% higher among Black women than among White women, yet the incidence of HR-positive breast cancer is 22% lower among Black women.

Similarly, mortality from HR-negative breast cancer is over twice as high among Black women as it is among White women – a substantially larger disparity, compared with the 65% relative difference in the incidence of HR-negative breast cancer between the two races.

“Universal health care coverage could reduce disparities in treatment for cancers of all subtypes, including triple-negative breast cancer,” Dr. Jatoi and colleagues emphasize.

“Ensuring universal access to high-quality medical care can substantially narrow the racial disparity in U.S. breast-cancer mortality,” they conclude. 

The authors have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Although breast cancer occurs less frequently in Black women, compared with White women, they have a much higher risk of dying from the disease.

In the United States, age-adjusted breast cancer mortality between 2014 and 2018 was approximately 40% higher among Black women than among non-Hispanic White women.

This mortality gap likely reflects the fact that Black women face substantial barriers to obtaining timely, high-quality medical care, compared with White women, lead author Ismail Jatoi, MD, PhD, University of Texas Health Science Center, San Antonio, and colleagues suggest in a recent opinion piece.

The article was published online  in The New England Journal of Medicine.

When the team examined the statistics for breast cancer mortality, they found a surprise: The mortality gap between races only dates back to 1980.

Prior to 1980, mortality from breast cancer among Black women was slightly lower than White women, Dr. Jatoi and colleagues point out.

That year was a turning point in breast cancer management, as in 1980, both mammography screening and adjuvant endocrine therapy became available.

This was also when the mortality gap between the races started to show up.

It was disparities in access to the two new interventions that precipitated the divergence, as the authors suggest. Why this occurred is fairly self-evident, they comment.

“Black women are more likely than White women to lack health insurance or to have inadequate coverage, which has limited their access to mammography screening and adversely affected therapeutic decisionmaking,” researchers point out.

Moreover, both mammography screening and endocrine therapy primarily benefit patients with hormone receptor (HR)-positive breast cancer, which is equally common in Black and White patients. However, Black women have a 65% higher rate of HR-negative cancers than White women – and HR-negative tumors are often detected during the interval between mammography screening exams as palpable cancers.

Black women also have an 81% higher rate of triple-negative breast cancer, so they have benefited less from mammography screening and adjuvant endocrine therapy, both of which favor the detection and treatment of HR-positive breast cancer, the authors emphasize.

Some have suggested that the excess HR-negative breast cancer in Black women might be explained by hereditary factors. Yet as Dr. Jatoi and colleagues point out, the incidence of HR-negative breast cancer has actually been falling across all races in the United States since 1992.

However, the declines have been slower among Black women, and reductions in its incidence have been smaller among White women living in less affluent regions of the United States compared with White women from more affluent regions.

These patterns suggest that social determinants of health influence not only access to and quality of health care but also the development of HR-negative breast cancers, as the authors observe.

“If all people with breast cancer benefited equally from effective medical interventions, racial differences in mortality for individual tumor subtypes would largely reflect differences in incidence,” Dr. Jatoi and colleagues continue.

Yet the statistics show that the substantial racial disparities in mortality for both HR-positive and HR-negative cancers between Black and White women cannot be explained by differences in the incidence of either tumor alone, they write.

For example, mortality for HR-positive breast cancer is 19% higher among Black women than among White women, yet the incidence of HR-positive breast cancer is 22% lower among Black women.

Similarly, mortality from HR-negative breast cancer is over twice as high among Black women as it is among White women – a substantially larger disparity, compared with the 65% relative difference in the incidence of HR-negative breast cancer between the two races.

“Universal health care coverage could reduce disparities in treatment for cancers of all subtypes, including triple-negative breast cancer,” Dr. Jatoi and colleagues emphasize.

“Ensuring universal access to high-quality medical care can substantially narrow the racial disparity in U.S. breast-cancer mortality,” they conclude. 

The authors have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Although breast cancer occurs less frequently in Black women, compared with White women, they have a much higher risk of dying from the disease.

In the United States, age-adjusted breast cancer mortality between 2014 and 2018 was approximately 40% higher among Black women than among non-Hispanic White women.

This mortality gap likely reflects the fact that Black women face substantial barriers to obtaining timely, high-quality medical care, compared with White women, lead author Ismail Jatoi, MD, PhD, University of Texas Health Science Center, San Antonio, and colleagues suggest in a recent opinion piece.

The article was published online  in The New England Journal of Medicine.

When the team examined the statistics for breast cancer mortality, they found a surprise: The mortality gap between races only dates back to 1980.

Prior to 1980, mortality from breast cancer among Black women was slightly lower than White women, Dr. Jatoi and colleagues point out.

That year was a turning point in breast cancer management, as in 1980, both mammography screening and adjuvant endocrine therapy became available.

This was also when the mortality gap between the races started to show up.

It was disparities in access to the two new interventions that precipitated the divergence, as the authors suggest. Why this occurred is fairly self-evident, they comment.

“Black women are more likely than White women to lack health insurance or to have inadequate coverage, which has limited their access to mammography screening and adversely affected therapeutic decisionmaking,” researchers point out.

Moreover, both mammography screening and endocrine therapy primarily benefit patients with hormone receptor (HR)-positive breast cancer, which is equally common in Black and White patients. However, Black women have a 65% higher rate of HR-negative cancers than White women – and HR-negative tumors are often detected during the interval between mammography screening exams as palpable cancers.

Black women also have an 81% higher rate of triple-negative breast cancer, so they have benefited less from mammography screening and adjuvant endocrine therapy, both of which favor the detection and treatment of HR-positive breast cancer, the authors emphasize.

Some have suggested that the excess HR-negative breast cancer in Black women might be explained by hereditary factors. Yet as Dr. Jatoi and colleagues point out, the incidence of HR-negative breast cancer has actually been falling across all races in the United States since 1992.

However, the declines have been slower among Black women, and reductions in its incidence have been smaller among White women living in less affluent regions of the United States compared with White women from more affluent regions.

These patterns suggest that social determinants of health influence not only access to and quality of health care but also the development of HR-negative breast cancers, as the authors observe.

“If all people with breast cancer benefited equally from effective medical interventions, racial differences in mortality for individual tumor subtypes would largely reflect differences in incidence,” Dr. Jatoi and colleagues continue.

Yet the statistics show that the substantial racial disparities in mortality for both HR-positive and HR-negative cancers between Black and White women cannot be explained by differences in the incidence of either tumor alone, they write.

For example, mortality for HR-positive breast cancer is 19% higher among Black women than among White women, yet the incidence of HR-positive breast cancer is 22% lower among Black women.

Similarly, mortality from HR-negative breast cancer is over twice as high among Black women as it is among White women – a substantially larger disparity, compared with the 65% relative difference in the incidence of HR-negative breast cancer between the two races.

“Universal health care coverage could reduce disparities in treatment for cancers of all subtypes, including triple-negative breast cancer,” Dr. Jatoi and colleagues emphasize.

“Ensuring universal access to high-quality medical care can substantially narrow the racial disparity in U.S. breast-cancer mortality,” they conclude. 

The authors have reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Hormone receptor positive (HR+) basal tumors are biologically analogous to triple negative breast cancer (TNBC), independent of race. That finding, suggested by transcriptomic analyses of a racially diverse cohort that identified racial disparities in the proportion of HR-positive basal tumors, underscores a need for diverse racial representation in clinical trials, researchers recently reported at the annual meeting of the American Society of Clinical Oncology.

The leading cause of cancer-associated death among Black women is breast cancer, and compared with White women, Black women are 41% more likely to die from breast cancer, said Sonya A. Reid, MD, MPH, a medical oncologist with the Vanderbilt-Ingram Cancer Center, Nashville, Tenn., and the study author.

Few studies, Dr. Reid said, have evaluated if tumor biology differences contribute to the racial outcome disparity. Hormone receptor-positive tumors classified as basal-type with Blueprint genomic analysis (HR+/Basal) are overrepresented among Black women. These tumors are thought to be similar to triple negative breast cancer tumors (TNBC) which are more aggressive and tend to have worse outcomes.

TNBC, Dr. Reid said, is associated with low ACKR1 expression, which encodes the Duffy antigen and correlates with worse breast cancer outcomes. Given the overrepresentation and worse outcomes among Black women with HR-positive basal tumors, Dr. Reid and colleagues compared differentially expressed genes (DEGs) by race and subtype.

Their analysis of data from 2,657 women with stage 1, 2, and 3 breast cancer, showed that among 455 Black women, 315 had luminal (HR-positive luminal) and 140 had basal tumors (66 HR-positive basal and 74 HR-negative basal). Among White women included as a reference group (n = 2,202), tumors were were HR-positive luminal in 1,825 and HR-positive basal or HR-negative basal in 158 and 219, respectively. The proportion of Black women with HR-positive basal tumors was significantly higher, compared with White women (15% versus 7%; P <0.001) as was the proportion of Black women with HR-negative basal tumors, compared with White women (16% versus 10%; P <0.001).

Women included in the study were participants in the ongoing BEST study (5R01CA204819) at Vanderbilt University Medical Center, Nashvlile, Tenn., or FLEX study (NCT03053193). In a multidimensional scaling analysis, HR-positive basal tumors clustered with TNBC rather than with HR-positive luminal tumors. While a differential gene expression analysis comparing HR-positive basal with HR-positive luminal tumors resulted in over 700 differently expressed genes in Black women, no such genes were identified when comparing HR-positive basal tumors with TNBC. ACKR1 expression in HR-positive basal tumors was comparable to TNBC in Black women (P = 0.81) and White women (P = 0.46). In contrast, HR-positive basal tumors had significantly lower ACKR1 expression than HR-positive luminal tumors in Black (P < 0.01) and White women (P < 0.01).

The findings highlight the importance of further genomic classification for patients with HR-positive tumors, Dr. Reid said.

“Molecular subtype classification is not standard of care for patients with localized breast cancer. However, the current analysis suggests that genomic classification could have important clinical implications. Women with HR-positive basal tumors should not be treated uniformly with HR-poisitive luminal tumors. Our data suggest that HR-positive basal tumors are transcriptomically similar to TNBC tumors and should potentially be treated similar to TNBC,” she said.

There are several genomic tests that are widely available clinically to guide treatment decisions and are covered by insurance, Dr. Reid said. Prior studies have shown racial disparity in the omission of genomic tests to guide treatment decisions, however. “Increasing access [to] and awareness of genomic testing will improve guideline-adherent care for all patients. We must intentionally recruit minority patients into clinical trials, knowing that Black women are more likely to die of their breast cancer,” she said.

A further impediment lies in the fact that while most minority patients receive their care in the community, most clinical trials are offered at large academic centers, Dr. Reid said. Future trials, she urged, should include a predetermined percentage of racial/ethnic groups in the clinical trial design to reflect the breast cancer population.

Limitations of the study included that race was self-reported. She noted further that the data for survival are not yet mature. She added, “We will also be evaluating the association of different systemic treatment options across the different molecular subtypes.”

Dr. Reid reported no relevant disclosures.

Hormone receptor positive (HR+) basal tumors are biologically analogous to triple negative breast cancer (TNBC), independent of race. That finding, suggested by transcriptomic analyses of a racially diverse cohort that identified racial disparities in the proportion of HR-positive basal tumors, underscores a need for diverse racial representation in clinical trials, researchers recently reported at the annual meeting of the American Society of Clinical Oncology.

The leading cause of cancer-associated death among Black women is breast cancer, and compared with White women, Black women are 41% more likely to die from breast cancer, said Sonya A. Reid, MD, MPH, a medical oncologist with the Vanderbilt-Ingram Cancer Center, Nashville, Tenn., and the study author.

Few studies, Dr. Reid said, have evaluated if tumor biology differences contribute to the racial outcome disparity. Hormone receptor-positive tumors classified as basal-type with Blueprint genomic analysis (HR+/Basal) are overrepresented among Black women. These tumors are thought to be similar to triple negative breast cancer tumors (TNBC) which are more aggressive and tend to have worse outcomes.

TNBC, Dr. Reid said, is associated with low ACKR1 expression, which encodes the Duffy antigen and correlates with worse breast cancer outcomes. Given the overrepresentation and worse outcomes among Black women with HR-positive basal tumors, Dr. Reid and colleagues compared differentially expressed genes (DEGs) by race and subtype.

Their analysis of data from 2,657 women with stage 1, 2, and 3 breast cancer, showed that among 455 Black women, 315 had luminal (HR-positive luminal) and 140 had basal tumors (66 HR-positive basal and 74 HR-negative basal). Among White women included as a reference group (n = 2,202), tumors were were HR-positive luminal in 1,825 and HR-positive basal or HR-negative basal in 158 and 219, respectively. The proportion of Black women with HR-positive basal tumors was significantly higher, compared with White women (15% versus 7%; P <0.001) as was the proportion of Black women with HR-negative basal tumors, compared with White women (16% versus 10%; P <0.001).

Women included in the study were participants in the ongoing BEST study (5R01CA204819) at Vanderbilt University Medical Center, Nashvlile, Tenn., or FLEX study (NCT03053193). In a multidimensional scaling analysis, HR-positive basal tumors clustered with TNBC rather than with HR-positive luminal tumors. While a differential gene expression analysis comparing HR-positive basal with HR-positive luminal tumors resulted in over 700 differently expressed genes in Black women, no such genes were identified when comparing HR-positive basal tumors with TNBC. ACKR1 expression in HR-positive basal tumors was comparable to TNBC in Black women (P = 0.81) and White women (P = 0.46). In contrast, HR-positive basal tumors had significantly lower ACKR1 expression than HR-positive luminal tumors in Black (P < 0.01) and White women (P < 0.01).

The findings highlight the importance of further genomic classification for patients with HR-positive tumors, Dr. Reid said.

“Molecular subtype classification is not standard of care for patients with localized breast cancer. However, the current analysis suggests that genomic classification could have important clinical implications. Women with HR-positive basal tumors should not be treated uniformly with HR-poisitive luminal tumors. Our data suggest that HR-positive basal tumors are transcriptomically similar to TNBC tumors and should potentially be treated similar to TNBC,” she said.

There are several genomic tests that are widely available clinically to guide treatment decisions and are covered by insurance, Dr. Reid said. Prior studies have shown racial disparity in the omission of genomic tests to guide treatment decisions, however. “Increasing access [to] and awareness of genomic testing will improve guideline-adherent care for all patients. We must intentionally recruit minority patients into clinical trials, knowing that Black women are more likely to die of their breast cancer,” she said.

A further impediment lies in the fact that while most minority patients receive their care in the community, most clinical trials are offered at large academic centers, Dr. Reid said. Future trials, she urged, should include a predetermined percentage of racial/ethnic groups in the clinical trial design to reflect the breast cancer population.

Limitations of the study included that race was self-reported. She noted further that the data for survival are not yet mature. She added, “We will also be evaluating the association of different systemic treatment options across the different molecular subtypes.”

Dr. Reid reported no relevant disclosures.

Hormone receptor positive (HR+) basal tumors are biologically analogous to triple negative breast cancer (TNBC), independent of race. That finding, suggested by transcriptomic analyses of a racially diverse cohort that identified racial disparities in the proportion of HR-positive basal tumors, underscores a need for diverse racial representation in clinical trials, researchers recently reported at the annual meeting of the American Society of Clinical Oncology.

The leading cause of cancer-associated death among Black women is breast cancer, and compared with White women, Black women are 41% more likely to die from breast cancer, said Sonya A. Reid, MD, MPH, a medical oncologist with the Vanderbilt-Ingram Cancer Center, Nashville, Tenn., and the study author.

Few studies, Dr. Reid said, have evaluated if tumor biology differences contribute to the racial outcome disparity. Hormone receptor-positive tumors classified as basal-type with Blueprint genomic analysis (HR+/Basal) are overrepresented among Black women. These tumors are thought to be similar to triple negative breast cancer tumors (TNBC) which are more aggressive and tend to have worse outcomes.

TNBC, Dr. Reid said, is associated with low ACKR1 expression, which encodes the Duffy antigen and correlates with worse breast cancer outcomes. Given the overrepresentation and worse outcomes among Black women with HR-positive basal tumors, Dr. Reid and colleagues compared differentially expressed genes (DEGs) by race and subtype.

Their analysis of data from 2,657 women with stage 1, 2, and 3 breast cancer, showed that among 455 Black women, 315 had luminal (HR-positive luminal) and 140 had basal tumors (66 HR-positive basal and 74 HR-negative basal). Among White women included as a reference group (n = 2,202), tumors were were HR-positive luminal in 1,825 and HR-positive basal or HR-negative basal in 158 and 219, respectively. The proportion of Black women with HR-positive basal tumors was significantly higher, compared with White women (15% versus 7%; P <0.001) as was the proportion of Black women with HR-negative basal tumors, compared with White women (16% versus 10%; P <0.001).

Women included in the study were participants in the ongoing BEST study (5R01CA204819) at Vanderbilt University Medical Center, Nashvlile, Tenn., or FLEX study (NCT03053193). In a multidimensional scaling analysis, HR-positive basal tumors clustered with TNBC rather than with HR-positive luminal tumors. While a differential gene expression analysis comparing HR-positive basal with HR-positive luminal tumors resulted in over 700 differently expressed genes in Black women, no such genes were identified when comparing HR-positive basal tumors with TNBC. ACKR1 expression in HR-positive basal tumors was comparable to TNBC in Black women (P = 0.81) and White women (P = 0.46). In contrast, HR-positive basal tumors had significantly lower ACKR1 expression than HR-positive luminal tumors in Black (P < 0.01) and White women (P < 0.01).

The findings highlight the importance of further genomic classification for patients with HR-positive tumors, Dr. Reid said.

“Molecular subtype classification is not standard of care for patients with localized breast cancer. However, the current analysis suggests that genomic classification could have important clinical implications. Women with HR-positive basal tumors should not be treated uniformly with HR-poisitive luminal tumors. Our data suggest that HR-positive basal tumors are transcriptomically similar to TNBC tumors and should potentially be treated similar to TNBC,” she said.

There are several genomic tests that are widely available clinically to guide treatment decisions and are covered by insurance, Dr. Reid said. Prior studies have shown racial disparity in the omission of genomic tests to guide treatment decisions, however. “Increasing access [to] and awareness of genomic testing will improve guideline-adherent care for all patients. We must intentionally recruit minority patients into clinical trials, knowing that Black women are more likely to die of their breast cancer,” she said.

A further impediment lies in the fact that while most minority patients receive their care in the community, most clinical trials are offered at large academic centers, Dr. Reid said. Future trials, she urged, should include a predetermined percentage of racial/ethnic groups in the clinical trial design to reflect the breast cancer population.

Limitations of the study included that race was self-reported. She noted further that the data for survival are not yet mature. She added, “We will also be evaluating the association of different systemic treatment options across the different molecular subtypes.”

Dr. Reid reported no relevant disclosures.

CHICAGO – Metastatic invasive lobular breast cancers (ILC) that are hormone receptor (HR)-positive and HER2-negative have therapeutic outcomes similar to those of invasive ductal cancer (IDC) following treatment with endocrine therapy combined with a CDK4/6 inhibitor, mTOR inhibitor, or PI3K inhibitor, according to a new retrospective analysis of patients treated at MD Anderson Cancer Center.

The two conditions have historically been lumped together when studying treatment outcomes, but more recent research has shown key differences between the two subtypes, according to Jason A. Mouabbi, MD, who presented the results at the annual meeting of the American Society of Clinical Oncology.

“All the studies that were done were driven by ductal patients, so you can never take conclusions for the lobular patients. We have a big database at MD Anderson, so we can really study a large number of patients and get some signals whether or not patients would benefit from that therapy or not,” said Dr. Mouabbi, a lobular breast cancer specialist at MD Anderson Cancer Center.

The results of the study are important since patients often come to physicians with sophisticated understanding of their disease, he said. Patients with lobular cancer naturally wonder if a therapeutic regimen tested primarily in IDC will benefit them. “For the longest time, we said, ‘we have no data,’ ” said Dr. Mouabbi.

The new study should offer patients and physicians some reassurance. “We found that all of them benefit from it and most importantly, they all benefit from it (with) the same magnitude,” Dr. Mouabbi said.

The researchers analyzed data from 2,971 patients (82% IDC, 14% ILC, 4% mixed) treated between 2010 and 2021. The median age was 50 in all groups. Eighty percent were White, 10% were Hispanic, and 5% were Black. Ninety-nine percent had estrogen receptor (ER) + tumors, and 88% had progesterone positive (PR) + tumors.

A total of 1,895 patients received CDK4/6 inhibitors, 1,027 received everolimus, and 49 received alpelisib. There was no statistically significant difference in overall survival or progression-free survival between the two cancer types in any of the treatment groups.

Despite the similar outcomes, the two conditions remain unique. IDC is a disease of cells from the ducts that deliver milk, while ILC arises in cells that produce milk. Nearly 95% of ILC cases are hormone-positive, compared to 50%-55% of IDC.

So, while existing treatments seem to benefit both groups, there are nonetheless plans to develop therapeutic strategies tailored to lobular cancer.

Dr. Mouabbi’s group has compared molecular profiles of ILC and IDC tumors to better understand how to target them individually. Almost all ILC cancers have a mutation in a gene called CDH1, which leads to loss of an anchoring protein. They believe this causes a unique growth pattern of thin tendrils, rather than the onion-like growths of IDC. A therapy targeting this mutation could provide a specific benefit for lobular breast cancer.

There are other differences: PI3 kinases are mutated in about 60% of ILC tumors, versus about 30% of IDC tumors, and other genes mutated at lower frequencies are also different between the two subtypes. “So there are a lot of (approaches) we are trying to initiate in lobular cancer because we have awareness now that they are different,” Dr. Mouabbi said.

The study received no external funding.

CHICAGO – Metastatic invasive lobular breast cancers (ILC) that are hormone receptor (HR)-positive and HER2-negative have therapeutic outcomes similar to those of invasive ductal cancer (IDC) following treatment with endocrine therapy combined with a CDK4/6 inhibitor, mTOR inhibitor, or PI3K inhibitor, according to a new retrospective analysis of patients treated at MD Anderson Cancer Center.

The two conditions have historically been lumped together when studying treatment outcomes, but more recent research has shown key differences between the two subtypes, according to Jason A. Mouabbi, MD, who presented the results at the annual meeting of the American Society of Clinical Oncology.

“All the studies that were done were driven by ductal patients, so you can never take conclusions for the lobular patients. We have a big database at MD Anderson, so we can really study a large number of patients and get some signals whether or not patients would benefit from that therapy or not,” said Dr. Mouabbi, a lobular breast cancer specialist at MD Anderson Cancer Center.

The results of the study are important since patients often come to physicians with sophisticated understanding of their disease, he said. Patients with lobular cancer naturally wonder if a therapeutic regimen tested primarily in IDC will benefit them. “For the longest time, we said, ‘we have no data,’ ” said Dr. Mouabbi.

The new study should offer patients and physicians some reassurance. “We found that all of them benefit from it and most importantly, they all benefit from it (with) the same magnitude,” Dr. Mouabbi said.

The researchers analyzed data from 2,971 patients (82% IDC, 14% ILC, 4% mixed) treated between 2010 and 2021. The median age was 50 in all groups. Eighty percent were White, 10% were Hispanic, and 5% were Black. Ninety-nine percent had estrogen receptor (ER) + tumors, and 88% had progesterone positive (PR) + tumors.

A total of 1,895 patients received CDK4/6 inhibitors, 1,027 received everolimus, and 49 received alpelisib. There was no statistically significant difference in overall survival or progression-free survival between the two cancer types in any of the treatment groups.

Despite the similar outcomes, the two conditions remain unique. IDC is a disease of cells from the ducts that deliver milk, while ILC arises in cells that produce milk. Nearly 95% of ILC cases are hormone-positive, compared to 50%-55% of IDC.

So, while existing treatments seem to benefit both groups, there are nonetheless plans to develop therapeutic strategies tailored to lobular cancer.

Dr. Mouabbi’s group has compared molecular profiles of ILC and IDC tumors to better understand how to target them individually. Almost all ILC cancers have a mutation in a gene called CDH1, which leads to loss of an anchoring protein. They believe this causes a unique growth pattern of thin tendrils, rather than the onion-like growths of IDC. A therapy targeting this mutation could provide a specific benefit for lobular breast cancer.

There are other differences: PI3 kinases are mutated in about 60% of ILC tumors, versus about 30% of IDC tumors, and other genes mutated at lower frequencies are also different between the two subtypes. “So there are a lot of (approaches) we are trying to initiate in lobular cancer because we have awareness now that they are different,” Dr. Mouabbi said.

The study received no external funding.

CHICAGO – Metastatic invasive lobular breast cancers (ILC) that are hormone receptor (HR)-positive and HER2-negative have therapeutic outcomes similar to those of invasive ductal cancer (IDC) following treatment with endocrine therapy combined with a CDK4/6 inhibitor, mTOR inhibitor, or PI3K inhibitor, according to a new retrospective analysis of patients treated at MD Anderson Cancer Center.

The two conditions have historically been lumped together when studying treatment outcomes, but more recent research has shown key differences between the two subtypes, according to Jason A. Mouabbi, MD, who presented the results at the annual meeting of the American Society of Clinical Oncology.

“All the studies that were done were driven by ductal patients, so you can never take conclusions for the lobular patients. We have a big database at MD Anderson, so we can really study a large number of patients and get some signals whether or not patients would benefit from that therapy or not,” said Dr. Mouabbi, a lobular breast cancer specialist at MD Anderson Cancer Center.

The results of the study are important since patients often come to physicians with sophisticated understanding of their disease, he said. Patients with lobular cancer naturally wonder if a therapeutic regimen tested primarily in IDC will benefit them. “For the longest time, we said, ‘we have no data,’ ” said Dr. Mouabbi.

The new study should offer patients and physicians some reassurance. “We found that all of them benefit from it and most importantly, they all benefit from it (with) the same magnitude,” Dr. Mouabbi said.

The researchers analyzed data from 2,971 patients (82% IDC, 14% ILC, 4% mixed) treated between 2010 and 2021. The median age was 50 in all groups. Eighty percent were White, 10% were Hispanic, and 5% were Black. Ninety-nine percent had estrogen receptor (ER) + tumors, and 88% had progesterone positive (PR) + tumors.

A total of 1,895 patients received CDK4/6 inhibitors, 1,027 received everolimus, and 49 received alpelisib. There was no statistically significant difference in overall survival or progression-free survival between the two cancer types in any of the treatment groups.

Despite the similar outcomes, the two conditions remain unique. IDC is a disease of cells from the ducts that deliver milk, while ILC arises in cells that produce milk. Nearly 95% of ILC cases are hormone-positive, compared to 50%-55% of IDC.

So, while existing treatments seem to benefit both groups, there are nonetheless plans to develop therapeutic strategies tailored to lobular cancer.

Dr. Mouabbi’s group has compared molecular profiles of ILC and IDC tumors to better understand how to target them individually. Almost all ILC cancers have a mutation in a gene called CDH1, which leads to loss of an anchoring protein. They believe this causes a unique growth pattern of thin tendrils, rather than the onion-like growths of IDC. A therapy targeting this mutation could provide a specific benefit for lobular breast cancer.

There are other differences: PI3 kinases are mutated in about 60% of ILC tumors, versus about 30% of IDC tumors, and other genes mutated at lower frequencies are also different between the two subtypes. “So there are a lot of (approaches) we are trying to initiate in lobular cancer because we have awareness now that they are different,” Dr. Mouabbi said.

The study received no external funding.

A study of elderly patients with HER2-positive/HR-negative metastatic breast cancer finds a significantly shorter median overall survival in actual clinical practice than younger counterparts.

After 46 months of treatment, the survival rate was only 25%, according to a study presented in June at the annual meeting of the American Society of Clinical Oncology. The finding suggests that older age is an important prognostic factor for breast cancer survival, said study author Zhonghui Jenny Ou, a doctoral candidate at the Massachusetts College of Pharmacy and Health Sciences in Boston.

For comparison, Ms. Ou cited the CLEOPATRA trial which showed a median overall survival of 57.1 months for patients who were treated with pertuzumab, docetaxel and trastuzumab versus 40.8 months for placebo with docetaxel plus trastuzumab.

The Ou study is based on an analysis of data between 2012 and 2016 from the SEER-Medicare database. The final analysis included 73 women (average age 75 years at diagnosis) with early-stage HER2-positive/HR-negative metastatic breast cancer. Fifty-six women were treated with trastuzumab with pertuzumab and chemotherapy as first-line treatment, and 17 were treated with chemotherapy only. The longest length of treatment with trastuzumab was over 44 months. And, the median follow-up for overall survival was 13 months (95% confidence interval, 12.7-18.7).

Between 2012 and 2016, five patients died from other causes, including lung cancer, cerebrovascular diseases, aortic aneurysm and dissection, pneumonia and influenza, and heart disease.

“While there are many clinical trials about HER2-positive metastatic breast cancer, these trials were all performed in younger and relatively healthier patients. Few studies included elderly patients 65 years or older,” Ms. Ou said.

According to the American Cancer Society, 31% of all newly diagnosed breast cancer cases are in women who are 70 years old or older, yet 47% of all breast cancer deaths each year are in women in this age group.

Undertreatment and lower treatment intensity have been cited by other studies as possible contributing factors to lower overall survival rates, but breast cancer in elderly women is a complex and understudied subject. Why the mortality rates for elderly women are disproportionately higher than those of younger women is attributable to a number of reasons, write the authors of one of the most recent studies on the subject.

“It is well established that receipt of adjuvant chemotherapy, trastuzumab, and hormonal therapy reduces risk of recurrence and death across all age groups, yet multiple studies document suboptimal systemic treatment and adherence for older patients, including omission of efficacious treatments, receipt of lower intensity and/or nonguideline treatment, or poor adherence to hormonal therapy,” Freedman et al. wrote in the May 15, 2018, issue of the journal Cancer.

While the Ou study sample size was small, the study’s real-world analysis is telling, Ms. Ou said.

“The major limitation of this study is that it has – after applying all the eligibility criteria to the 170,516 breast cancer patients from the SEER-Medicare database between 2012 and 2016 – a study population of just 73 patients. The number is sufficient to do survival analysis,” she said.

A study of elderly patients with HER2-positive/HR-negative metastatic breast cancer finds a significantly shorter median overall survival in actual clinical practice than younger counterparts.

After 46 months of treatment, the survival rate was only 25%, according to a study presented in June at the annual meeting of the American Society of Clinical Oncology. The finding suggests that older age is an important prognostic factor for breast cancer survival, said study author Zhonghui Jenny Ou, a doctoral candidate at the Massachusetts College of Pharmacy and Health Sciences in Boston.

For comparison, Ms. Ou cited the CLEOPATRA trial which showed a median overall survival of 57.1 months for patients who were treated with pertuzumab, docetaxel and trastuzumab versus 40.8 months for placebo with docetaxel plus trastuzumab.

The Ou study is based on an analysis of data between 2012 and 2016 from the SEER-Medicare database. The final analysis included 73 women (average age 75 years at diagnosis) with early-stage HER2-positive/HR-negative metastatic breast cancer. Fifty-six women were treated with trastuzumab with pertuzumab and chemotherapy as first-line treatment, and 17 were treated with chemotherapy only. The longest length of treatment with trastuzumab was over 44 months. And, the median follow-up for overall survival was 13 months (95% confidence interval, 12.7-18.7).

Between 2012 and 2016, five patients died from other causes, including lung cancer, cerebrovascular diseases, aortic aneurysm and dissection, pneumonia and influenza, and heart disease.

“While there are many clinical trials about HER2-positive metastatic breast cancer, these trials were all performed in younger and relatively healthier patients. Few studies included elderly patients 65 years or older,” Ms. Ou said.

According to the American Cancer Society, 31% of all newly diagnosed breast cancer cases are in women who are 70 years old or older, yet 47% of all breast cancer deaths each year are in women in this age group.

Undertreatment and lower treatment intensity have been cited by other studies as possible contributing factors to lower overall survival rates, but breast cancer in elderly women is a complex and understudied subject. Why the mortality rates for elderly women are disproportionately higher than those of younger women is attributable to a number of reasons, write the authors of one of the most recent studies on the subject.

“It is well established that receipt of adjuvant chemotherapy, trastuzumab, and hormonal therapy reduces risk of recurrence and death across all age groups, yet multiple studies document suboptimal systemic treatment and adherence for older patients, including omission of efficacious treatments, receipt of lower intensity and/or nonguideline treatment, or poor adherence to hormonal therapy,” Freedman et al. wrote in the May 15, 2018, issue of the journal Cancer.

While the Ou study sample size was small, the study’s real-world analysis is telling, Ms. Ou said.

“The major limitation of this study is that it has – after applying all the eligibility criteria to the 170,516 breast cancer patients from the SEER-Medicare database between 2012 and 2016 – a study population of just 73 patients. The number is sufficient to do survival analysis,” she said.

A study of elderly patients with HER2-positive/HR-negative metastatic breast cancer finds a significantly shorter median overall survival in actual clinical practice than younger counterparts.

After 46 months of treatment, the survival rate was only 25%, according to a study presented in June at the annual meeting of the American Society of Clinical Oncology. The finding suggests that older age is an important prognostic factor for breast cancer survival, said study author Zhonghui Jenny Ou, a doctoral candidate at the Massachusetts College of Pharmacy and Health Sciences in Boston.

For comparison, Ms. Ou cited the CLEOPATRA trial which showed a median overall survival of 57.1 months for patients who were treated with pertuzumab, docetaxel and trastuzumab versus 40.8 months for placebo with docetaxel plus trastuzumab.

The Ou study is based on an analysis of data between 2012 and 2016 from the SEER-Medicare database. The final analysis included 73 women (average age 75 years at diagnosis) with early-stage HER2-positive/HR-negative metastatic breast cancer. Fifty-six women were treated with trastuzumab with pertuzumab and chemotherapy as first-line treatment, and 17 were treated with chemotherapy only. The longest length of treatment with trastuzumab was over 44 months. And, the median follow-up for overall survival was 13 months (95% confidence interval, 12.7-18.7).

Between 2012 and 2016, five patients died from other causes, including lung cancer, cerebrovascular diseases, aortic aneurysm and dissection, pneumonia and influenza, and heart disease.

“While there are many clinical trials about HER2-positive metastatic breast cancer, these trials were all performed in younger and relatively healthier patients. Few studies included elderly patients 65 years or older,” Ms. Ou said.

According to the American Cancer Society, 31% of all newly diagnosed breast cancer cases are in women who are 70 years old or older, yet 47% of all breast cancer deaths each year are in women in this age group.

Undertreatment and lower treatment intensity have been cited by other studies as possible contributing factors to lower overall survival rates, but breast cancer in elderly women is a complex and understudied subject. Why the mortality rates for elderly women are disproportionately higher than those of younger women is attributable to a number of reasons, write the authors of one of the most recent studies on the subject.

“It is well established that receipt of adjuvant chemotherapy, trastuzumab, and hormonal therapy reduces risk of recurrence and death across all age groups, yet multiple studies document suboptimal systemic treatment and adherence for older patients, including omission of efficacious treatments, receipt of lower intensity and/or nonguideline treatment, or poor adherence to hormonal therapy,” Freedman et al. wrote in the May 15, 2018, issue of the journal Cancer.

While the Ou study sample size was small, the study’s real-world analysis is telling, Ms. Ou said.

“The major limitation of this study is that it has – after applying all the eligibility criteria to the 170,516 breast cancer patients from the SEER-Medicare database between 2012 and 2016 – a study population of just 73 patients. The number is sufficient to do survival analysis,” she said.

Eight-year follow-up of the ASTRRA trial confirmed and extended support for adding 2 years of ovarian function suppression with goserelin to tamoxifen, compared with tamoxifen alone.

“Adding ovarian suppression to tamoxifen should be considered for this population of women,” said senior author Hee Jeong Kim, MD, a breast cancer surgeon with the Asan Medical Center, Seoul, South Korea. Dr. Kim presented the data earlier this month at the annual meeting of the American Society of Clinical Oncology.

The median disease-free survival rate of 85.4% for tamoxifen plus ovarian function suppression versus 80.2% for tamoxifen alone (HR, 0.67; 95% confidence interval, 0.514-0.869; P = .0027) was consistent with recent findings from SOFT (Suppression of Ovarian Function Trial), which also showed a clear survival benefit in breast cancer events with the addition of ovarian function suppression to tamoxifen for women who remain premenopausal after chemotherapy. SOFT trial analyses of disease-free survival at 5 and 8 years demonstrated hazard ratios of 0.82 and 0.76 respectively.

Dr. Kim’s study is a post-trial follow-up of the ASTRRA trial, or the Addition of Ovarian Suppression to Tamoxifen in Young Women With Hormone-Sensitive Breast Cancer Who Remain Premenopausal or Regain Vaginal Bleeding After Chemotherapy, which randomly assigned 1,298 patients with breast cancer in a one-to-one ratio to receive tamoxifen only (n = 647) or tamoxifen plus ovarian function suppression (n = 635). The primary endpoint was disease-free survival and the secondary endpoint was overall survival.

Earlier ASTRRA analysis at 5-year follow-up had shown disease-free survival rates of 89.9% for tamoxifen plus ovarian function suppression versus 87.2% for tamoxifen alone in women with hormone-sensitive breast cancer who remained premenopausal or had premenopausal status restored after chemotherapy. Overall survival, a secondary endpoint, also favored adding ovarian function suppression (HR, 0.31; 95% CI, 0.10-0.94; P = .029). The absolute difference for disease-free survival adding ovarian function suppression at the later median follow-up of 106.4 months was 5.2%. The difference at 5 years had been 2.7%, Dr. Kim pointed out. Also, these findings were calculated from time of enrollment. When calculated from time of randomization, the disease-free survival rates were 84.1% and 78.1%, respectively, for tamoxifen plus ovarian function suppression and tamoxifen alone, with a 6.0% absolute difference (HR, 0.67; 95% CI, 0.516-0.872); P = .0025).

The benefit of adding ovarian function suppression to tamoxifen for the secondary endpoint of overall survival at 8 years (96.5% versus 95.3%) did not achieve statistical significance (HR, 0.78; 95% CI, 0.486-1.253); P = .3). “Although it’s not statistically significant, there are absolute differences between the two groups favoring tamoxifen plus ovarian function suppression,” Dr. Kim said in an interview. She pointed out also that for distant metastasis-free survival the hazard ratio was 0.71, significantly favoring tamoxifen plus ovarian function suppression. “More than 95% were still surviving at 8 years with tamoxifen plus ovarian function suppression. So, we need more events to fully evaluate the overall survival benefit.”

A study limitation, Dr. Kim acknowledged in the interview, is that safety and adverse event data were not collected. “As ovarian function suppression has been widely used in clinical practice for decades, and the side effects of its relatively short-term use were considered to be well-understood in previous studies, we focused on the oncologic efficacy of ovarian function suppression in this study,” she said.

Eight-year follow-up of the ASTRRA trial confirmed and extended support for adding 2 years of ovarian function suppression with goserelin to tamoxifen, compared with tamoxifen alone.

“Adding ovarian suppression to tamoxifen should be considered for this population of women,” said senior author Hee Jeong Kim, MD, a breast cancer surgeon with the Asan Medical Center, Seoul, South Korea. Dr. Kim presented the data earlier this month at the annual meeting of the American Society of Clinical Oncology.

The median disease-free survival rate of 85.4% for tamoxifen plus ovarian function suppression versus 80.2% for tamoxifen alone (HR, 0.67; 95% confidence interval, 0.514-0.869; P = .0027) was consistent with recent findings from SOFT (Suppression of Ovarian Function Trial), which also showed a clear survival benefit in breast cancer events with the addition of ovarian function suppression to tamoxifen for women who remain premenopausal after chemotherapy. SOFT trial analyses of disease-free survival at 5 and 8 years demonstrated hazard ratios of 0.82 and 0.76 respectively.

Dr. Kim’s study is a post-trial follow-up of the ASTRRA trial, or the Addition of Ovarian Suppression to Tamoxifen in Young Women With Hormone-Sensitive Breast Cancer Who Remain Premenopausal or Regain Vaginal Bleeding After Chemotherapy, which randomly assigned 1,298 patients with breast cancer in a one-to-one ratio to receive tamoxifen only (n = 647) or tamoxifen plus ovarian function suppression (n = 635). The primary endpoint was disease-free survival and the secondary endpoint was overall survival.

Earlier ASTRRA analysis at 5-year follow-up had shown disease-free survival rates of 89.9% for tamoxifen plus ovarian function suppression versus 87.2% for tamoxifen alone in women with hormone-sensitive breast cancer who remained premenopausal or had premenopausal status restored after chemotherapy. Overall survival, a secondary endpoint, also favored adding ovarian function suppression (HR, 0.31; 95% CI, 0.10-0.94; P = .029). The absolute difference for disease-free survival adding ovarian function suppression at the later median follow-up of 106.4 months was 5.2%. The difference at 5 years had been 2.7%, Dr. Kim pointed out. Also, these findings were calculated from time of enrollment. When calculated from time of randomization, the disease-free survival rates were 84.1% and 78.1%, respectively, for tamoxifen plus ovarian function suppression and tamoxifen alone, with a 6.0% absolute difference (HR, 0.67; 95% CI, 0.516-0.872); P = .0025).

The benefit of adding ovarian function suppression to tamoxifen for the secondary endpoint of overall survival at 8 years (96.5% versus 95.3%) did not achieve statistical significance (HR, 0.78; 95% CI, 0.486-1.253); P = .3). “Although it’s not statistically significant, there are absolute differences between the two groups favoring tamoxifen plus ovarian function suppression,” Dr. Kim said in an interview. She pointed out also that for distant metastasis-free survival the hazard ratio was 0.71, significantly favoring tamoxifen plus ovarian function suppression. “More than 95% were still surviving at 8 years with tamoxifen plus ovarian function suppression. So, we need more events to fully evaluate the overall survival benefit.”

A study limitation, Dr. Kim acknowledged in the interview, is that safety and adverse event data were not collected. “As ovarian function suppression has been widely used in clinical practice for decades, and the side effects of its relatively short-term use were considered to be well-understood in previous studies, we focused on the oncologic efficacy of ovarian function suppression in this study,” she said.

Eight-year follow-up of the ASTRRA trial confirmed and extended support for adding 2 years of ovarian function suppression with goserelin to tamoxifen, compared with tamoxifen alone.

“Adding ovarian suppression to tamoxifen should be considered for this population of women,” said senior author Hee Jeong Kim, MD, a breast cancer surgeon with the Asan Medical Center, Seoul, South Korea. Dr. Kim presented the data earlier this month at the annual meeting of the American Society of Clinical Oncology.

The median disease-free survival rate of 85.4% for tamoxifen plus ovarian function suppression versus 80.2% for tamoxifen alone (HR, 0.67; 95% confidence interval, 0.514-0.869; P = .0027) was consistent with recent findings from SOFT (Suppression of Ovarian Function Trial), which also showed a clear survival benefit in breast cancer events with the addition of ovarian function suppression to tamoxifen for women who remain premenopausal after chemotherapy. SOFT trial analyses of disease-free survival at 5 and 8 years demonstrated hazard ratios of 0.82 and 0.76 respectively.

Dr. Kim’s study is a post-trial follow-up of the ASTRRA trial, or the Addition of Ovarian Suppression to Tamoxifen in Young Women With Hormone-Sensitive Breast Cancer Who Remain Premenopausal or Regain Vaginal Bleeding After Chemotherapy, which randomly assigned 1,298 patients with breast cancer in a one-to-one ratio to receive tamoxifen only (n = 647) or tamoxifen plus ovarian function suppression (n = 635). The primary endpoint was disease-free survival and the secondary endpoint was overall survival.

Earlier ASTRRA analysis at 5-year follow-up had shown disease-free survival rates of 89.9% for tamoxifen plus ovarian function suppression versus 87.2% for tamoxifen alone in women with hormone-sensitive breast cancer who remained premenopausal or had premenopausal status restored after chemotherapy. Overall survival, a secondary endpoint, also favored adding ovarian function suppression (HR, 0.31; 95% CI, 0.10-0.94; P = .029). The absolute difference for disease-free survival adding ovarian function suppression at the later median follow-up of 106.4 months was 5.2%. The difference at 5 years had been 2.7%, Dr. Kim pointed out. Also, these findings were calculated from time of enrollment. When calculated from time of randomization, the disease-free survival rates were 84.1% and 78.1%, respectively, for tamoxifen plus ovarian function suppression and tamoxifen alone, with a 6.0% absolute difference (HR, 0.67; 95% CI, 0.516-0.872); P = .0025).

The benefit of adding ovarian function suppression to tamoxifen for the secondary endpoint of overall survival at 8 years (96.5% versus 95.3%) did not achieve statistical significance (HR, 0.78; 95% CI, 0.486-1.253); P = .3). “Although it’s not statistically significant, there are absolute differences between the two groups favoring tamoxifen plus ovarian function suppression,” Dr. Kim said in an interview. She pointed out also that for distant metastasis-free survival the hazard ratio was 0.71, significantly favoring tamoxifen plus ovarian function suppression. “More than 95% were still surviving at 8 years with tamoxifen plus ovarian function suppression. So, we need more events to fully evaluate the overall survival benefit.”

A study limitation, Dr. Kim acknowledged in the interview, is that safety and adverse event data were not collected. “As ovarian function suppression has been widely used in clinical practice for decades, and the side effects of its relatively short-term use were considered to be well-understood in previous studies, we focused on the oncologic efficacy of ovarian function suppression in this study,” she said.

A neighborhood analysis of socioeconomic status conducted in the Pittsburgh area found worse metastatic breast cancer survival outcomes among patients of low socioeconomic status. The findings suggest that race is not a relevant factor in outcomes.

“This study demonstrates that metastatic breast cancer patients of low socioeconomic status have worse outcomes than those with higher socioeconomic status at our center. It also underscores the idea that race is not so much a biological construct but more a consequence of socioeconomic issues. The effect of race is likely mediated by lower socioeconomic status,” said Susrutha Puthanmadhom Narayanan, MD, who presented the results of her study earlier this month in Chicago at the annual meeting of the American Society of Clinical Oncology.

“The current study should make clinicians cognizant of the potential for biases in the management of metastatic breast cancer in terms of socioeconomic status and race. One should think of socioeconomic status as a predictor of bad outcomes, almost like a comorbidity, and think of [associations between race and outcomes], as a consequence of socioeconomic inequality,” said Dr. Puthanmadhom Narayanan, who is an internal medicine resident at University of Pittsburgh Medical Center.

She and her colleagues intend to dig deeper into the relationships. “We are interested in looking at utilization of different treatment options for metastatic breast cancer between the socioeconomic status groups. In the preliminary analysis, we saw that ER-positive metastatic breast cancer patients with lower socioeconomic status get treated with tamoxifen more often than aromatase inhibitors and newer agents. And, we have plans to study stress signaling and inflammation as mediators of bad outcomes in the low socioeconomic status population,” Dr. Puthanmadhom Narayanan said.

In fact, that tendency for lower socioeconomic status patients to receive older treatments should be a call to action for physicians. “This study should make clinicians cognizant of the potential for biases in management of metastatic breast cancer in terms of socioeconomic status and race,” she said.

The study is based on an analysis of data from the Neighborhood Atlas in which a Neighborhood Deprivation Index (NDI) score was calculated. An NDI score in the bottom tertile meant that patients were better off than patients with mid to high range NDI scores. In this study, socioeconomic status was described as “low deprivation” or “high depreviation.” Higher deprivation correlated with lower overall survival. And, there were more Black patients in the higher deprivation group (10.5%), compared with the low deprivation group (3.7%). In multivariate Cox proportional hazard model, socioeconomic status, but not race, had a significant effect on overall survival (HR for high deprivation was 1.19 [95% confidence interval; 1.04-1.37], P = 0.01).

It included 1,246 patients who were treated at the University of Pittsburgh Medical Center between 2000 and 2017. Of 1,246 patients, 414 patients considered in the bottom tertile of NDI as having low deprivation, while 832 patients in the middle or top tertiles were classified as having high deprivation.

The two socioeconomic status groups were similar in baseline characteristics, with the exception of race: 10.5% of the high deprivation group were African American, compared with 3.7% of the low deprivation group (P =.000093).

Univariate analyses showed worse survival in both Black women and women in the lower socioeconomic status group, but a multivariate analysis found only socioeconomic status was associated with overall survival (hazard ratio for lower socioeconomic status, 1.19; P = .01).

The study had several strengths, according to Rachel Freedman, MD, MPH, who served as a discussant for the abstract. “It included both de novo and recurrent metastatic breast cancer, unlike previous studies based on the Surveillance, Epidemiology, and End Results (SEER) database that only included de novo cases. It also employed a novel tool to define socioeconomic status in the form of the Neighborhood Atlas. The study “adds more evidence that socioeconomic status likely mediates much of what we see when it comes to racial disparities,” said Dr. Freedman, who is a senior physician at Dana Farber Cancer Institute.

Nevertheless, more work needs to be done. Dr. Freedman pointed out that the current study did not include information on treatment.

The findings underscore the failure to date to address disparities in breast cancer treatment, an effort that is hampered by difficulty in teasing out complex factors that may impact survival. “We need to standardize the way that we collect social determinants of health and act upon findings, and we need to standardize patient navigation, and we need to commit as a community to diverse clinical trial populations,” Dr. Freedman said.

Dr. Narayanan has no relevant financial disclosures. Dr. Freedman is an employee and stockholder of Firefly Health.

A neighborhood analysis of socioeconomic status conducted in the Pittsburgh area found worse metastatic breast cancer survival outcomes among patients of low socioeconomic status. The findings suggest that race is not a relevant factor in outcomes.

“This study demonstrates that metastatic breast cancer patients of low socioeconomic status have worse outcomes than those with higher socioeconomic status at our center. It also underscores the idea that race is not so much a biological construct but more a consequence of socioeconomic issues. The effect of race is likely mediated by lower socioeconomic status,” said Susrutha Puthanmadhom Narayanan, MD, who presented the results of her study earlier this month in Chicago at the annual meeting of the American Society of Clinical Oncology.

“The current study should make clinicians cognizant of the potential for biases in the management of metastatic breast cancer in terms of socioeconomic status and race. One should think of socioeconomic status as a predictor of bad outcomes, almost like a comorbidity, and think of [associations between race and outcomes], as a consequence of socioeconomic inequality,” said Dr. Puthanmadhom Narayanan, who is an internal medicine resident at University of Pittsburgh Medical Center.

She and her colleagues intend to dig deeper into the relationships. “We are interested in looking at utilization of different treatment options for metastatic breast cancer between the socioeconomic status groups. In the preliminary analysis, we saw that ER-positive metastatic breast cancer patients with lower socioeconomic status get treated with tamoxifen more often than aromatase inhibitors and newer agents. And, we have plans to study stress signaling and inflammation as mediators of bad outcomes in the low socioeconomic status population,” Dr. Puthanmadhom Narayanan said.

In fact, that tendency for lower socioeconomic status patients to receive older treatments should be a call to action for physicians. “This study should make clinicians cognizant of the potential for biases in management of metastatic breast cancer in terms of socioeconomic status and race,” she said.

The study is based on an analysis of data from the Neighborhood Atlas in which a Neighborhood Deprivation Index (NDI) score was calculated. An NDI score in the bottom tertile meant that patients were better off than patients with mid to high range NDI scores. In this study, socioeconomic status was described as “low deprivation” or “high depreviation.” Higher deprivation correlated with lower overall survival. And, there were more Black patients in the higher deprivation group (10.5%), compared with the low deprivation group (3.7%). In multivariate Cox proportional hazard model, socioeconomic status, but not race, had a significant effect on overall survival (HR for high deprivation was 1.19 [95% confidence interval; 1.04-1.37], P = 0.01).

It included 1,246 patients who were treated at the University of Pittsburgh Medical Center between 2000 and 2017. Of 1,246 patients, 414 patients considered in the bottom tertile of NDI as having low deprivation, while 832 patients in the middle or top tertiles were classified as having high deprivation.

The two socioeconomic status groups were similar in baseline characteristics, with the exception of race: 10.5% of the high deprivation group were African American, compared with 3.7% of the low deprivation group (P =.000093).

Univariate analyses showed worse survival in both Black women and women in the lower socioeconomic status group, but a multivariate analysis found only socioeconomic status was associated with overall survival (hazard ratio for lower socioeconomic status, 1.19; P = .01).

The study had several strengths, according to Rachel Freedman, MD, MPH, who served as a discussant for the abstract. “It included both de novo and recurrent metastatic breast cancer, unlike previous studies based on the Surveillance, Epidemiology, and End Results (SEER) database that only included de novo cases. It also employed a novel tool to define socioeconomic status in the form of the Neighborhood Atlas. The study “adds more evidence that socioeconomic status likely mediates much of what we see when it comes to racial disparities,” said Dr. Freedman, who is a senior physician at Dana Farber Cancer Institute.

Nevertheless, more work needs to be done. Dr. Freedman pointed out that the current study did not include information on treatment.

The findings underscore the failure to date to address disparities in breast cancer treatment, an effort that is hampered by difficulty in teasing out complex factors that may impact survival. “We need to standardize the way that we collect social determinants of health and act upon findings, and we need to standardize patient navigation, and we need to commit as a community to diverse clinical trial populations,” Dr. Freedman said.

Dr. Narayanan has no relevant financial disclosures. Dr. Freedman is an employee and stockholder of Firefly Health.

A neighborhood analysis of socioeconomic status conducted in the Pittsburgh area found worse metastatic breast cancer survival outcomes among patients of low socioeconomic status. The findings suggest that race is not a relevant factor in outcomes.

“This study demonstrates that metastatic breast cancer patients of low socioeconomic status have worse outcomes than those with higher socioeconomic status at our center. It also underscores the idea that race is not so much a biological construct but more a consequence of socioeconomic issues. The effect of race is likely mediated by lower socioeconomic status,” said Susrutha Puthanmadhom Narayanan, MD, who presented the results of her study earlier this month in Chicago at the annual meeting of the American Society of Clinical Oncology.

“The current study should make clinicians cognizant of the potential for biases in the management of metastatic breast cancer in terms of socioeconomic status and race. One should think of socioeconomic status as a predictor of bad outcomes, almost like a comorbidity, and think of [associations between race and outcomes], as a consequence of socioeconomic inequality,” said Dr. Puthanmadhom Narayanan, who is an internal medicine resident at University of Pittsburgh Medical Center.

She and her colleagues intend to dig deeper into the relationships. “We are interested in looking at utilization of different treatment options for metastatic breast cancer between the socioeconomic status groups. In the preliminary analysis, we saw that ER-positive metastatic breast cancer patients with lower socioeconomic status get treated with tamoxifen more often than aromatase inhibitors and newer agents. And, we have plans to study stress signaling and inflammation as mediators of bad outcomes in the low socioeconomic status population,” Dr. Puthanmadhom Narayanan said.

In fact, that tendency for lower socioeconomic status patients to receive older treatments should be a call to action for physicians. “This study should make clinicians cognizant of the potential for biases in management of metastatic breast cancer in terms of socioeconomic status and race,” she said.

The study is based on an analysis of data from the Neighborhood Atlas in which a Neighborhood Deprivation Index (NDI) score was calculated. An NDI score in the bottom tertile meant that patients were better off than patients with mid to high range NDI scores. In this study, socioeconomic status was described as “low deprivation” or “high depreviation.” Higher deprivation correlated with lower overall survival. And, there were more Black patients in the higher deprivation group (10.5%), compared with the low deprivation group (3.7%). In multivariate Cox proportional hazard model, socioeconomic status, but not race, had a significant effect on overall survival (HR for high deprivation was 1.19 [95% confidence interval; 1.04-1.37], P = 0.01).

It included 1,246 patients who were treated at the University of Pittsburgh Medical Center between 2000 and 2017. Of 1,246 patients, 414 patients considered in the bottom tertile of NDI as having low deprivation, while 832 patients in the middle or top tertiles were classified as having high deprivation.

The two socioeconomic status groups were similar in baseline characteristics, with the exception of race: 10.5% of the high deprivation group were African American, compared with 3.7% of the low deprivation group (P =.000093).

Univariate analyses showed worse survival in both Black women and women in the lower socioeconomic status group, but a multivariate analysis found only socioeconomic status was associated with overall survival (hazard ratio for lower socioeconomic status, 1.19; P = .01).

The study had several strengths, according to Rachel Freedman, MD, MPH, who served as a discussant for the abstract. “It included both de novo and recurrent metastatic breast cancer, unlike previous studies based on the Surveillance, Epidemiology, and End Results (SEER) database that only included de novo cases. It also employed a novel tool to define socioeconomic status in the form of the Neighborhood Atlas. The study “adds more evidence that socioeconomic status likely mediates much of what we see when it comes to racial disparities,” said Dr. Freedman, who is a senior physician at Dana Farber Cancer Institute.

Nevertheless, more work needs to be done. Dr. Freedman pointed out that the current study did not include information on treatment.

The findings underscore the failure to date to address disparities in breast cancer treatment, an effort that is hampered by difficulty in teasing out complex factors that may impact survival. “We need to standardize the way that we collect social determinants of health and act upon findings, and we need to standardize patient navigation, and we need to commit as a community to diverse clinical trial populations,” Dr. Freedman said.

Dr. Narayanan has no relevant financial disclosures. Dr. Freedman is an employee and stockholder of Firefly Health.

In a surprising discovery that flies in the face of conventional medicine, McGill University researchers report that treating pain with anti-inflammatory medication, like ibuprofen or aspirin, may promote pain in the long term.

The paper, published in Science Translational Medicine, suggests that inflammation, a normal part of injury recovery, helps resolve acute pain and prevents it from becoming chronic. Blocking that inflammation may interfere with this process, leading to harder-to-treat pain.

“What we’ve been doing for decades not only appears to be wrong, but appears to be 180 degrees wrong,” says senior study author Jeffrey Mogil, PhD, a professor in the department of psychology at McGill University in Montreal. “You should not be blocking inflammation. You should be letting inflammation happen. That’s what stops chronic pain.”
 

Inflammation: Nature’s pain reliever

Wanting to know why pain goes away for some but drags on (and on) for others, the researchers looked at pain mechanisms in both humans and mice. They found that a type of white blood cell known as a neutrophil seems to play a key role.

“In analyzing the genes of people suffering from lower back pain, we observed active changes in genes over time in people whose pain went away,” says Luda Diatchenko, PhD, a professor in the faculty of medicine and Canada excellence research chair in human pain genetics at McGill. “Changes in the blood cells and their activity seemed to be the most important factor, especially in cells called neutrophils.”

To test this link, the researchers blocked neutrophils in mice and found the pain lasted 2-10 times longer than normal. Anti-inflammatory drugs, despite providing short-term relief, had the same pain-prolonging effect – though injecting neutrophils into the mice seemed to keep that from happening.

The findings are supported by a separate analysis of 500,000 people in the United Kingdom that showed those taking anti-inflammatory drugs to treat their pain were more likely to have pain 2-10 years later.

“Inflammation occurs for a reason,” says Dr. Mogil, “and it looks like it’s dangerous to interfere with it.”
 

Rethinking how we treat pain

Neutrophils arrive early during inflammation, at the onset of injury – just when many of us reach for pain medication. This research suggests it might be better not to block inflammation, instead letting the neutrophils “do their thing.” Taking an analgesic that alleviates pain without blocking neutrophils, like acetaminophen, may be better than taking an anti-inflammatory drug or steroid, says Dr. Mogil.

Still, while the findings are compelling, clinical trials are needed to directly compare anti-inflammatory drugs to other painkillers, the researchers said. This research may also lay the groundwork for new drug development for chronic pain patients, Dr. Mogil says.

“Our data strongly suggests that neutrophils act like analgesics themselves, which is potentially useful in terms of analgesic development,” Dr. Mogil says. “And of course, we need new analgesics.”

A version of this article first appeared on WebMD.com.

In a surprising discovery that flies in the face of conventional medicine, McGill University researchers report that treating pain with anti-inflammatory medication, like ibuprofen or aspirin, may promote pain in the long term.

The paper, published in Science Translational Medicine, suggests that inflammation, a normal part of injury recovery, helps resolve acute pain and prevents it from becoming chronic. Blocking that inflammation may interfere with this process, leading to harder-to-treat pain.

“What we’ve been doing for decades not only appears to be wrong, but appears to be 180 degrees wrong,” says senior study author Jeffrey Mogil, PhD, a professor in the department of psychology at McGill University in Montreal. “You should not be blocking inflammation. You should be letting inflammation happen. That’s what stops chronic pain.”
 

Inflammation: Nature’s pain reliever

Wanting to know why pain goes away for some but drags on (and on) for others, the researchers looked at pain mechanisms in both humans and mice. They found that a type of white blood cell known as a neutrophil seems to play a key role.

“In analyzing the genes of people suffering from lower back pain, we observed active changes in genes over time in people whose pain went away,” says Luda Diatchenko, PhD, a professor in the faculty of medicine and Canada excellence research chair in human pain genetics at McGill. “Changes in the blood cells and their activity seemed to be the most important factor, especially in cells called neutrophils.”

To test this link, the researchers blocked neutrophils in mice and found the pain lasted 2-10 times longer than normal. Anti-inflammatory drugs, despite providing short-term relief, had the same pain-prolonging effect – though injecting neutrophils into the mice seemed to keep that from happening.

The findings are supported by a separate analysis of 500,000 people in the United Kingdom that showed those taking anti-inflammatory drugs to treat their pain were more likely to have pain 2-10 years later.

“Inflammation occurs for a reason,” says Dr. Mogil, “and it looks like it’s dangerous to interfere with it.”
 

Rethinking how we treat pain

Neutrophils arrive early during inflammation, at the onset of injury – just when many of us reach for pain medication. This research suggests it might be better not to block inflammation, instead letting the neutrophils “do their thing.” Taking an analgesic that alleviates pain without blocking neutrophils, like acetaminophen, may be better than taking an anti-inflammatory drug or steroid, says Dr. Mogil.

Still, while the findings are compelling, clinical trials are needed to directly compare anti-inflammatory drugs to other painkillers, the researchers said. This research may also lay the groundwork for new drug development for chronic pain patients, Dr. Mogil says.

“Our data strongly suggests that neutrophils act like analgesics themselves, which is potentially useful in terms of analgesic development,” Dr. Mogil says. “And of course, we need new analgesics.”

A version of this article first appeared on WebMD.com.

In a surprising discovery that flies in the face of conventional medicine, McGill University researchers report that treating pain with anti-inflammatory medication, like ibuprofen or aspirin, may promote pain in the long term.

The paper, published in Science Translational Medicine, suggests that inflammation, a normal part of injury recovery, helps resolve acute pain and prevents it from becoming chronic. Blocking that inflammation may interfere with this process, leading to harder-to-treat pain.

“What we’ve been doing for decades not only appears to be wrong, but appears to be 180 degrees wrong,” says senior study author Jeffrey Mogil, PhD, a professor in the department of psychology at McGill University in Montreal. “You should not be blocking inflammation. You should be letting inflammation happen. That’s what stops chronic pain.”
 

Inflammation: Nature’s pain reliever

Wanting to know why pain goes away for some but drags on (and on) for others, the researchers looked at pain mechanisms in both humans and mice. They found that a type of white blood cell known as a neutrophil seems to play a key role.

“In analyzing the genes of people suffering from lower back pain, we observed active changes in genes over time in people whose pain went away,” says Luda Diatchenko, PhD, a professor in the faculty of medicine and Canada excellence research chair in human pain genetics at McGill. “Changes in the blood cells and their activity seemed to be the most important factor, especially in cells called neutrophils.”

To test this link, the researchers blocked neutrophils in mice and found the pain lasted 2-10 times longer than normal. Anti-inflammatory drugs, despite providing short-term relief, had the same pain-prolonging effect – though injecting neutrophils into the mice seemed to keep that from happening.

The findings are supported by a separate analysis of 500,000 people in the United Kingdom that showed those taking anti-inflammatory drugs to treat their pain were more likely to have pain 2-10 years later.

“Inflammation occurs for a reason,” says Dr. Mogil, “and it looks like it’s dangerous to interfere with it.”
 

Rethinking how we treat pain

Neutrophils arrive early during inflammation, at the onset of injury – just when many of us reach for pain medication. This research suggests it might be better not to block inflammation, instead letting the neutrophils “do their thing.” Taking an analgesic that alleviates pain without blocking neutrophils, like acetaminophen, may be better than taking an anti-inflammatory drug or steroid, says Dr. Mogil.

Still, while the findings are compelling, clinical trials are needed to directly compare anti-inflammatory drugs to other painkillers, the researchers said. This research may also lay the groundwork for new drug development for chronic pain patients, Dr. Mogil says.

“Our data strongly suggests that neutrophils act like analgesics themselves, which is potentially useful in terms of analgesic development,” Dr. Mogil says. “And of course, we need new analgesics.”

A version of this article first appeared on WebMD.com.

It all began with the question, “Has your butt been getting enough attention?”

Though that may seem unorthodox, it led researchers to discovering a treatment that may help prevent anal cancer in people with HIV/AIDS. It’s still featured on their study’s website, with this further explanation: “You get your viral load checked, your T-cell count checked, but what about your anus? Did you know that half of HIV+ men have cell changes in their anus caused by HPV?”

The Anal Cancer/HSIL Outcomes Research (ANCHOR) study, led by Joel Palefsky, MD, was published  in The New England Journal of Medicine. Dr. Palefsky, an infectious disease expert at the University of California, San Francisco, and his team set out to determine whether a treatment that prevents cervical cancer in people with human papillomavirus (HPV) would benefit people with HIV/AIDS. The new treatment reduced the likelihood of anal cancer by more than 50%.

The team worked over 7 years, during which time they tested 4,459 men, women, transgender, and nonbinary individuals at 25 sites across the United States. The participants were sorted into two groups: Some received treatment for high-grade squamous intraepithelial lesions (HSILs), and some did not but were monitored for signs of disease. These included individuals over 35 who were living with HIV/AIDS and who were found to have patches of abnormal cells in their rectal lining.

HSILs are the cells gynecologists look for in performing a pap smear. They are precancerous cells commonly found in the cervix of persons with HPV. Finding HSILs during a gynecologic examination alerts clinicians to potential problems.

HSILs can also be found in the anal tract of men and women with HIV. Dr. Palefsky therefore hypothesized that, as with HPV and cervical cancer, these anal HSILs may be a precursor of anal cancer.

The scientists decided to treat these cells the same way they would treat them if found in the cervix and to see whether that reduced the risk of cancer. Doctors used lidocaine to numb the area, then removed the HSILs with an electric probe. The team then assessed whether the treatment prevented people from getting cancer.

It turns out that in many cases, it did. The study concluded after 30 of the participants developed anal cancer. Of those, 21 patients had not received HSIL treatment, compared with nine who did receive the treatment. The treatment resulted in a 57% reduction in the rate of anal cancer among patients who received treatment for their HSILs.

These results are encouraging, said Aasma Shaukat, MD, director of outcomes research in the Division of Gastroenterology and Hepatology at NYU Langone Health. Dr. Shaukat was not involved with the study. She believes it’s going to cause ripples across the field.

“The study is likely to change guidelines in favor of active and early treatment for HSIL and away from watchful waiting in individuals living with HIV to reduce the risk of developing anal squamous cell carcinoma, akin to removing polyps during colonoscopy to progression to and incidence of colorectal cancer,” she said in an email interview.

Treatments for this group of patients are more important now than ever. Since the beginning of the AIDS epidemic in the 1980s, the number of people with HIV has increased, Dr. Palefsky detailed in a press conference announcing the ANCHOR results. That’s partially because of new transmissions and partially owing to the fact that new treatments make it possible for people with HIV to live long, healthy lives. So as more people with HIV move into their sunset years, there are more people at risk for developing cancer, which is a disease associated with aging. Anal cancer sits at the intersection of risk for aging people who have HIV.

Any defense we have against the risk of cancer in this growing demographic is a good thing, says Hanna K. Sanoff, MD, a gastrointestinal oncologist at the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, who was also not involved in the study. Although it’s not ready to be applied in doctors’ offices now, it could be a tool in the future. “Anything we can do to try and decrease the chance of precancerous lesions progressing to a real invasive cancer is of great importance. This kind of prevention work is critical to helping minimize the burden of cancer on our communities,” Dr. Sanoff said in an interview.

The study was funded by the National Cancer Institute of the National Institutes of Health and was conducted through the NCI-supported AIDS Malignancy Consortium. Dr. Shaukat and Dr. Sanoff report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

It all began with the question, “Has your butt been getting enough attention?”

Though that may seem unorthodox, it led researchers to discovering a treatment that may help prevent anal cancer in people with HIV/AIDS. It’s still featured on their study’s website, with this further explanation: “You get your viral load checked, your T-cell count checked, but what about your anus? Did you know that half of HIV+ men have cell changes in their anus caused by HPV?”

The Anal Cancer/HSIL Outcomes Research (ANCHOR) study, led by Joel Palefsky, MD, was published  in The New England Journal of Medicine. Dr. Palefsky, an infectious disease expert at the University of California, San Francisco, and his team set out to determine whether a treatment that prevents cervical cancer in people with human papillomavirus (HPV) would benefit people with HIV/AIDS. The new treatment reduced the likelihood of anal cancer by more than 50%.

The team worked over 7 years, during which time they tested 4,459 men, women, transgender, and nonbinary individuals at 25 sites across the United States. The participants were sorted into two groups: Some received treatment for high-grade squamous intraepithelial lesions (HSILs), and some did not but were monitored for signs of disease. These included individuals over 35 who were living with HIV/AIDS and who were found to have patches of abnormal cells in their rectal lining.

HSILs are the cells gynecologists look for in performing a pap smear. They are precancerous cells commonly found in the cervix of persons with HPV. Finding HSILs during a gynecologic examination alerts clinicians to potential problems.

HSILs can also be found in the anal tract of men and women with HIV. Dr. Palefsky therefore hypothesized that, as with HPV and cervical cancer, these anal HSILs may be a precursor of anal cancer.

The scientists decided to treat these cells the same way they would treat them if found in the cervix and to see whether that reduced the risk of cancer. Doctors used lidocaine to numb the area, then removed the HSILs with an electric probe. The team then assessed whether the treatment prevented people from getting cancer.

It turns out that in many cases, it did. The study concluded after 30 of the participants developed anal cancer. Of those, 21 patients had not received HSIL treatment, compared with nine who did receive the treatment. The treatment resulted in a 57% reduction in the rate of anal cancer among patients who received treatment for their HSILs.

These results are encouraging, said Aasma Shaukat, MD, director of outcomes research in the Division of Gastroenterology and Hepatology at NYU Langone Health. Dr. Shaukat was not involved with the study. She believes it’s going to cause ripples across the field.

“The study is likely to change guidelines in favor of active and early treatment for HSIL and away from watchful waiting in individuals living with HIV to reduce the risk of developing anal squamous cell carcinoma, akin to removing polyps during colonoscopy to progression to and incidence of colorectal cancer,” she said in an email interview.

Treatments for this group of patients are more important now than ever. Since the beginning of the AIDS epidemic in the 1980s, the number of people with HIV has increased, Dr. Palefsky detailed in a press conference announcing the ANCHOR results. That’s partially because of new transmissions and partially owing to the fact that new treatments make it possible for people with HIV to live long, healthy lives. So as more people with HIV move into their sunset years, there are more people at risk for developing cancer, which is a disease associated with aging. Anal cancer sits at the intersection of risk for aging people who have HIV.

Any defense we have against the risk of cancer in this growing demographic is a good thing, says Hanna K. Sanoff, MD, a gastrointestinal oncologist at the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, who was also not involved in the study. Although it’s not ready to be applied in doctors’ offices now, it could be a tool in the future. “Anything we can do to try and decrease the chance of precancerous lesions progressing to a real invasive cancer is of great importance. This kind of prevention work is critical to helping minimize the burden of cancer on our communities,” Dr. Sanoff said in an interview.

The study was funded by the National Cancer Institute of the National Institutes of Health and was conducted through the NCI-supported AIDS Malignancy Consortium. Dr. Shaukat and Dr. Sanoff report no relevant financial relationships.

A version of this article first appeared on Medscape.com.

It all began with the question, “Has your butt been getting enough attention?”

Though that may seem unorthodox, it led researchers to discovering a treatment that may help prevent anal cancer in people with HIV/AIDS. It’s still featured on their study’s website, with this further explanation: “You get your viral load checked, your T-cell count checked, but what about your anus? Did you know that half of HIV+ men have cell changes in their anus caused by HPV?”

The Anal Cancer/HSIL Outcomes Research (ANCHOR) study, led by Joel Palefsky, MD, was published  in The New England Journal of Medicine. Dr. Palefsky, an infectious disease expert at the University of California, San Francisco, and his team set out to determine whether a treatment that prevents cervical cancer in people with human papillomavirus (HPV) would benefit people with HIV/AIDS. The new treatment reduced the likelihood of anal cancer by more than 50%.

The team worked over 7 years, during which time they tested 4,459 men, women, transgender, and nonbinary individuals at 25 sites across the United States. The participants were sorted into two groups: Some received treatment for high-grade squamous intraepithelial lesions (HSILs), and some did not but were monitored for signs of disease. These included individuals over 35 who were living with HIV/AIDS and who were found to have patches of abnormal cells in their rectal lining.

HSILs are the cells gynecologists look for in performing a pap smear. They are precancerous cells commonly found in the cervix of persons with HPV. Finding HSILs during a gynecologic examination alerts clinicians to potential problems.

HSILs can also be found in the anal tract of men and women with HIV. Dr. Palefsky therefore hypothesized that, as with HPV and cervical cancer, these anal HSILs may be a precursor of anal cancer.

The scientists decided to treat these cells the same way they would treat them if found in the cervix and to see whether that reduced the risk of cancer. Doctors used lidocaine to numb the area, then removed the HSILs with an electric probe. The team then assessed whether the treatment prevented people from getting cancer.

It turns out that in many cases, it did. The study concluded after 30 of the participants developed anal cancer. Of those, 21 patients had not received HSIL treatment, compared with nine who did receive the treatment. The treatment resulted in a 57% reduction in the rate of anal cancer among patients who received treatment for their HSILs.

These results are encouraging, said Aasma Shaukat, MD, director of outcomes research in the Division of Gastroenterology and Hepatology at NYU Langone Health. Dr. Shaukat was not involved with the study. She believes it’s going to cause ripples across the field.

“The study is likely to change guidelines in favor of active and early treatment for HSIL and away from watchful waiting in individuals living with HIV to reduce the risk of developing anal squamous cell carcinoma, akin to removing polyps during colonoscopy to progression to and incidence of colorectal cancer,” she said in an email interview.

Treatments for this group of patients are more important now than ever. Since the beginning of the AIDS epidemic in the 1980s, the number of people with HIV has increased, Dr. Palefsky detailed in a press conference announcing the ANCHOR results. That’s partially because of new transmissions and partially owing to the fact that new treatments make it possible for people with HIV to live long, healthy lives. So as more people with HIV move into their sunset years, there are more people at risk for developing cancer, which is a disease associated with aging. Anal cancer sits at the intersection of risk for aging people who have HIV.

Any defense we have against the risk of cancer in this growing demographic is a good thing, says Hanna K. Sanoff, MD, a gastrointestinal oncologist at the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, who was also not involved in the study. Although it’s not ready to be applied in doctors’ offices now, it could be a tool in the future. “Anything we can do to try and decrease the chance of precancerous lesions progressing to a real invasive cancer is of great importance. This kind of prevention work is critical to helping minimize the burden of cancer on our communities,” Dr. Sanoff said in an interview.

The study was funded by the National Cancer Institute of the National Institutes of Health and was conducted through the NCI-supported AIDS Malignancy Consortium. Dr. Shaukat and Dr. Sanoff report no relevant financial relationships.

A version of this article first appeared on Medscape.com.