Editor’s note: “Everything We Say and Do” is an informational series developed by SHM’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experience of care. Each article will focus on how the contributor applies one or more of the “key communication” tactics in practice to maintain provider accountability for “everything we say and do that affects our patients’ thoughts, feelings, and well-being.”

View a chart outlining key communication tactics

What I Say and Do

I sit down at patients’ eye level during patient visits and use a team brochure/personal business card for all new patients.

Why I Do It

One of the major concerns expressed by patients is the time spent with them by their provider. Sitting down at patients’ eye level lets them know that you are not in a hurry and you are there to give them whatever time they need. Sitting also causes your patients to perceive that you spent more time with them than if you spent the same amount of time while standing. This practice is not only advocated by patient-care consultants but is something I had reinforced during my firsthand experience as a patient several years ago when I had a surgical procedure. Every time the surgeon came into my hospital room, he sat in the chair, leisurely crossed his legs, and spoke to me from that position while writing in the chart. I knew exactly what he was doing, and it still made a difference to me! It put me more at ease and made me feel that he was there for me, ready to give me whatever time I needed and answer any questions that I had (and I had them). Sitting also puts you on an even level with your patients so they feel that you are talking with them, not down to them. This eases tension, adds comfort and trust to the situation, and is much more engaging.

How I Do It

After I greet patients, I look for a place to sit. If there is a chair, I pull it over to the bedside, sit in a relaxed manner, and continue the visit. If there is no chair in the room, I will sit on the windowsill, the bedside table (I have even been known to lower the bedside tray table and sit on the end with the support post if there is room on it), or whatever I can utilize to physically put myself on patients’ level. As a last resort, as long as there is not an isolatable infection, I will ask permission to sit on the edge of the bed. I make a point of telling them during this process that I am looking for a place to sit and talk so that they know this is my goal.

After the initial conversation and exam, if the patients are new to the service, I walk them through our team brochure and reiterate how we act as their PCP in the hospital and how we communicate with their PCP. I also make a point to show the team photo roster, which personalizes our team to patients, and say, “I also want you to have one of my baseball cards. We call our business cards ‘baseball cards’ because they have our pictures and a lot of ‘stats’ on them: our training, personal interests. That way, you know more about the person who is helping to take care of you.” I almost always see these cards out on patients’ trays or bedside tables on subsequent visits. Patients seem appreciative of the cards and the information. If I see another provider’s baseball card, I will ask patients a question about that provider as a way to continue to foster relations between our patients and our team. The more our patients can relate to us, the more they will trust us and the better their experience will be. TH

Dr. Sharp is a chief hospitalist with Sound Physicians at UF Health in Jacksonville, Fla.

Editor’s note: “Everything We Say and Do” is an informational series developed by SHM’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experience of care. Each article will focus on how the contributor applies one or more of the “key communication” tactics in practice to maintain provider accountability for “everything we say and do that affects our patients’ thoughts, feelings, and well-being.”

View a chart outlining key communication tactics

What I Say and Do

I sit down at patients’ eye level during patient visits and use a team brochure/personal business card for all new patients.

Why I Do It

One of the major concerns expressed by patients is the time spent with them by their provider. Sitting down at patients’ eye level lets them know that you are not in a hurry and you are there to give them whatever time they need. Sitting also causes your patients to perceive that you spent more time with them than if you spent the same amount of time while standing. This practice is not only advocated by patient-care consultants but is something I had reinforced during my firsthand experience as a patient several years ago when I had a surgical procedure. Every time the surgeon came into my hospital room, he sat in the chair, leisurely crossed his legs, and spoke to me from that position while writing in the chart. I knew exactly what he was doing, and it still made a difference to me! It put me more at ease and made me feel that he was there for me, ready to give me whatever time I needed and answer any questions that I had (and I had them). Sitting also puts you on an even level with your patients so they feel that you are talking with them, not down to them. This eases tension, adds comfort and trust to the situation, and is much more engaging.

How I Do It

After I greet patients, I look for a place to sit. If there is a chair, I pull it over to the bedside, sit in a relaxed manner, and continue the visit. If there is no chair in the room, I will sit on the windowsill, the bedside table (I have even been known to lower the bedside tray table and sit on the end with the support post if there is room on it), or whatever I can utilize to physically put myself on patients’ level. As a last resort, as long as there is not an isolatable infection, I will ask permission to sit on the edge of the bed. I make a point of telling them during this process that I am looking for a place to sit and talk so that they know this is my goal.

After the initial conversation and exam, if the patients are new to the service, I walk them through our team brochure and reiterate how we act as their PCP in the hospital and how we communicate with their PCP. I also make a point to show the team photo roster, which personalizes our team to patients, and say, “I also want you to have one of my baseball cards. We call our business cards ‘baseball cards’ because they have our pictures and a lot of ‘stats’ on them: our training, personal interests. That way, you know more about the person who is helping to take care of you.” I almost always see these cards out on patients’ trays or bedside tables on subsequent visits. Patients seem appreciative of the cards and the information. If I see another provider’s baseball card, I will ask patients a question about that provider as a way to continue to foster relations between our patients and our team. The more our patients can relate to us, the more they will trust us and the better their experience will be. TH

Dr. Sharp is a chief hospitalist with Sound Physicians at UF Health in Jacksonville, Fla.

Editor’s note: “Everything We Say and Do” is an informational series developed by SHM’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experience of care. Each article will focus on how the contributor applies one or more of the “key communication” tactics in practice to maintain provider accountability for “everything we say and do that affects our patients’ thoughts, feelings, and well-being.”

View a chart outlining key communication tactics

What I Say and Do

I sit down at patients’ eye level during patient visits and use a team brochure/personal business card for all new patients.

Why I Do It

One of the major concerns expressed by patients is the time spent with them by their provider. Sitting down at patients’ eye level lets them know that you are not in a hurry and you are there to give them whatever time they need. Sitting also causes your patients to perceive that you spent more time with them than if you spent the same amount of time while standing. This practice is not only advocated by patient-care consultants but is something I had reinforced during my firsthand experience as a patient several years ago when I had a surgical procedure. Every time the surgeon came into my hospital room, he sat in the chair, leisurely crossed his legs, and spoke to me from that position while writing in the chart. I knew exactly what he was doing, and it still made a difference to me! It put me more at ease and made me feel that he was there for me, ready to give me whatever time I needed and answer any questions that I had (and I had them). Sitting also puts you on an even level with your patients so they feel that you are talking with them, not down to them. This eases tension, adds comfort and trust to the situation, and is much more engaging.

How I Do It

After I greet patients, I look for a place to sit. If there is a chair, I pull it over to the bedside, sit in a relaxed manner, and continue the visit. If there is no chair in the room, I will sit on the windowsill, the bedside table (I have even been known to lower the bedside tray table and sit on the end with the support post if there is room on it), or whatever I can utilize to physically put myself on patients’ level. As a last resort, as long as there is not an isolatable infection, I will ask permission to sit on the edge of the bed. I make a point of telling them during this process that I am looking for a place to sit and talk so that they know this is my goal.

After the initial conversation and exam, if the patients are new to the service, I walk them through our team brochure and reiterate how we act as their PCP in the hospital and how we communicate with their PCP. I also make a point to show the team photo roster, which personalizes our team to patients, and say, “I also want you to have one of my baseball cards. We call our business cards ‘baseball cards’ because they have our pictures and a lot of ‘stats’ on them: our training, personal interests. That way, you know more about the person who is helping to take care of you.” I almost always see these cards out on patients’ trays or bedside tables on subsequent visits. Patients seem appreciative of the cards and the information. If I see another provider’s baseball card, I will ask patients a question about that provider as a way to continue to foster relations between our patients and our team. The more our patients can relate to us, the more they will trust us and the better their experience will be. TH

Dr. Sharp is a chief hospitalist with Sound Physicians at UF Health in Jacksonville, Fla.

Purpose: To disseminate information regarding the Louis Stokes Cleveland VAMC process for CT guided bone marrow aspiration and biopsies (BMAB).

Relevant Background/Problem: With timely access to quality care at the forefront of many VA-based initiatives we sought to decrease wait times for new patients with hematology concerns. Upon review of clinic utilization we recognized that many established patients requiring BMAB were scheduled into a new patient slot to allow enough time for the procedure. At the same time, our colleagues in Interventional Radiology (IR) approached us regarding the feasibility of performing BMAB using CT guidance.

Methods: We performed a retrospective review of all BMAB done between September 2014 and August 2015 before the IR guided procedure was offered to determine number of procedures performed. We then examined those cases performed from September 2015 to June 2016 after rollout of IR guided BMAB to determine numbers of cases, location of procedure (IR versus Hematology/Oncology), operator (IR versus staff versus fellow), and complications.

Data Analysis: From September 2014 to August 2015, 211 BMAB were performed, averaging 17 per month. From September 2015 to June 2016, 207 BMAB were performed with an average of 20 per month. During the latter time period, 50% of BMAB were performed using IR guidance with the other 50% performed by either Hematology/Oncology staff or fellows. There were no complications reported regardless of location and operator. Exposure to radiation dose was extremely low.

Results: IR guided BMAB is a safe and feasible option for patients and Hematology/Oncology providers.

Implications: IR guided BMAB can be one option to decompress already overbooked Hematology/Oncology clinics and to provide quicker access to care for patients with newly diagnosed hematologic and oncologic conditions.

Purpose: To disseminate information regarding the Louis Stokes Cleveland VAMC process for CT guided bone marrow aspiration and biopsies (BMAB).

Relevant Background/Problem: With timely access to quality care at the forefront of many VA-based initiatives we sought to decrease wait times for new patients with hematology concerns. Upon review of clinic utilization we recognized that many established patients requiring BMAB were scheduled into a new patient slot to allow enough time for the procedure. At the same time, our colleagues in Interventional Radiology (IR) approached us regarding the feasibility of performing BMAB using CT guidance.

Methods: We performed a retrospective review of all BMAB done between September 2014 and August 2015 before the IR guided procedure was offered to determine number of procedures performed. We then examined those cases performed from September 2015 to June 2016 after rollout of IR guided BMAB to determine numbers of cases, location of procedure (IR versus Hematology/Oncology), operator (IR versus staff versus fellow), and complications.

Data Analysis: From September 2014 to August 2015, 211 BMAB were performed, averaging 17 per month. From September 2015 to June 2016, 207 BMAB were performed with an average of 20 per month. During the latter time period, 50% of BMAB were performed using IR guidance with the other 50% performed by either Hematology/Oncology staff or fellows. There were no complications reported regardless of location and operator. Exposure to radiation dose was extremely low.

Results: IR guided BMAB is a safe and feasible option for patients and Hematology/Oncology providers.

Implications: IR guided BMAB can be one option to decompress already overbooked Hematology/Oncology clinics and to provide quicker access to care for patients with newly diagnosed hematologic and oncologic conditions.

Purpose: To disseminate information regarding the Louis Stokes Cleveland VAMC process for CT guided bone marrow aspiration and biopsies (BMAB).

Relevant Background/Problem: With timely access to quality care at the forefront of many VA-based initiatives we sought to decrease wait times for new patients with hematology concerns. Upon review of clinic utilization we recognized that many established patients requiring BMAB were scheduled into a new patient slot to allow enough time for the procedure. At the same time, our colleagues in Interventional Radiology (IR) approached us regarding the feasibility of performing BMAB using CT guidance.

Methods: We performed a retrospective review of all BMAB done between September 2014 and August 2015 before the IR guided procedure was offered to determine number of procedures performed. We then examined those cases performed from September 2015 to June 2016 after rollout of IR guided BMAB to determine numbers of cases, location of procedure (IR versus Hematology/Oncology), operator (IR versus staff versus fellow), and complications.

Data Analysis: From September 2014 to August 2015, 211 BMAB were performed, averaging 17 per month. From September 2015 to June 2016, 207 BMAB were performed with an average of 20 per month. During the latter time period, 50% of BMAB were performed using IR guidance with the other 50% performed by either Hematology/Oncology staff or fellows. There were no complications reported regardless of location and operator. Exposure to radiation dose was extremely low.

Results: IR guided BMAB is a safe and feasible option for patients and Hematology/Oncology providers.

Implications: IR guided BMAB can be one option to decompress already overbooked Hematology/Oncology clinics and to provide quicker access to care for patients with newly diagnosed hematologic and oncologic conditions.

Background: CSP 380-Risk Factors for Large Colonic Adenomas, a screening colonoscopy study, enrolled 3,121 patients from 1994-97 at 13 VA sites. We report 10 year outcomes based on risk group after baseline colonoscopy.

Methods: Asymptomatic veterans age 50-75 who had not undergone colorectal cancer (CRC) screening in the prior 10 years underwent colonoscopy and were classified into 6 risk groups: no neoplasia, 1-2 small adenomas, 3-10 adenomas, > 10 adenomas, advanced adenoma (polyp ≥ 1 cm, villous histology, or high grade dysplasia), and CRC. Subjects were followed for 10 years until death or last colonoscopy. We report the proportions who developed advanced neoplasia (AN, defined as advanced adenoma or CRC) and CRC.

Results: Of the patients enrolled, 1,917 had at least one follow-up colonoscopy. Of these 1,917, 933 had no neoplasia at baseline; 4.0% developed AN, including 0.8% with CRC. At baseline, 560 patients had 1-2 small adenomas; 5.9% developed AN, including 0.9% with CRC. For those with 3-10 adenomas (134), 15.7% developed AN, including 0.7% with CRC. Two had > 10 adenomas; neither developed AN or CRC. At baseline, 265 patients had advanced adenoma; 19.2% developed AN, including 1.9% with CRC. Twenty-three patients had baseline CRC; 34.8% developed AN, including 21.7% with CRC. Patients with baseline CRC were at highest risk of developing AN. Those with advanced adenoma or 3-10 adenomas were at moderate risk. Those with no neoplasia or 1-2 small adenomas were at lowest risk. Except for those with baseline CRC, all risk groups showed a dramatic decline in CRC incidence after 3 years, with 10-year CRC risk similar to those with no neoplasia at baseline.

Conclusion: 1) Baseline colonoscopy result is a predictor of future risk for AN. 2) Those with baseline CRC remain at risk for recurrence. Intensive surveillance is warranted. 3) Those with 1-2 small adenomas or no adenomas at baseline have a low risk of AN after 2-3 years, and may not need surveillance. 4) Those with baseline advanced adenoma or > 3 adenomas show a dramatic decline in CRC risk after 3 years, suggesting that frequent surveillance may only be necessary in the first 5 years.

Background: CSP 380-Risk Factors for Large Colonic Adenomas, a screening colonoscopy study, enrolled 3,121 patients from 1994-97 at 13 VA sites. We report 10 year outcomes based on risk group after baseline colonoscopy.

Methods: Asymptomatic veterans age 50-75 who had not undergone colorectal cancer (CRC) screening in the prior 10 years underwent colonoscopy and were classified into 6 risk groups: no neoplasia, 1-2 small adenomas, 3-10 adenomas, > 10 adenomas, advanced adenoma (polyp ≥ 1 cm, villous histology, or high grade dysplasia), and CRC. Subjects were followed for 10 years until death or last colonoscopy. We report the proportions who developed advanced neoplasia (AN, defined as advanced adenoma or CRC) and CRC.

Results: Of the patients enrolled, 1,917 had at least one follow-up colonoscopy. Of these 1,917, 933 had no neoplasia at baseline; 4.0% developed AN, including 0.8% with CRC. At baseline, 560 patients had 1-2 small adenomas; 5.9% developed AN, including 0.9% with CRC. For those with 3-10 adenomas (134), 15.7% developed AN, including 0.7% with CRC. Two had > 10 adenomas; neither developed AN or CRC. At baseline, 265 patients had advanced adenoma; 19.2% developed AN, including 1.9% with CRC. Twenty-three patients had baseline CRC; 34.8% developed AN, including 21.7% with CRC. Patients with baseline CRC were at highest risk of developing AN. Those with advanced adenoma or 3-10 adenomas were at moderate risk. Those with no neoplasia or 1-2 small adenomas were at lowest risk. Except for those with baseline CRC, all risk groups showed a dramatic decline in CRC incidence after 3 years, with 10-year CRC risk similar to those with no neoplasia at baseline.

Conclusion: 1) Baseline colonoscopy result is a predictor of future risk for AN. 2) Those with baseline CRC remain at risk for recurrence. Intensive surveillance is warranted. 3) Those with 1-2 small adenomas or no adenomas at baseline have a low risk of AN after 2-3 years, and may not need surveillance. 4) Those with baseline advanced adenoma or > 3 adenomas show a dramatic decline in CRC risk after 3 years, suggesting that frequent surveillance may only be necessary in the first 5 years.

Background: CSP 380-Risk Factors for Large Colonic Adenomas, a screening colonoscopy study, enrolled 3,121 patients from 1994-97 at 13 VA sites. We report 10 year outcomes based on risk group after baseline colonoscopy.

Methods: Asymptomatic veterans age 50-75 who had not undergone colorectal cancer (CRC) screening in the prior 10 years underwent colonoscopy and were classified into 6 risk groups: no neoplasia, 1-2 small adenomas, 3-10 adenomas, > 10 adenomas, advanced adenoma (polyp ≥ 1 cm, villous histology, or high grade dysplasia), and CRC. Subjects were followed for 10 years until death or last colonoscopy. We report the proportions who developed advanced neoplasia (AN, defined as advanced adenoma or CRC) and CRC.

Results: Of the patients enrolled, 1,917 had at least one follow-up colonoscopy. Of these 1,917, 933 had no neoplasia at baseline; 4.0% developed AN, including 0.8% with CRC. At baseline, 560 patients had 1-2 small adenomas; 5.9% developed AN, including 0.9% with CRC. For those with 3-10 adenomas (134), 15.7% developed AN, including 0.7% with CRC. Two had > 10 adenomas; neither developed AN or CRC. At baseline, 265 patients had advanced adenoma; 19.2% developed AN, including 1.9% with CRC. Twenty-three patients had baseline CRC; 34.8% developed AN, including 21.7% with CRC. Patients with baseline CRC were at highest risk of developing AN. Those with advanced adenoma or 3-10 adenomas were at moderate risk. Those with no neoplasia or 1-2 small adenomas were at lowest risk. Except for those with baseline CRC, all risk groups showed a dramatic decline in CRC incidence after 3 years, with 10-year CRC risk similar to those with no neoplasia at baseline.

Conclusion: 1) Baseline colonoscopy result is a predictor of future risk for AN. 2) Those with baseline CRC remain at risk for recurrence. Intensive surveillance is warranted. 3) Those with 1-2 small adenomas or no adenomas at baseline have a low risk of AN after 2-3 years, and may not need surveillance. 4) Those with baseline advanced adenoma or > 3 adenomas show a dramatic decline in CRC risk after 3 years, suggesting that frequent surveillance may only be necessary in the first 5 years.

Background: Colorectal cancer (CRC) screening guidelines in the U.S. recommend genetic evaluation for individuals with ≥ 10 cumulative colorectal adenomas, as they are thought to have an increased risk for underlying hereditary CRC syndromes. However, little is known about the prevalence, clinical characteristics, and long-term outcomes of patients with ≥ 10 cumulative adenomas.

Aims: To estimate the proportion of patients in a screening cohort who are found to have ≥ 10 cumulative adenomas, examine the demographic and baseline clinical risk factors associated with having ≥ 10 cumulative adenomas, and describe the prevalence of advanced neoplasia (AN) and CRC in these patients.

Patients and Methods: The CSP 380 cohort comprises 3,121 asymptomatic veterans aged 50-75 from 13 VA sites who underwent a screening colonoscopy from 1994-97 and were followed for 10 years until death or last colonoscopy. Of these 3,121 patients, 3,089 did not have CRC at baseline. We identified patients with ≥ 10 cumulative adenomas and compared baseline factors (gender, race, family history of CRC, age, BMI, tobacco use, and alcohol use) in patients with and without ≥ 10 cumulative adenomas. We then estimated the age to ≥ 10 cumulative adenomas. Finally, we calculated the prevalence of AN (polyp ≥ 1 cm, villous histology, high grade dysplasia, or CRC) in patients with ≥ 10 adenomas and those with 0-9 adenomas.

Results: Ten or more cumulative adenomas were found in 66 (2.1%) of the 3089 patients in a 10-year period. Age 60-69 is the single baseline risk factor associated with this outcome. Of the 3,023 patients with 0-9 cumulative adenomas, 348 (11.5%) developed AN, including 23 (0.8%) with CRC. Of the 66 patients with ≥ 10 adenomas, 42 (63.6%) developed AN, including 2 (3.0%) with CRC.

Conclusion: The prevalence of ≥ 10 cumulative adenomas was 2% in this screening population, with few cases before age 60. Few patients with this outcome, however, develop CRC within a 10-year period. Future work could identify additional risk factors associated with the development of ≥ 10 cumulative adenomas in order to create a risk stratification tool that may lead to the earlier detection of patients at high risk for hereditary CRC syndromes, AN, and CRC.

Background: Colorectal cancer (CRC) screening guidelines in the U.S. recommend genetic evaluation for individuals with ≥ 10 cumulative colorectal adenomas, as they are thought to have an increased risk for underlying hereditary CRC syndromes. However, little is known about the prevalence, clinical characteristics, and long-term outcomes of patients with ≥ 10 cumulative adenomas.

Aims: To estimate the proportion of patients in a screening cohort who are found to have ≥ 10 cumulative adenomas, examine the demographic and baseline clinical risk factors associated with having ≥ 10 cumulative adenomas, and describe the prevalence of advanced neoplasia (AN) and CRC in these patients.

Patients and Methods: The CSP 380 cohort comprises 3,121 asymptomatic veterans aged 50-75 from 13 VA sites who underwent a screening colonoscopy from 1994-97 and were followed for 10 years until death or last colonoscopy. Of these 3,121 patients, 3,089 did not have CRC at baseline. We identified patients with ≥ 10 cumulative adenomas and compared baseline factors (gender, race, family history of CRC, age, BMI, tobacco use, and alcohol use) in patients with and without ≥ 10 cumulative adenomas. We then estimated the age to ≥ 10 cumulative adenomas. Finally, we calculated the prevalence of AN (polyp ≥ 1 cm, villous histology, high grade dysplasia, or CRC) in patients with ≥ 10 adenomas and those with 0-9 adenomas.

Results: Ten or more cumulative adenomas were found in 66 (2.1%) of the 3089 patients in a 10-year period. Age 60-69 is the single baseline risk factor associated with this outcome. Of the 3,023 patients with 0-9 cumulative adenomas, 348 (11.5%) developed AN, including 23 (0.8%) with CRC. Of the 66 patients with ≥ 10 adenomas, 42 (63.6%) developed AN, including 2 (3.0%) with CRC.

Conclusion: The prevalence of ≥ 10 cumulative adenomas was 2% in this screening population, with few cases before age 60. Few patients with this outcome, however, develop CRC within a 10-year period. Future work could identify additional risk factors associated with the development of ≥ 10 cumulative adenomas in order to create a risk stratification tool that may lead to the earlier detection of patients at high risk for hereditary CRC syndromes, AN, and CRC.

Background: Colorectal cancer (CRC) screening guidelines in the U.S. recommend genetic evaluation for individuals with ≥ 10 cumulative colorectal adenomas, as they are thought to have an increased risk for underlying hereditary CRC syndromes. However, little is known about the prevalence, clinical characteristics, and long-term outcomes of patients with ≥ 10 cumulative adenomas.

Aims: To estimate the proportion of patients in a screening cohort who are found to have ≥ 10 cumulative adenomas, examine the demographic and baseline clinical risk factors associated with having ≥ 10 cumulative adenomas, and describe the prevalence of advanced neoplasia (AN) and CRC in these patients.

Patients and Methods: The CSP 380 cohort comprises 3,121 asymptomatic veterans aged 50-75 from 13 VA sites who underwent a screening colonoscopy from 1994-97 and were followed for 10 years until death or last colonoscopy. Of these 3,121 patients, 3,089 did not have CRC at baseline. We identified patients with ≥ 10 cumulative adenomas and compared baseline factors (gender, race, family history of CRC, age, BMI, tobacco use, and alcohol use) in patients with and without ≥ 10 cumulative adenomas. We then estimated the age to ≥ 10 cumulative adenomas. Finally, we calculated the prevalence of AN (polyp ≥ 1 cm, villous histology, high grade dysplasia, or CRC) in patients with ≥ 10 adenomas and those with 0-9 adenomas.

Results: Ten or more cumulative adenomas were found in 66 (2.1%) of the 3089 patients in a 10-year period. Age 60-69 is the single baseline risk factor associated with this outcome. Of the 3,023 patients with 0-9 cumulative adenomas, 348 (11.5%) developed AN, including 23 (0.8%) with CRC. Of the 66 patients with ≥ 10 adenomas, 42 (63.6%) developed AN, including 2 (3.0%) with CRC.

Conclusion: The prevalence of ≥ 10 cumulative adenomas was 2% in this screening population, with few cases before age 60. Few patients with this outcome, however, develop CRC within a 10-year period. Future work could identify additional risk factors associated with the development of ≥ 10 cumulative adenomas in order to create a risk stratification tool that may lead to the earlier detection of patients at high risk for hereditary CRC syndromes, AN, and CRC.

Background: Prostate cancer is the second leading cause of cancer death in American men, diagnosed mainly in older men. Treatment options for stage 3 prostate cancer include external beam radiation plus hormone therapy (HT) vs external beam radiation plus brachytherapy vs radical prostatectomy in selected cases.

Methodology: A total of 52,384 patients with stage 3 prostate cancer have been studied from national cancer database comparing Veterans Affairs Hospital (VAH) vs Academic Centers from years 2003-2013. Fisher exact test was used to make direct comparisons between centers and treatment type. We used a Bonferroni-adjusted P.

Results: Within both the 50-59 and 60-69-year-old age groups, when compared to Academic hospitals, VAH performed surgery alone at a lower rate (87.6% vs 77.4% and 86.1% vs 77.7%, respectively) and performed Surgery + Radiation and Radiation + Hormone therapy at a significantly higher rate (8.2% vs 15.0% and 6.8% vs 10.0%, respectively). In 70-79 year age group, when compared to Academic hospitals, VAH performed surgery alone at a lower rate (73.5% vs 43.1%) and Hormone therapy only and Radiation + Hormone therapy at significantly higher rate (3.7% vs 17.3% and 20.8% vs 33.9%, respectively) (all P < .001).

Conclusion: In VAH, people within age groups of 50-59, 60-69 years had more surgery plus radiation, radiation plus HT and less surgery alone than Academic centers. In 70-79 age group, VAH performed much more HT only, radiation plus HT and less surgery alone than Academic Centers.

Background: Prostate cancer is the second leading cause of cancer death in American men, diagnosed mainly in older men. Treatment options for stage 3 prostate cancer include external beam radiation plus hormone therapy (HT) vs external beam radiation plus brachytherapy vs radical prostatectomy in selected cases.

Methodology: A total of 52,384 patients with stage 3 prostate cancer have been studied from national cancer database comparing Veterans Affairs Hospital (VAH) vs Academic Centers from years 2003-2013. Fisher exact test was used to make direct comparisons between centers and treatment type. We used a Bonferroni-adjusted P.

Results: Within both the 50-59 and 60-69-year-old age groups, when compared to Academic hospitals, VAH performed surgery alone at a lower rate (87.6% vs 77.4% and 86.1% vs 77.7%, respectively) and performed Surgery + Radiation and Radiation + Hormone therapy at a significantly higher rate (8.2% vs 15.0% and 6.8% vs 10.0%, respectively). In 70-79 year age group, when compared to Academic hospitals, VAH performed surgery alone at a lower rate (73.5% vs 43.1%) and Hormone therapy only and Radiation + Hormone therapy at significantly higher rate (3.7% vs 17.3% and 20.8% vs 33.9%, respectively) (all P < .001).

Conclusion: In VAH, people within age groups of 50-59, 60-69 years had more surgery plus radiation, radiation plus HT and less surgery alone than Academic centers. In 70-79 age group, VAH performed much more HT only, radiation plus HT and less surgery alone than Academic Centers.

Background: Prostate cancer is the second leading cause of cancer death in American men, diagnosed mainly in older men. Treatment options for stage 3 prostate cancer include external beam radiation plus hormone therapy (HT) vs external beam radiation plus brachytherapy vs radical prostatectomy in selected cases.

Methodology: A total of 52,384 patients with stage 3 prostate cancer have been studied from national cancer database comparing Veterans Affairs Hospital (VAH) vs Academic Centers from years 2003-2013. Fisher exact test was used to make direct comparisons between centers and treatment type. We used a Bonferroni-adjusted P.

Results: Within both the 50-59 and 60-69-year-old age groups, when compared to Academic hospitals, VAH performed surgery alone at a lower rate (87.6% vs 77.4% and 86.1% vs 77.7%, respectively) and performed Surgery + Radiation and Radiation + Hormone therapy at a significantly higher rate (8.2% vs 15.0% and 6.8% vs 10.0%, respectively). In 70-79 year age group, when compared to Academic hospitals, VAH performed surgery alone at a lower rate (73.5% vs 43.1%) and Hormone therapy only and Radiation + Hormone therapy at significantly higher rate (3.7% vs 17.3% and 20.8% vs 33.9%, respectively) (all P < .001).

Conclusion: In VAH, people within age groups of 50-59, 60-69 years had more surgery plus radiation, radiation plus HT and less surgery alone than Academic centers. In 70-79 age group, VAH performed much more HT only, radiation plus HT and less surgery alone than Academic Centers.

The VA’s National Oncology Program Office is an active participant in the White House’s Cancer Moonshot Initiative. This presentation will summarize efforts underway to provide Veterans with state of the art cancer care in a learning healthcare system. To achieve the goals of the Cancer Moonshot Initiative and Precision Oncology, the VA needs to: Provide all Veterans with timely access to coordinated, interdisciplinary, disease-specific cancer care; identify and facilitate VA medical center participation in compelling clinical trials that are designed to test novel therapeutics targeted at mutations with a high prevalence among Veterans; and, improve the infrastructure and capability for VA clinicians to practice in a learning healthcare system through decision support tool and robust data analytics.

The VA National Program Office has partnered with the National Cancer Institute (NCI) and the White House to implement innovations designed to achieve these objectives. It has received funding to provide Veterans access to next generation sequencing of tumor tissue. Data generated from analysis of the cancer genome will be analyzed by IBM’s Watson computers.

We are also developing a governance structure for national, multisite clinical trials. It will be similar in formatto NCI’s cooperative groups with oncologists leading diseases committees to evaluate which treatment clinical trials should be conducted nationally within the VA. We have developed national contract research agreements with the large pharmaceutical companies to facilitate national clinical trials. We have also developed agreements with VA Central Office and NCI that will allow industry funded studies to be submitted to the VA Centralized Institutional Review Boards (C-IRB) and VAMCs will be able to accept studies that have been approved by NCI’s centralized IRB. We are leveraging Connected/Tele-health technologies to develop Virtual Tumors Boards and Virtual Cancer Centers. These Virtual Cancer Centers are designed to provide access to expedited workup by specialized clinicians using evidence-based guidelines and clinical care pathways.

The VA’s National Oncology Program Office is an active participant in the White House’s Cancer Moonshot Initiative. This presentation will summarize efforts underway to provide Veterans with state of the art cancer care in a learning healthcare system. To achieve the goals of the Cancer Moonshot Initiative and Precision Oncology, the VA needs to: Provide all Veterans with timely access to coordinated, interdisciplinary, disease-specific cancer care; identify and facilitate VA medical center participation in compelling clinical trials that are designed to test novel therapeutics targeted at mutations with a high prevalence among Veterans; and, improve the infrastructure and capability for VA clinicians to practice in a learning healthcare system through decision support tool and robust data analytics.

The VA National Program Office has partnered with the National Cancer Institute (NCI) and the White House to implement innovations designed to achieve these objectives. It has received funding to provide Veterans access to next generation sequencing of tumor tissue. Data generated from analysis of the cancer genome will be analyzed by IBM’s Watson computers.

We are also developing a governance structure for national, multisite clinical trials. It will be similar in formatto NCI’s cooperative groups with oncologists leading diseases committees to evaluate which treatment clinical trials should be conducted nationally within the VA. We have developed national contract research agreements with the large pharmaceutical companies to facilitate national clinical trials. We have also developed agreements with VA Central Office and NCI that will allow industry funded studies to be submitted to the VA Centralized Institutional Review Boards (C-IRB) and VAMCs will be able to accept studies that have been approved by NCI’s centralized IRB. We are leveraging Connected/Tele-health technologies to develop Virtual Tumors Boards and Virtual Cancer Centers. These Virtual Cancer Centers are designed to provide access to expedited workup by specialized clinicians using evidence-based guidelines and clinical care pathways.

The VA’s National Oncology Program Office is an active participant in the White House’s Cancer Moonshot Initiative. This presentation will summarize efforts underway to provide Veterans with state of the art cancer care in a learning healthcare system. To achieve the goals of the Cancer Moonshot Initiative and Precision Oncology, the VA needs to: Provide all Veterans with timely access to coordinated, interdisciplinary, disease-specific cancer care; identify and facilitate VA medical center participation in compelling clinical trials that are designed to test novel therapeutics targeted at mutations with a high prevalence among Veterans; and, improve the infrastructure and capability for VA clinicians to practice in a learning healthcare system through decision support tool and robust data analytics.

The VA National Program Office has partnered with the National Cancer Institute (NCI) and the White House to implement innovations designed to achieve these objectives. It has received funding to provide Veterans access to next generation sequencing of tumor tissue. Data generated from analysis of the cancer genome will be analyzed by IBM’s Watson computers.

We are also developing a governance structure for national, multisite clinical trials. It will be similar in formatto NCI’s cooperative groups with oncologists leading diseases committees to evaluate which treatment clinical trials should be conducted nationally within the VA. We have developed national contract research agreements with the large pharmaceutical companies to facilitate national clinical trials. We have also developed agreements with VA Central Office and NCI that will allow industry funded studies to be submitted to the VA Centralized Institutional Review Boards (C-IRB) and VAMCs will be able to accept studies that have been approved by NCI’s centralized IRB. We are leveraging Connected/Tele-health technologies to develop Virtual Tumors Boards and Virtual Cancer Centers. These Virtual Cancer Centers are designed to provide access to expedited workup by specialized clinicians using evidence-based guidelines and clinical care pathways.

Neutrophil engulfing bacteria

Image by Volker Brinkmann

Developing blood cells are caught in a tug of war between competing gene regulatory networks before finally deciding what type of cell to become, according to a study published in Nature.

Researchers found that, as developing blood cells are triggered by a multitude of genetic signals firing on and off, they are pulled back and forth in fluctuating multi-lineage states before finally becoming specific cell types.

The team still doesn’t understand exactly what drives the cells to an eventual fate, but their work suggests that competing gene networks induce dynamic instability, resulting in mixed-lineage states that are necessary to prime newly forming cells for that decision.

“It is somewhat chaotic, but, from that chaos, results order,” said study author Harinder Singh, PhD, of Cincinnati Children’s Hospital Medical Center in Ohio.

“It’s a finding that helps us address a fundamental question of developmental biology: What are the nature of the intermediate states and the networks of regulatory genes that underlie cell-type specification?”

Although the finding requires additional study to better understand the back-and-forth nature of this process, the research may eventually provide new insights into developmental miscues that cause disease, according to study author H. Leighton Grimes, PhD, of Cincinnati Children’s.

“How do blood cells know to become neutrophils or monocytes?” Dr Grimes asked. “Two thirds of your bone marrow is taken up with this activity, and the number of cells has to be exquisitely balanced. Too many or too few of either can kill you.”

For this study, Dr Grimes and his colleagues looked specifically at the formation of neutrophils and macrophages. The researchers studied mouse cells as they developed in a natural state using single-cell RNA sequencing.

The team also used a bioinformatics computer program known as iterative clustering and guide-gene selection (ICGS). They used ICGS to process and analyze sequencing and biological data to identify the various transitioning or shifting genomic and cellular states of developing blood cells.

Dynamic instability

Researchers previously proposed that neutrophils and macrophages result from a bi-stable gene regulatory network—one that can manifest either of 2 stable states. But the different cellular transition states and underlying molecular dynamics of development have remained unknown.

Dr Grimes and his colleagues said their analysis of developing blood cells captured a prevalent mixed-lineage intermediate.

These intermediates expressed a combination of genes, including those typical of hematopoietic stem and progenitor cells and some genes that are specific for red blood cells, platelets, macrophages, and neutrophils. This seemed to reflect competing genetic programs.

The researchers also observed the developing cells moving through a rare state where they encountered turbulence known as dynamic instability. This was caused by 2 counteracting myeloid gene regulatory networks.

Two key components of the counteracting gene networks were Irf8 and Gfi1, genes that are involved in blood cell formation. When Irf8 and Gfi1 were eliminated from the picture, the rare cells could be trapped in an intermediate state.

As they continue this work, the researchers want to gain a clearer understanding of what finally causes cells in intermediate states of dynamic instability to assume specific fates.

The team suggests the influence of 2 simultaneous and counteracting gene networks generates internal oscillations that are eventually stabilized by unknown mechanisms to generate 1 of 2 different cell fates.

Neutrophil engulfing bacteria

Image by Volker Brinkmann

Developing blood cells are caught in a tug of war between competing gene regulatory networks before finally deciding what type of cell to become, according to a study published in Nature.

Researchers found that, as developing blood cells are triggered by a multitude of genetic signals firing on and off, they are pulled back and forth in fluctuating multi-lineage states before finally becoming specific cell types.

The team still doesn’t understand exactly what drives the cells to an eventual fate, but their work suggests that competing gene networks induce dynamic instability, resulting in mixed-lineage states that are necessary to prime newly forming cells for that decision.

“It is somewhat chaotic, but, from that chaos, results order,” said study author Harinder Singh, PhD, of Cincinnati Children’s Hospital Medical Center in Ohio.

“It’s a finding that helps us address a fundamental question of developmental biology: What are the nature of the intermediate states and the networks of regulatory genes that underlie cell-type specification?”

Although the finding requires additional study to better understand the back-and-forth nature of this process, the research may eventually provide new insights into developmental miscues that cause disease, according to study author H. Leighton Grimes, PhD, of Cincinnati Children’s.

“How do blood cells know to become neutrophils or monocytes?” Dr Grimes asked. “Two thirds of your bone marrow is taken up with this activity, and the number of cells has to be exquisitely balanced. Too many or too few of either can kill you.”

For this study, Dr Grimes and his colleagues looked specifically at the formation of neutrophils and macrophages. The researchers studied mouse cells as they developed in a natural state using single-cell RNA sequencing.

The team also used a bioinformatics computer program known as iterative clustering and guide-gene selection (ICGS). They used ICGS to process and analyze sequencing and biological data to identify the various transitioning or shifting genomic and cellular states of developing blood cells.

Dynamic instability

Researchers previously proposed that neutrophils and macrophages result from a bi-stable gene regulatory network—one that can manifest either of 2 stable states. But the different cellular transition states and underlying molecular dynamics of development have remained unknown.

Dr Grimes and his colleagues said their analysis of developing blood cells captured a prevalent mixed-lineage intermediate.

These intermediates expressed a combination of genes, including those typical of hematopoietic stem and progenitor cells and some genes that are specific for red blood cells, platelets, macrophages, and neutrophils. This seemed to reflect competing genetic programs.

The researchers also observed the developing cells moving through a rare state where they encountered turbulence known as dynamic instability. This was caused by 2 counteracting myeloid gene regulatory networks.

Two key components of the counteracting gene networks were Irf8 and Gfi1, genes that are involved in blood cell formation. When Irf8 and Gfi1 were eliminated from the picture, the rare cells could be trapped in an intermediate state.

As they continue this work, the researchers want to gain a clearer understanding of what finally causes cells in intermediate states of dynamic instability to assume specific fates.

The team suggests the influence of 2 simultaneous and counteracting gene networks generates internal oscillations that are eventually stabilized by unknown mechanisms to generate 1 of 2 different cell fates.

Neutrophil engulfing bacteria

Image by Volker Brinkmann

Developing blood cells are caught in a tug of war between competing gene regulatory networks before finally deciding what type of cell to become, according to a study published in Nature.

Researchers found that, as developing blood cells are triggered by a multitude of genetic signals firing on and off, they are pulled back and forth in fluctuating multi-lineage states before finally becoming specific cell types.

The team still doesn’t understand exactly what drives the cells to an eventual fate, but their work suggests that competing gene networks induce dynamic instability, resulting in mixed-lineage states that are necessary to prime newly forming cells for that decision.

“It is somewhat chaotic, but, from that chaos, results order,” said study author Harinder Singh, PhD, of Cincinnati Children’s Hospital Medical Center in Ohio.

“It’s a finding that helps us address a fundamental question of developmental biology: What are the nature of the intermediate states and the networks of regulatory genes that underlie cell-type specification?”

Although the finding requires additional study to better understand the back-and-forth nature of this process, the research may eventually provide new insights into developmental miscues that cause disease, according to study author H. Leighton Grimes, PhD, of Cincinnati Children’s.

“How do blood cells know to become neutrophils or monocytes?” Dr Grimes asked. “Two thirds of your bone marrow is taken up with this activity, and the number of cells has to be exquisitely balanced. Too many or too few of either can kill you.”

For this study, Dr Grimes and his colleagues looked specifically at the formation of neutrophils and macrophages. The researchers studied mouse cells as they developed in a natural state using single-cell RNA sequencing.

The team also used a bioinformatics computer program known as iterative clustering and guide-gene selection (ICGS). They used ICGS to process and analyze sequencing and biological data to identify the various transitioning or shifting genomic and cellular states of developing blood cells.

Dynamic instability

Researchers previously proposed that neutrophils and macrophages result from a bi-stable gene regulatory network—one that can manifest either of 2 stable states. But the different cellular transition states and underlying molecular dynamics of development have remained unknown.

Dr Grimes and his colleagues said their analysis of developing blood cells captured a prevalent mixed-lineage intermediate.

These intermediates expressed a combination of genes, including those typical of hematopoietic stem and progenitor cells and some genes that are specific for red blood cells, platelets, macrophages, and neutrophils. This seemed to reflect competing genetic programs.

The researchers also observed the developing cells moving through a rare state where they encountered turbulence known as dynamic instability. This was caused by 2 counteracting myeloid gene regulatory networks.

Two key components of the counteracting gene networks were Irf8 and Gfi1, genes that are involved in blood cell formation. When Irf8 and Gfi1 were eliminated from the picture, the rare cells could be trapped in an intermediate state.

As they continue this work, the researchers want to gain a clearer understanding of what finally causes cells in intermediate states of dynamic instability to assume specific fates.

The team suggests the influence of 2 simultaneous and counteracting gene networks generates internal oscillations that are eventually stabilized by unknown mechanisms to generate 1 of 2 different cell fates.

A once-daily inhaled combination of fluticasone furoate and vilanterol was associated with an 8% lower rate of exacerbations in chronic obstructive pulmonary disease (COPD) than was usual care, with no increase in adverse effects, according to a multicenter trial designed to reflect real-world practice.

“Future effectiveness studies [like this one] are likely to influence clinical guidelines, not only for COPD but [also] for many other chronic diseases,” said Jørgen Vestbo, MD, of University Hospital of South Manchester NHS Foundation Trust, Manchester, England, and his associates, for the Salford Lung Study investigators. The findings were presented at the annual congress of the European Respiratory Society and published simultaneously in the New England Journal of Medicine.

©designer491/Thinkstock

Current COPD guidelines are based on clinical trials of carefully selected and monitored patients, which substantially limits their usefulness in everyday practice, the researchers said. To help address that problem, their 12-month, prospective, open-label, parallel-group, randomized study enrolled 2,799 COPD patients in 75 general practices within a single urban area in the United Kingdom. Patients received 100 mcg of fluticasone furoate and 25 mcg of vilanterol or usual care. The primary outcome was the rate of moderate or severe exacerbations among patients who had experienced an exacerbation within 1 year before enrollment. Patients received all treatment from their usual providers and were monitored remotely for safety through electronic health records (N Engl J Med. 2016 Sep 4. doi: 10.1056/NEJMoa1608033).

Fluticasone furoate/vilanterol was associated with 1.74 moderate or severe exacerbations per year, compared with 1.9 events per year with usual-care group, for a statistically significant difference of 8.4% (95% confidence interval, 1.1%-15.2%; P = .02). The trial arms had similar rates of COPD-related health care visits and first moderate or severe exacerbations. They also did not notably differ in terms of serious adverse events of special interest, such as cardiovascular events (which affected 8% of patients in each group) or pneumonia (which affected 7% of fluticasone furoate/vilanterol patients and 6% of usual-care patients). Thirteen patients in each group developed fatal pneumonia, of which one case was considered related to usual care. The only other treatment-related death involved of deep-vein thrombosis and pulmonary embolism in a patient receiving fluticasone furoate/vilanterol.

Medication switches were about twice as common (22%) in the intervention group than in the usual care group (11%), perhaps because of the open-label nature of the trial, the researchers said. Only 4% of patients receiving fluticasone furoate/vilanterol needed better disease control, half the rate of the usual care group.

GlaxoSmithKline funded the trial. Dr. Vestbo reported personal fees from GlaxoSmithKline while the study was conducted.

A once-daily inhaled combination of fluticasone furoate and vilanterol was associated with an 8% lower rate of exacerbations in chronic obstructive pulmonary disease (COPD) than was usual care, with no increase in adverse effects, according to a multicenter trial designed to reflect real-world practice.

“Future effectiveness studies [like this one] are likely to influence clinical guidelines, not only for COPD but [also] for many other chronic diseases,” said Jørgen Vestbo, MD, of University Hospital of South Manchester NHS Foundation Trust, Manchester, England, and his associates, for the Salford Lung Study investigators. The findings were presented at the annual congress of the European Respiratory Society and published simultaneously in the New England Journal of Medicine.

©designer491/Thinkstock

Current COPD guidelines are based on clinical trials of carefully selected and monitored patients, which substantially limits their usefulness in everyday practice, the researchers said. To help address that problem, their 12-month, prospective, open-label, parallel-group, randomized study enrolled 2,799 COPD patients in 75 general practices within a single urban area in the United Kingdom. Patients received 100 mcg of fluticasone furoate and 25 mcg of vilanterol or usual care. The primary outcome was the rate of moderate or severe exacerbations among patients who had experienced an exacerbation within 1 year before enrollment. Patients received all treatment from their usual providers and were monitored remotely for safety through electronic health records (N Engl J Med. 2016 Sep 4. doi: 10.1056/NEJMoa1608033).

Fluticasone furoate/vilanterol was associated with 1.74 moderate or severe exacerbations per year, compared with 1.9 events per year with usual-care group, for a statistically significant difference of 8.4% (95% confidence interval, 1.1%-15.2%; P = .02). The trial arms had similar rates of COPD-related health care visits and first moderate or severe exacerbations. They also did not notably differ in terms of serious adverse events of special interest, such as cardiovascular events (which affected 8% of patients in each group) or pneumonia (which affected 7% of fluticasone furoate/vilanterol patients and 6% of usual-care patients). Thirteen patients in each group developed fatal pneumonia, of which one case was considered related to usual care. The only other treatment-related death involved of deep-vein thrombosis and pulmonary embolism in a patient receiving fluticasone furoate/vilanterol.

Medication switches were about twice as common (22%) in the intervention group than in the usual care group (11%), perhaps because of the open-label nature of the trial, the researchers said. Only 4% of patients receiving fluticasone furoate/vilanterol needed better disease control, half the rate of the usual care group.

GlaxoSmithKline funded the trial. Dr. Vestbo reported personal fees from GlaxoSmithKline while the study was conducted.

A once-daily inhaled combination of fluticasone furoate and vilanterol was associated with an 8% lower rate of exacerbations in chronic obstructive pulmonary disease (COPD) than was usual care, with no increase in adverse effects, according to a multicenter trial designed to reflect real-world practice.

“Future effectiveness studies [like this one] are likely to influence clinical guidelines, not only for COPD but [also] for many other chronic diseases,” said Jørgen Vestbo, MD, of University Hospital of South Manchester NHS Foundation Trust, Manchester, England, and his associates, for the Salford Lung Study investigators. The findings were presented at the annual congress of the European Respiratory Society and published simultaneously in the New England Journal of Medicine.

©designer491/Thinkstock

Current COPD guidelines are based on clinical trials of carefully selected and monitored patients, which substantially limits their usefulness in everyday practice, the researchers said. To help address that problem, their 12-month, prospective, open-label, parallel-group, randomized study enrolled 2,799 COPD patients in 75 general practices within a single urban area in the United Kingdom. Patients received 100 mcg of fluticasone furoate and 25 mcg of vilanterol or usual care. The primary outcome was the rate of moderate or severe exacerbations among patients who had experienced an exacerbation within 1 year before enrollment. Patients received all treatment from their usual providers and were monitored remotely for safety through electronic health records (N Engl J Med. 2016 Sep 4. doi: 10.1056/NEJMoa1608033).

Fluticasone furoate/vilanterol was associated with 1.74 moderate or severe exacerbations per year, compared with 1.9 events per year with usual-care group, for a statistically significant difference of 8.4% (95% confidence interval, 1.1%-15.2%; P = .02). The trial arms had similar rates of COPD-related health care visits and first moderate or severe exacerbations. They also did not notably differ in terms of serious adverse events of special interest, such as cardiovascular events (which affected 8% of patients in each group) or pneumonia (which affected 7% of fluticasone furoate/vilanterol patients and 6% of usual-care patients). Thirteen patients in each group developed fatal pneumonia, of which one case was considered related to usual care. The only other treatment-related death involved of deep-vein thrombosis and pulmonary embolism in a patient receiving fluticasone furoate/vilanterol.

Medication switches were about twice as common (22%) in the intervention group than in the usual care group (11%), perhaps because of the open-label nature of the trial, the researchers said. Only 4% of patients receiving fluticasone furoate/vilanterol needed better disease control, half the rate of the usual care group.

GlaxoSmithKline funded the trial. Dr. Vestbo reported personal fees from GlaxoSmithKline while the study was conducted.

Purpose: Develop ordersets that seamlessly enter chemotherapy and biologics orders from CPRS to Pharmacy’s VISTA program (pVista) and CPRS notes within the VISN.

Background: Hematology/Oncology orders ranged from paper to CPRS within the VISN. CPRS orders must be reentered into pVistA by the pharmacist, a safety issue. Commercial proprietary programs were expensive and didn’t translate to pVistA. The COEMS program isn’t available within the VA may not interface seamlessly with pVistA. Therefore, VISN 09 Medicine Service Line’s Oncology Committee (MSLOC) decided to develop ordersets in CPRS that enter treatment notes and orders into pVistA.

Methods: Ordersets development was MSLOC highest priority (2015). MSLOC met monthly by phone identifying resources, reviewing available ordersets, and translating into pVistA. MSLOC developed a timeline for orderset implementation. Progress was discussed monthly and documented with screen shots. Site visits will be completed before 2017.

Data Analysis: Flowsheets included: 1. facility resources: treatment area, providers, staffing, oncology pharmacy, ADPACs, and CACs; 2. Mechanisms of orders and notes entering/ recording; 3. Dosing and safety checks; 4. Available ordersets.

Results: In 2016 our ordersets were established as a “best practice”. VISN issued a suspense to implement electronic ordersets by 2017. The timeline included: 1. team development (fall 2015)-providers, pharmacists, pharmacy ADPAC, CACs; 2. Review of available ordersets (winter 2016); 3. Orderset development (winter-spring 2016); 4. Progress assessment (spring 2016); 5. Site visits (summer 2016). Results varied by VISN site: 2/5 of VAs were already paperless; 4/5 are now paperless; 2/5 have completely updated ordersets; 1/5 still uses paper and have only begun implementing ordersets. 1/5 ordersets completed chemotherapy notes; this will be implemented at all sites.

Implications: Using limited VA resources, ordersets can seamlessly enter pVistA. Results vary within VISN sites; switching from paper to electronic requires a paradigm shift. In approximately 18 months ordersets have been revised and updated. Chemotherapy ordersets now are generated electronically in 4/5 VAs. A team of MSLOC, providers, and staff have implemented this. In 2017 MSLOC will quantify the effectiveness of the initiative to improve patient care, safety, and efficiency.

Purpose: Develop ordersets that seamlessly enter chemotherapy and biologics orders from CPRS to Pharmacy’s VISTA program (pVista) and CPRS notes within the VISN.

Background: Hematology/Oncology orders ranged from paper to CPRS within the VISN. CPRS orders must be reentered into pVistA by the pharmacist, a safety issue. Commercial proprietary programs were expensive and didn’t translate to pVistA. The COEMS program isn’t available within the VA may not interface seamlessly with pVistA. Therefore, VISN 09 Medicine Service Line’s Oncology Committee (MSLOC) decided to develop ordersets in CPRS that enter treatment notes and orders into pVistA.

Methods: Ordersets development was MSLOC highest priority (2015). MSLOC met monthly by phone identifying resources, reviewing available ordersets, and translating into pVistA. MSLOC developed a timeline for orderset implementation. Progress was discussed monthly and documented with screen shots. Site visits will be completed before 2017.

Data Analysis: Flowsheets included: 1. facility resources: treatment area, providers, staffing, oncology pharmacy, ADPACs, and CACs; 2. Mechanisms of orders and notes entering/ recording; 3. Dosing and safety checks; 4. Available ordersets.

Results: In 2016 our ordersets were established as a “best practice”. VISN issued a suspense to implement electronic ordersets by 2017. The timeline included: 1. team development (fall 2015)-providers, pharmacists, pharmacy ADPAC, CACs; 2. Review of available ordersets (winter 2016); 3. Orderset development (winter-spring 2016); 4. Progress assessment (spring 2016); 5. Site visits (summer 2016). Results varied by VISN site: 2/5 of VAs were already paperless; 4/5 are now paperless; 2/5 have completely updated ordersets; 1/5 still uses paper and have only begun implementing ordersets. 1/5 ordersets completed chemotherapy notes; this will be implemented at all sites.

Implications: Using limited VA resources, ordersets can seamlessly enter pVistA. Results vary within VISN sites; switching from paper to electronic requires a paradigm shift. In approximately 18 months ordersets have been revised and updated. Chemotherapy ordersets now are generated electronically in 4/5 VAs. A team of MSLOC, providers, and staff have implemented this. In 2017 MSLOC will quantify the effectiveness of the initiative to improve patient care, safety, and efficiency.

Purpose: Develop ordersets that seamlessly enter chemotherapy and biologics orders from CPRS to Pharmacy’s VISTA program (pVista) and CPRS notes within the VISN.

Background: Hematology/Oncology orders ranged from paper to CPRS within the VISN. CPRS orders must be reentered into pVistA by the pharmacist, a safety issue. Commercial proprietary programs were expensive and didn’t translate to pVistA. The COEMS program isn’t available within the VA may not interface seamlessly with pVistA. Therefore, VISN 09 Medicine Service Line’s Oncology Committee (MSLOC) decided to develop ordersets in CPRS that enter treatment notes and orders into pVistA.

Methods: Ordersets development was MSLOC highest priority (2015). MSLOC met monthly by phone identifying resources, reviewing available ordersets, and translating into pVistA. MSLOC developed a timeline for orderset implementation. Progress was discussed monthly and documented with screen shots. Site visits will be completed before 2017.

Data Analysis: Flowsheets included: 1. facility resources: treatment area, providers, staffing, oncology pharmacy, ADPACs, and CACs; 2. Mechanisms of orders and notes entering/ recording; 3. Dosing and safety checks; 4. Available ordersets.

Results: In 2016 our ordersets were established as a “best practice”. VISN issued a suspense to implement electronic ordersets by 2017. The timeline included: 1. team development (fall 2015)-providers, pharmacists, pharmacy ADPAC, CACs; 2. Review of available ordersets (winter 2016); 3. Orderset development (winter-spring 2016); 4. Progress assessment (spring 2016); 5. Site visits (summer 2016). Results varied by VISN site: 2/5 of VAs were already paperless; 4/5 are now paperless; 2/5 have completely updated ordersets; 1/5 still uses paper and have only begun implementing ordersets. 1/5 ordersets completed chemotherapy notes; this will be implemented at all sites.

Implications: Using limited VA resources, ordersets can seamlessly enter pVistA. Results vary within VISN sites; switching from paper to electronic requires a paradigm shift. In approximately 18 months ordersets have been revised and updated. Chemotherapy ordersets now are generated electronically in 4/5 VAs. A team of MSLOC, providers, and staff have implemented this. In 2017 MSLOC will quantify the effectiveness of the initiative to improve patient care, safety, and efficiency.

Purpose: To identify DEL amongst veteran patients with diffuse large B cell lymphoma (DLBCL) and its outcome.

Background: Molecular profile determines prognosis in DLBCL. Activated B-cell (ABC), a subtype of DLBCL, is associated with poor outcome compared to germinal center Bcell (GCB). Poor response to standard chemotherapy is seen with double-hit lymphomas as detected by FISH (5% -10% of DLBCL) and DELs that express both MYC and BCL-2 as detected by immunohistochemistry (IHC) (cutoffs—30% MYC, 40% BCL-2), with a median overall survival of <12 months.

Methods: Sixty-nine DLBCL patients diagnosed at DC VAMC from 1/1996-4/2016 were identified utilizing cancer registry. IHC stains were reviewed for CD3, CD10, CD20, BCL-2, BCL-6, C-MYC, MUM-1, MIB1, and p53. DLBCL were sub-classified as GCB and ABC based on CD10, BCL6 and MUM1 stains. Demographic data, diagnosis, treatment and outcome in terms of relapse and death are analyzed and will be presented at the meeting.

Results: Of the 69 DLBCL cases, only 37 met inclusion criteria; 32 were excluded due to unavailable blocks (20, mostly sent to outside institutions), tissue exhaustion with incomplete IHC data (6), T-cell rich B cell lymphoma (5) and pending (1). 20 cases are GCB and 17 ABC. All cases are CD20 positive with high mib1. MYC is positive in 17 cases (46%) and 15 of them double positive for BCL-2 (40%).

Implications/Future Directions: DLBCL veterans at the DC VAMC have a high percentage of double expressors when compared to the literature. It will be important to examine clinical data, treatment, and outcome to develop better treatment guidelines for double-expressor DLBCL. Future studies are in plan to compare double hit lymphomas to double expressors.

Purpose: To identify DEL amongst veteran patients with diffuse large B cell lymphoma (DLBCL) and its outcome.

Background: Molecular profile determines prognosis in DLBCL. Activated B-cell (ABC), a subtype of DLBCL, is associated with poor outcome compared to germinal center Bcell (GCB). Poor response to standard chemotherapy is seen with double-hit lymphomas as detected by FISH (5% -10% of DLBCL) and DELs that express both MYC and BCL-2 as detected by immunohistochemistry (IHC) (cutoffs—30% MYC, 40% BCL-2), with a median overall survival of <12 months.

Methods: Sixty-nine DLBCL patients diagnosed at DC VAMC from 1/1996-4/2016 were identified utilizing cancer registry. IHC stains were reviewed for CD3, CD10, CD20, BCL-2, BCL-6, C-MYC, MUM-1, MIB1, and p53. DLBCL were sub-classified as GCB and ABC based on CD10, BCL6 and MUM1 stains. Demographic data, diagnosis, treatment and outcome in terms of relapse and death are analyzed and will be presented at the meeting.

Results: Of the 69 DLBCL cases, only 37 met inclusion criteria; 32 were excluded due to unavailable blocks (20, mostly sent to outside institutions), tissue exhaustion with incomplete IHC data (6), T-cell rich B cell lymphoma (5) and pending (1). 20 cases are GCB and 17 ABC. All cases are CD20 positive with high mib1. MYC is positive in 17 cases (46%) and 15 of them double positive for BCL-2 (40%).

Implications/Future Directions: DLBCL veterans at the DC VAMC have a high percentage of double expressors when compared to the literature. It will be important to examine clinical data, treatment, and outcome to develop better treatment guidelines for double-expressor DLBCL. Future studies are in plan to compare double hit lymphomas to double expressors.

Purpose: To identify DEL amongst veteran patients with diffuse large B cell lymphoma (DLBCL) and its outcome.

Background: Molecular profile determines prognosis in DLBCL. Activated B-cell (ABC), a subtype of DLBCL, is associated with poor outcome compared to germinal center Bcell (GCB). Poor response to standard chemotherapy is seen with double-hit lymphomas as detected by FISH (5% -10% of DLBCL) and DELs that express both MYC and BCL-2 as detected by immunohistochemistry (IHC) (cutoffs—30% MYC, 40% BCL-2), with a median overall survival of <12 months.

Methods: Sixty-nine DLBCL patients diagnosed at DC VAMC from 1/1996-4/2016 were identified utilizing cancer registry. IHC stains were reviewed for CD3, CD10, CD20, BCL-2, BCL-6, C-MYC, MUM-1, MIB1, and p53. DLBCL were sub-classified as GCB and ABC based on CD10, BCL6 and MUM1 stains. Demographic data, diagnosis, treatment and outcome in terms of relapse and death are analyzed and will be presented at the meeting.

Results: Of the 69 DLBCL cases, only 37 met inclusion criteria; 32 were excluded due to unavailable blocks (20, mostly sent to outside institutions), tissue exhaustion with incomplete IHC data (6), T-cell rich B cell lymphoma (5) and pending (1). 20 cases are GCB and 17 ABC. All cases are CD20 positive with high mib1. MYC is positive in 17 cases (46%) and 15 of them double positive for BCL-2 (40%).

Implications/Future Directions: DLBCL veterans at the DC VAMC have a high percentage of double expressors when compared to the literature. It will be important to examine clinical data, treatment, and outcome to develop better treatment guidelines for double-expressor DLBCL. Future studies are in plan to compare double hit lymphomas to double expressors.