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Exposure to Particulate Air Pollutants Associated With Numerous Types of Cancer163834/28/2016 4:36:04 PM Releases/AllItems.aspx886False2016-04-29T04:05:00Z<div class="ExternalClassEFFF549B4255449788A367B57F51E377"><p>​PHILADELPHIA — Long-term exposure to ambient fine particulate matter, a mixture of environmental pollutants, was associated with increased risk of mortality for many types of cancer in an elderly Hong Kong population, according to a study published in <a href="http&#58;//"><em>Cancer Epidemiology, Biomarkers &amp; Prevention</em></a>, a journal of the <a href="/">American Association for Cancer Research</a>. <img alt="Thuan Quoc Thach" src="/Newsroom/PublishingImages/Thach_Thuan%20Quoc_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Long-term exposure to particulate matter has been associated with mortality mainly from cardiopulmonary causes and lung cancer, but there have been few studies showing an association with mortality from other cancers,” said the study’s co-lead author, <a href="http&#58;//" target="_blank">Thuan Quoc Thach, PhD</a>, a scientific officer at the <a href="http&#58;//" target="_blank">School of Public Health </a>at the <a href="http&#58;//" target="_blank">University of Hong Kong</a>. “Co-lead author <a href="http&#58;//" target="_blank">Neil Thomas </a>and I suspected that these particulates could have an equivalent effect on cancers elsewhere in the body.” Thomas, MPhil, PhD, is a reader in epidemiology in the Department of Public Health, Epidemiology and Biostatistics in the Institute of Applied Health of the College of Medical and Dental Sciences at <a href="http&#58;//">The University of Birmingham</a>.<img alt="G. Neil Thomas" src="/Newsroom/PublishingImages/Thomas_Neil_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>Particulate matter is the term for particles found in the air, including hydrocarbons and heavy metals produced by transportation and power generation, among other sources, Thach explained. This study focused on ambient fine particulate matter, or matter with an aerodynamic diameter of less than 2.5 micrometers (PM<sub>2.5</sub>). </p><p>For this study, Thach, Thomas, and colleagues enrolled 66,280 people who were age 65 or older when initially recruited between 1998 and 2001. The researchers did not have data on whether they had cancer before they were enrolled. Researchers followed the study subjects until 2011, ascertaining causes of death from Hong Kong registrations. Annual concentrations of PM<sub>2.5</sub> at their homes were estimated using data from satellite data and fixed-site monitors. </p><p>After adjusting for smoking status and excluding deaths that had occurred within three years of the baseline to control for competing diseases, the study showed that for every 10 microgram per cubic meter (µg/m3) of increased exposure to PM<sub>2.5</sub>, the risk of dying from any cancer rose by 22 percent. Increases of 10 µg/m3 of PM<sub>2.5 </sub>were associated with a 42 percent increased risk of mortality from cancer in the upper digestive tract and a 35 percent increased risk of mortality from accessory digestive organs, which include the liver, bile ducts, gall bladder, and pancreas.</p><p>For women, every 10 µg/m3 increase in exposure to PM<sub>2.5</sub> was associated with an 80 percent increased risk of mortality from breast cancer, and men experienced a 36 percent increased risk of dying of lung cancer for every 10 µg/m3 increased exposure to PM<sub>2.5</sub>. </p><p>Thach and Thomas indicated possible explanations for the association between PM<sub>2.5</sub> and cancer could include defects in DNA repair function, alterations in the body’s immune response, or inflammation that triggers angiogenesis, the growth of new blood vessels that allows tumors to spread. In the case of the digestive organs, heavy metal pollution could affect gut microbiota and influence the development of cancer, the authors added. </p><p>In 2015, the <a href="http&#58;//" target="_blank">International Agency for Research on Cancer </a>(IARC) published a series of monographs on the evaluation of various carcinogenic risks. In a <a href="http&#58;//" target="_blank">monograph on air pollution</a>, the organization pointed out the difficulty of assessing the effects of pollution on multiple types of cancers, given their different etiologies, risk factors, and variability in the composition of air pollutants in space and time. The IARC also identified certain key components of air pollution, including particulates. The large scale of Thach and Thomas’s study, as well as its documentation of cancer-specific mortality, enables the detailed investigation of the contribution of particulate matter to these cancers, the authors said.</p><p>Thomas added that further research would be required to determine whether other countries experience similar associations between PM<sub>2.5 </sub>and cancer deaths, but this study combined with existing research suggests that other urban populations may carry the same risks. </p><p>“The implications for other similar cities around the world are that PM<sub>2.5</sub> must be reduced as much and as fast as possible,” he said. “Air pollution remains a clear, modifiable public health concern.” </p><p>Thach said a limitation of the study is that it focused solely on PM<sub>2.5</sub>. He said emerging research is beginning to study the effects of exposure to multiple pollutants on human health. He also cautioned that pollution is just one risk factor for cancer, and others, such as diet and exercise, may be more significant and more modifiable risk factors. </p><p>This study was funded by the Wellcome Trust. Thach and Thomas declare no conflicts of interest. </p><p>&#160;</p></div>
AACR CEO Margaret Foti Recognized With Honorary Member Award 163764/28/2016 3:34:10 PM Releases/AllItems.aspx885False2016-04-28T14:30:00Z<div class="ExternalClass6CE8976137A446E6B5CE862D7E8B5352"><p>​PHILADELPHIA — Margaret Foti, PhD, MD (hc), chief executive officer (CEO) of the American Association for Cancer Research (AACR), was honored this morning during the opening ceremony of the <a href="http&#58;//" target="_blank">41st Annual Congress</a> of the Oncology Nursing Society (ONS) in San Antonio, Texas, with the Honorary Member Award for her unwavering dedication to improving cancer care and her unstinting commitment to the prevention and cure of all cancers.</p><p>The <a href="https&#58;//" target="_blank">Honorary Member Award</a> is awarded by the ONS to thank and honor an individual who is not otherwise eligible for ONS membership for his or her contributions to oncology nursing, support of the ONS, and conduct consistent with the ONS mission and core values.</p><p>&quot;I am deeply honored to be recognized by the Oncology Nursing Society with the Honorary Member Award,&quot; said Foti. &quot;Oncology nurses are playing a vital role in quality cancer care, and the compassion and deep commitment with which they care for patients and support caregivers are extraordinary in their impact. It has been exciting to work since 2002 with these dedicated health care professionals from ONS in the development of a series of sessions that underscore the importance of the science behind what is done in the clinic. I look forward to what we will do together in the future to address our shared mission. If we are to accelerate the pace of progress against cancer, we must collaborate as individual professionals and organizations, and ONS continues to be a synergistic partner in the cancer field.&quot;</p><p>During Foti's tenure as CEO of the AACR, her leadership has increased the organization's membership, which has grown from about 3,000 to more than 35,000 laboratory, translational, and clinical researchers; population scientists; other health care professionals; and cancer advocates residing in 104 countries and territories around the world. In addition, the organization's scientific meetings, peer-reviewed journals, and science policy work have furthered progress against all cancers through research, education, communication, and collaboration.</p><p>Under Foti's guidance, the AACR has become an outspoken proponent of policies that support all aspects of cancer research and prevention. The organization engages with policymakers through its Science Policy and Government Affairs Committee in Washington, D.C., which opened in 2007 to amplify the voice of cancer researchers, patients, survivors, and caregivers on Capitol Hill. The AACR's commitment to advocacy is evident through the leading role it plays in organizing the annual Rally for Medical Research Hill Day. The Rally brings together several hundred organizations, including the ONS, to raise awareness among the nation's policymakers about the need to make funding for the National Institutes of Health a national priority. More recently, the AACR has been providing thought leadership to Vice President Joe Biden as he begins to lead a new national effort against cancer, and the organization will continue to collaborate to provide valuable insights and creative thinking about how to reduce cancer incidence and mortality.</p><p>Foti's contributions have been widely recognized by numerous awards from organizations around the world. Her extensive list of formal recognitions includes honorary degrees in medicine and surgery from the University of Rome La Sapienza and the University of Catania in Sicily, and an honorary degree in medicine from the University CEU of San Pablo in Madrid. Most recently, she was honored by the Society of Surgical Oncology with the 2016 James Ewing Layperson's Award and by Massachusetts General Hospital Cancer Center as a 2015 honoree of &quot;the one hundred.&quot; She was also the recipient of the Children's Champion Award from Children's Hospital of Philadelphia in 2015, the 2014 Ellen V. Sigal Advocacy Leadership Award from Friends of Cancer Research, the 2014 Morton M. Kligerman Visiting Professorship Award from the University of Pennsylvania, the 2013 Stanley P. Reimann Honor Award from Fox Chase Cancer Center, and the 2013 Distinguished Partner in Hope Award from the Abramson Cancer Center of the University of Pennsylvania.</p></div>
Vice President Biden and Dr. Jill Biden Address the Cancer Research Community at the AACR Annual Meeting 2016161934/28/2016 7:57:20 PM Releases/AllItems.aspx884False2016-04-21T02:00:00Z<div class="ExternalClassA20379D726D74EADA44BA30B55A24807"><div>NEW ORLEANS —Vice President Joe Biden and Dr. Jill Biden today addressed over 4,000 attendees during the American Association for Cancer Research (AACR) Annual Meeting 2016 to thank members of the cancer research community for devoting their lives to cancer research, and to encourage them to share their ideas to more rapidly accelerate progress against cancer.&#160; <img alt="BidenAM.jpg" src="/Newsroom/PublishingImages/Lists/News%20Releases/AllItems/BidenAM.jpg" style="margin&#58;5px 10px;float&#58;right;" /></div><div>&#160;</div><div>Vice President Biden conveyed, &quot;There is more brain power in this room than exists in many countries. And we need you.&quot; He added, &quot;You're the very best we have.&quot; </div><div>&#160;</div><div>Biden talked about the importance of removing political barriers, fostering collaborations and data-sharing, and re-aligning incentives in cancer research to better serve patients. </div><div>&#160;</div><div><a href="http&#58;//;" target="_blank">View the webcast</a> of Dr. Jill Biden's and Vice President Biden's full remarks. <br><br>&quot;On behalf of the American Association for Cancer Research, I would like to thank Vice President Joe Biden and Dr. Jill Biden for delivering such inspirational remarks to our attendees at the AACR Annual Meeting 2016 this afternoon,&quot; said Margaret Foti, PhD, MD (hc), chief executive officer of the AACR. &quot;We are at a watershed moment in cancer research, and their remarks serve to motivate us to work even harder to hasten the pace of progress against cancer. We are in a new era of transformational breakthroughs in cancer research, and we look forward to continuing to work with Vice President Biden and his staff as well as to collaborating with all stakeholders to help chart a course to end cancer.” </div><div>&#160;</div><div>Biden selected the AACR Annual Meeting as a platform for his remarks, which drew a record number of 19,500 cancer community stakeholders from research, health care, academia, industry, government, and advocacy, all dedicated to propelling cancer research forward.</div><div>&#160;</div><div>AACR Past President José Baselga, MD, PhD, physician-in-chief and chief medical officer, Memorial Sloan Kettering Cancer Center, thanked President Barack Obama and Vice President Biden for launching the National Cancer Moonshot Initiative on behalf of the AACR's 36,000 members comprised of laboratory researchers, physicians and scientists, other medical professionals, and patient advocates nationally and internationally.</div><div>&#160;</div><div>Sophia Lunt, PhD, assistant professor, Michigan State University, introduced Dr. Jill Biden. Lunt is a recipient of the AACR NextGen Grant for Transformative Cancer Research, a funding initiative to stimulate highly innovative research conducted by young investigators.</div><div>&#160;</div><div>Dr. Jill Biden reinforced their personal commitment by saying, &quot;Joe and I know, this is personal for us…but it's also bigger than us. It affects millions of people around the world every day.&quot;</div><div>&#160;</div><div>Hosting Biden at the AACR Annual Meeting 2016 builds upon the AACR's thought leadership in this national effort to cure cancer. Prior to the announcement of the vice president's cancer moonshot initiative, 15 distinguished AACR leaders and members representing 10 medical institutions and nine states met with Biden's staff to discuss areas of major promise in cancer research including precision medicine, immunotherapy, and potential collaboration around big data, citing AACR's Project GENIE as an example. Shortly thereafter, Biden invited the AACR's president and two past presidents to offer their perspectives and guidance at a special session, &quot;Cancer Moonshot&#58; A Call to Action,&quot; at the World Economic Forum in Davos, Switzerland. Since then, Biden has continued to meet with AACR members as he tours cancer centers throughout the U.S.​</div><div>&#160;</div></div>
​Stand Up To Cancer Supports Innovative Research Grants for 10 Early-career Scientists161774/20/2016 3:34:59 PM Releases/AllItems.aspx883False2016-04-20T16:00:00Z2016 class brings total of IRGs awarded to 36<div class="ExternalClass80C3FD5089374989915B502508EB302E"><p>NEW ORLEANS — Stand Up To Cancer (SU2C) announced Monday that it is awarding 10 grants of $750,000 each to early-career scientists to support innovative, high-risk, high-reward projects in cancer research. The announcement was made at the 2016 Annual Meeting of the American Association for Cancer Research, SU2C’s Scientific Partner.</p><p>“We have selected 10 scientists and projects that we believe use new insights and fresh approaches and have high potential to make a difference for people with cancer,” said William G. Kaelin Jr., MD, professor of medicine at the Dana-Farber Cancer Institute in Boston and chairman of the SU2C Innovative Research Grant (IRG) review committee. “Just as importantly, SU2C is investing in the future of cancer research by supporting an outstanding group of early-career investigators whom we believe are rising stars in science.”</p><p>The announcement marks the third time SU2C has selected a class of Innovative Research Grant recipients. Previous classes were announced in 2009 and 2011. With the new class of IRGs, the total number of recipients now stands at 36.</p><p>Serving as Stand Up To Cancer’s celebrity ambassador at the event is Sonequa Martin-Green, 31, an actress and producer who is a main cast member in the hit television show “The Walking Dead,” in which she plays a survivor of the zombie apocalypse.&#160;In real life, she has lost several members of her extended family to cancer, and has other relatives, including her mother, who are cancer survivors.</p><p>“I have seen the terrible toll that cancer can take in a single family, so I respect and fully support these outstanding researchers in their battle against cancer,” Martin-Green said. “Hopefully the innovative ideas they are pursuing will one day spare other families the losses that my family, and so many other families have endured.”</p><p>The 10 grant recipients work at eight different institutions across the country where they have their own, independent laboratories. These innovative projects are characterized as “high-risk” because they either challenge existing paradigms, utilize novel concepts or approaches, and because in order to receive a grant, the applicants were not required—as they would be by most conventional funding mechanisms—to have already conducted a portion of the research resulting in an established base of evidence. If successful, the projects have the potential for “high-reward” in terms of saving lives.</p><p>“We’re trying to find the superstars of tomorrow and set them on their course by giving them funding so they don’t have to worry about that at this earlier stage of their career,” said Sara A. Courtneidge, PhD, associate director for translational sciences of the Knight Cancer Institute at Oregon Health &amp; Science University and vice-chairperson of the review committee.</p><p>“These grants will allow them to get off to a really good start in their independent research programs, take this research to the next level and then apply for more traditional funding mechanisms to take it forward,” she said.&#160; “I see it as a really good opportunity for young people not to have to worry so much about where their next grant is coming from until they've got themselves established.”</p><p>The scope of the projects selected range from tumor metabolism to imaging of drug response in single cells to mathematical models of combination drug therapy to the use of certain enzymes as new anticancer targets, among other topics.</p><p>With their institutions and the titles of their proposals, the IRG recipients are&#58;<br>•&#160;John G. Albeck, PhD, University of California, Davis&#58; Targeting cellular plasticity in individual basal-type breast cancer cells;<br>•&#160;Kara A. Bernstein, PhD, University of Pittsburgh&#58; Uncovering how RAD51 paralog mutations contribute to cancer predisposition;<br>•&#160;Juan R. Cubillos-Ruiz, PhD, Weill Cornell Medicine&#58;&#160; Phospholipid messengers as drivers of dendritic cell dysfunction in cancer;<br>•&#160;Greg Michael Delgoffe, PhD, University of Pittsburgh&#58;&#160; Metabolic reprogramming using oncolytic viruses to improve immunotherapy;<br>•&#160;Martin Kampmann, PhD, University of California, San Francisco&#58; &quot;Weak links” in cancer proteostasis networks as new therapeutic targets;<br>•&#160;Dan A. Landau, MD, PhD, Weill Cornell Medicine&#58; Algorithmically-driven quantitative combination cancer therapy engineering;<br>•&#160;Li Ma, PhD, The University of Texas MD Anderson Cancer Center&#58; Deubiquitinating enzymes as novel anticancer targets;<br>•&#160;Melissa Skala, PhD, Vanderbilt University (moving to Morgridge Institute for Research, University of Wisconsin-Madison)&#58; Imaging cell-level heterogeneity in solid tumors for personalized treatment;<br>•&#160;Matthew G. Vander Heiden, MD, PhD, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology&#58;&#160; Defining the metabolic dependencies of tumors; and<br>•&#160;Hao Zhu, MD, University of Texas Southwestern Medical Center&#58; Defining the mechanistic connections between injury, regeneration, and cancer.</p><p>More than 250 applications were received, from which 16 finalists were chosen to make presentations in person to a committee of senior scientists.</p><p>“They were all incredibly good,” said William G. Nelson, MD, PhD, vice-chair of the review committee and director of the Johns Hopkins Kimmel Cancer Center in Baltimore. “Very hard-working, ambitious, and imaginative, each and every one of them. Their ideas were high-risk and high-reward, but the young scientists themselves were sure bets. They are going to go places.”</p><p>The term of the grants begins July 1 and runs for three years. The scientists will report their progress twice a year to SU2C and the AACR, which organized the application and review process and will administer the grants.</p><p>Since 2008, SU2C has successfully launched 19 Dream Teams, two Translational Research Teams, and 36 Innovative Research Grants with funds committed by philanthropic, organizational, corporate and individual donors, as well as non-profit collaborators.</p><p>&#160;</p></div>
​Certain Oral Bacteria Associated With Increased Pancreatic Cancer Risk​160944/15/2016 7:54:15 PM Releases/AllItems.aspx876False2016-04-19T20:00:00Z<div class="ExternalClass3E820D27A2FA4E65826F7E3B4C51AED8"><p>NEW ORLEANS — The presence of two species of bacteria linked to periodontal disease in the mouths of healthy individuals was associated with an increased risk of subsequently developing <a href="https&#58;//">pancreatic cancer</a>, according to research presented here at the <a href="https&#58;//">AACR Annual Meeting 2016</a>, April 16-20.<img alt="Jiyoung Ahn" src="/PublishingImages/Ahn_Jiyoung_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Previous studies have shown that indicators of poor oral health, including a history of periodontal disease and lots of missing teeth, are associated with an increased risk of pancreatic cancer,” said <a href="http&#58;//" target="_blank">Jiyoung Ahn, PhD</a>, associate professor of population health and associate director of population sciences at the <a href="http&#58;//" target="_blank">Laura and Isaac Perlmutter Cancer Center at NYU Langone Medical Center </a>in New York. “To test the idea that this association is driven by species of oral bacteria linked to periodontal disease, we first needed to determine whether these bacteria are even associated with pancreatic cancer risk.</p><p>“We found that Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, two species of bacteria linked to periodontal disease, were associated with a more than 50 percent increased risk of pancreatic cancer,” Ahn continued. “These data do not show a causal relationship, but they are the first steps in understanding a potential new risk factor for pancreatic cancer, which is vital if we are to develop new approaches for pancreatic cancer prevention and early detection in the future.”</p><p>Ahn, Xiaozhou Fan, a graduate student working in Ahn’s laboratory, and colleagues conducted a nested case-control study using samples and data from the <a href="http&#58;//" target="_blank">Cancer Prevention Study II </a>and the <a href="http&#58;//" target="_blank">Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial </a>cohorts. Both these cohorts enrolled healthy people and followed them over a long period for a variety of outcomes, including development of cancer.</p><p>The researchers analyzed oral wash samples collected at study enrollment from 361 people who later went on to develop pancreatic cancer and from 371 matched controls. They used genomic technologies to generate a profile of the bacterial species present in each sample and performed logistic regression analysis to study the association between individual species of bacteria and risk of pancreatic cancer, controlling for other risk factors, including age, smoking status, and body mass index.</p><p>The presence of P. gingivalis in oral wash samples was associated with a 59 percent increased risk for pancreatic cancer and the presence of A. actinomycetemcomitans was associated with a 119 percent increased risk. Risks remained even after excluding samples from people who developed pancreatic cancer within two years of collection of their oral wash samples, which increased the research team’s confidence in the associations that were identified, according to Ahn.</p><p>“About 1.5 percent of U.S. men and women will be diagnosed with pancreatic cancer at some point in their life,” explained Ahn. “However, only 5 percent survive five years or more after their diagnosis. New approaches to pancreatic cancer prevention and early detection are urgently needed. Although our new findings cannot be directly translated into such approaches, if they are confirmed in additional studies, they could point to new ways to screen for the disease, and if the associations are found to be causal, they could point to potential prevention approaches.”</p><p>According to Ahn, a major limitation of the study was that the population studied was not very diverse—it was predominantly non-Hispanic white and healthy—so the results might not be generalizable to the whole population.</p><p>This study was funded by the National Cancer Institute. Ahn and Fan declare no conflicts of interest.</p><p><br>&#160;</p></div>
Noninvasive Test Detected Colorectal Cancer in Previously Unscreened Patients160904/15/2016 7:17:49 PM Releases/AllItems.aspx875False2016-04-19T17:00:00ZHigh compliance reveals significant colon cancer and advanced adenoma detection<div class="ExternalClass7555B0F8CBD74242BD7012EF6D4B7084"><p>NEW ORLEANS — A noninvasive colorectal cancer screening test detected the disease in patients who had previously avoided more invasive screening measures, according to research presented here at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=63&amp;DetailItemID=365">AACR Annual Meeting 2016</a>, April 16-20. The study of nearly 400 patients revealed four patients with cancers and 21 with advanced adenoma, or polyps.<img alt="Mark Prince" src="/PublishingImages/Prince_Mark_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Despite the availability of various colon cancer screening options, more than 40 percent of Americans are not getting screened,” said <a href="http&#58;//" target="_blank">Mark Prince, MD, MBA</a>, a director of gastroenterology with <a href="http&#58;//" target="_blank">USMD Physician Services</a>, a health system based in Dallas, Texas. “This study highlights the opportunity to expand the screening population by offering new, patient-friendly methods.”</p><p>In August 2014, the U.S. Food and Drug Administration <a href="http&#58;//">approved </a>Cologuard, a multi-target stool DNA test (mt-sDNA) that detects the presence of red blood cells and DNA mutations that can be associated with colon cancer. In October 2014, Cologuard was approved for Medicare coverage.&#160; </p><p>A 10,000-patient, prospectively conducted clinical trial for Cologuard, which was <a href="http&#58;//">published in The New England Journal of Medicine</a>, showed that Cologuard is 92 percent sensitive for detecting colorectal cancer and 42 percent sensitive for precancer, with a specificity of 87 percent. </p><p>In this study, Prince and colleagues performed a retrospective medical records review of Medicare-eligible patients treated by physicians in the USMD Physician Services. The study focused on patients at average risk for colorectal cancer—those without symptoms, a personal or family history of colorectal cancer, or polyps— who were not previously compliant with recommended guidelines for screening. </p><p>“We were interested to see whether the ‘real-life’ experience with Cologuard in clinical practice would be similar to the results seen in the clinical trial,” Prince said. The patients’ clinicians offered Cologuard screening to patients who had not had a colonoscopy screening in 10 or more years, or a fecal occult blood test in a year or more. During the 12-month study period, from October 2014 to September 2015, USMD providers ordered 393 mt-sDNA studies, and 347 patients completed the test, achieving 88.3 percent compliance. Fifty-one patients, representing 14.7 percent of the total, tested positive by Cologuard and were referred for diagnostic colonoscopies.</p><p>According to Prince, 46 patients, or 90.2 percent of those referred, received the follow-up colonoscopies. Three patients refused the procedure and two patients did not respond to physicians’ attempts to follow up.&#160;</p><p>Among the 46 patients who had follow-up colonoscopies, four were diagnosed with colon cancer. Twenty-one were diagnosed with advanced adenoma, or polyps; nine had non-advanced adenoma; and 12 tested negative.</p><p>Prince said the discovery of four cases of colon cancer and numerous polyps, which have the potential to develop into cancer, supported the findings of the clinical trial. He noted that none of the patients had reported any symptoms and all had previously refused colonoscopies.</p><p>“Colon cancer screening saves lives,” Prince said. “Colonoscopy is the best form of colon cancer screening, but for patients who will not have a colonoscopy, a noninvasive screening test like Cologuard is needed.”</p><p>Colorectal cancer is the second deadliest form of cancer in the United States. This year, nearly 135,000 Americans will be diagnosed with the disease and 50,000 Americans will die of it.</p><p>Prince said a limitation of the study is that it involved only patients who were eligible for Medicare. “It will be interesting to analyze the use in commercially insured patients when insurance coverage becomes more widespread,” he said. Prince also cautioned that any positive results from noninvasive screening tests should be followed up by a colonoscopy.</p><p>Prince is a speaker for Exact Sciences Corp., the maker of Cologuard.</p><p>&#160;</p></div>
​​​Pembrolizumab Yielded Durable Responses in Patients With Advanced Merkel Cell Carcinoma160494/22/2016 6:23:48 PM Releases/AllItems.aspx864False2016-04-19T13:30:00Z<div class="ExternalClass653B67E0FED349C7BED1202EF7273FF3"><p>NEW ORLEANS — Many patients with advanced Merkel cell carcinoma (MCC), an aggressive type of skin cancer, who received the immunotherapeutic pembrolizumab as first-line therapy in a <a target="_blank" href="https&#58;//;rank=1">phase II clinical trial </a>had durable responses, and responses were seen in those whose cancers were driven by a virus as well as those whose cancers were induced by exposure to ultraviolet (UV) light, according to research presented here at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=63&amp;DetailItemID=365">AACR Annual Meeting 2016</a>, April 16-20. <img src="/PublishingImages/Nghiem_Paul_150x200.jpg" alt="Paul Nghiem" style="margin&#58;10px;float&#58;right;" /></p><p>This study is being simultaneously published in <a target="_blank" href="http&#58;//"><em>The New England Journal of Medicine</em></a>.</p><p>“In this clinical trial, patients with metastatic Merkel cell carcinoma who received pembrolizumab had an objective response rate of 56 percent, which is similar to chemotherapy outcomes, but the duration of response to pembrolizumab appears to be significantly longer than that for chemotherapy,” said <a href="http&#58;//">Paul Ngheim, MD, PhD</a>, affiliate investigator of the Clinical Research Division at <a href="http&#58;//">Fred Hutchinson Cancer Research Center </a>in Seattle and professor of medicine, Division of Dermatology, at the <a href="http&#58;//">University of Washington School of Medicine</a>. </p><p>“While the study is still ongoing, the vast majority of patients [86 percent] who responded to pembrolizumab are still experiencing excellent disease control more than six months after starting therapy.” </p><p>MCC is a rare, aggressive type of skin cancer, and Merkel polyomavirus (MCPyV) is the driving factor in about 80 percent of MCC cases, Nghiem explained. About 2,000 new cases of MCC are diagnosed in the United States per year. MCC is 35-fold less common than melanoma, but on average, it is about three times more likely to kill a patient than melanoma. Response to chemotherapy is typically quite brief and half of patients develop progressive disease within three months of initiating treatment, he added.</p><p>Nghiem and colleagues enrolled 26 patients with advanced/metastatic MCC who had received no prior systemic therapy in this single-arm, open-label trial. Of them, 17 had MCPyV-positive disease. All patients received 2 mg/kg body weight of pembrolizumab every three weeks and responses were assessed every nine to 12 weeks. At the time of data analysis, patients had received four to 49 weeks of therapy.</p><p>The overall response rate was 63 percent in patients with virus-positive MCC and 44 percent in those with virus-negative (UV-induced) MCC. Four patients, three with virus-positive disease, had complete responses (CR), and 10 patients, seven with virus-positive disease, had partial responses (PR).</p><p>Adverse events in this trial were similar to other anti-PD-1 trials and were largely managed with steroid treatment and stopping the study drug, Nghiem added. The condition of two patients who developed severe drug-related toxicities improved with corticosteroid treatment and discontinuation of pembrolizumab. “Importantly, both these patients have ongoing antitumor responses many months after discontinuation of pembrolizumab,” he noted.</p><p>“We believe that the immune system is likely ‘seeing’ different targets in the virus-positive and virus-negative patients,” Nghiem said. He explained that the virus-positive tumors produce the viral proteins needed for the tumors to grow. These viral proteins may be readily seen by the immune system. In contrast, virus-negative MCC has extremely high numbers of mutations caused by sunlight. These mutations can change the normal cellular proteins so they no longer appear as “self” and the immune system can then see and attack these tumors.</p><p>Pembrolizumab acts by removing the “brakes” present on tumor-specific immune cells called T cells, thereby allowing the T cells to kill the cancer cells.</p><p>“Currently there are no FDA-approved drugs for the treatment of MCC. We are expanding this trial to recruit additional patients and we hope that these data will contribute to meaningful new therapeutic options becoming available for these patients,” Nghiem said.</p><p>“It was initially challenging to partner with pharmaceutical companies because of the rarity of MCC. We are very thankful that the National Cancer Institute (NCI)’s Cancer Therapy Evaluation Program (CTEP), the Cancer Immunotherapy Trials Network (CITN), Merck, and multiple clinical sites came together to carry out this challenging study, which we believe is providing significant hope for MCC patients,” he added.</p><p>Nghiem is a consultant for EMD Serono, Inc., and receives funding from Bristol-Myers Squibb to perform biomarker studies in MCC clinical trials.</p><p>&#160; <br></p></div>
New Mathematical Model May Help Better Define Roles of Environmental and Intrinsic Factors in Cancer Initiation160664/22/2016 6:24:58 PM Releases/AllItems.aspx868False2016-04-19T13:30:00Z<div class="ExternalClass9399409B0F4F40AE964602832C811C1C"><p>​NEW ORLEANS — A mathematical model that takes into account the number of mutations required to initiate a specific type of cancer to estimate mutational activity, rather than cancer initiation, as the elementary event (as reported in two studies last year, one of which generated the &quot;bad luck&quot; hypothesis) may help better define the contributions of environmental factors and cellular factors in cancer initiation, according to data presented here at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=63&amp;DetailItemID=365">AACR Annual Meeting 2016</a>, April 16-20.<img src="/PublishingImages/Bilke_Sven_150x200.jpg" alt="Sven Bilke" style="margin&#58;10px;float&#58;right;" /></p><p>&quot;Understanding the impact of environmental and cellular factors in causing cancer is important because it will help define the amount of emphasis needed on cancer prevention versus early detection,&quot; said Sven Bilke, PhD, staff scientist in the <a target="_blank" href="https&#58;//">Genetics Branch of the National Cancer Institute</a> (NCI). &quot;This knowledge would also give some insight into the feeling of guilt people may have when they are diagnosed with cancer.&quot;</p><p>Bilke and colleagues developed a new mathematical model to reanalyze the data that were used by Cristian Tomasetti and Bert Vogelstein in their study <a target="_blank" href="http&#58;//">published</a> in <em>Science</em> last year, which found a correlation between the number of cell divisions in different tissues and the risk of getting cancer in that tissue. The study concluded that about two-thirds of variations in cancer risk can be explained by the number of stem cell divisions.</p><p>Another paper <a target="_blank" href="http&#58;//">published</a> last year in <em>Nature</em> by Song Wu and colleagues questioned that interpretation by pointing out that the mathematical model the authors had chosen was intrinsically insensitive toward changes in the environment that can influence cancer risk, and therefore, cannot distinguish between environment and accident.</p><p>&quot;However, both Tomassetti and Wu analyzed 'cancer initiation' as the elementary process,&quot; Bilke explained. Both studies found that the cancer incidence rates closely track the number of cell cycles. But they disagreed on how to choose the baseline that defines the intrinsic cellular, or &quot;bad luck&quot; component of the risk, he said. Consequently, they disagreed on what constitutes the excess, environmentally driven cancer risk.</p><p>&quot;In our analysis, we studied 'cancer-driver mutations' as opposed to 'cancer initiation,'&quot; Bilke continued. &quot;It is well established that cancer is the consequence of driver mutations, and the immediate impact of environmental as well as accidental factors is mutation, not cancer initiation.&quot; Excess mutations caused by the environment (or lack thereof) should thus be seen in the mutation rate, with the cancer initiation rate recapitulating that excess in a complex way, he added.</p><p>&quot;Our work estimates this mutation rate from the same data the other two studies used by taking into account that different cancer types require a different number of driver mutations to occur. &#160;For example, it takes about six mutations on average to initiate colorectal cancer, while only two mutations are sufficient to initiate retinoblastoma,&quot; Bilke said.</p><p>Tomasetti and Vogelstein estimated that less than about 40 percent of cancer incidence is caused by environmental factors, with the exception of lung and skin cancer, and genomic predispositions, continued Bilke. Reinterpretation by Wu and colleagues led to a much higher estimate (more than 90 percent) of environmental contributions in many cancers.</p><p>&quot;In our study, we find that the mutation rate, <em>not cancer incidence</em>, follows a much narrower distribution, largely taking away the possibility for competing interpretations. We find that more than 80 percent of the mutation rate is accidental, with the exception of colorectal, skin, and lung cancer, where a significant excess was detectable,&quot; he added.</p><p>&quot;Using our mathematical approach, we found that with the exception of environmental factors such as smoking, ultraviolet (UV) radiation, and diet, which are associated with some cancers, in most cases, cancer-driving mutations are largely random chance occurrences,&quot; Bilke said. &quot;Even in the absence of excessive carcinogens in the environment, mutations still occur and are difficult to prevent. Therefore, it is paramount to follow cancer screening recommendations.&quot;</p><p>&quot;The results of our study do not at all question the carcinogenic role of smoking, diet, and UV radiation in lung, colon, and skin cancer, respectively. Instead it <em>confirms</em> their role by identifying an increased rate of mutation in these cancers compared with baseline, as in the case of lung cancer among smokers,&quot; Bilke noted. &quot;Carcinogens remain dangerous and should be avoided.&quot;</p><p>As a limitation, Bilke noted that the study estimated the number of required driver mutations using epidemiologic data based on somewhat stringent assumptions. Some frequent cancers not following these assumptions, like hormone-dependent cancers, were therefore not included in this study.</p><p>This study was funded by the intramural research program of the NCI. Bilke declares no conflicts of interest.</p><p>&#160;</p></div>
An Implantable Microdevice Has Potential to Identify Suitable Therapy for Cancer Patients160774/15/2016 2:03:06 PM Releases/AllItems.aspx869False2016-04-19T13:30:00Z<div class="ExternalClass3C636E7419E44D4EAA6B40DEDC86F19C"><p>​NEW ORLEANS — A microdevice implanted into a tumor could release up to 100 individual cancer therapeutics or combinations, and upon retrieval from the tumor and analyses, could identify the best treatment option for that tumor, according to preclinical research presented here at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=63&amp;DetailItemID=365">AACR Annual Meeting 2016</a>, April 16-20.<img alt="Oliver Jonas" src="/PublishingImages/Jonas_Oliver_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>The research team that developed this microdevice has <a href="https&#58;//;rank=1" target="_blank">initiated a clinical trial</a> to test the safety and feasibility of placing and removing the microdevice in patients with early-stage HER-2 positive or triple-negative breast cancer. </p><p>“Currently, there are about 150 cancer drugs approved by the U.S. Food and Drug Administration, and many cancer patients have different drugs to choose from to treat their specific disease. However, patients respond differently to different drugs, and often, no two patients have the same response to a specific drug. It has been a major challenge to determine which drug or combination of drugs to give to which patient,” said Oliver Jonas, a postdoctoral fellow appointed jointly in the laboratories of <a href="http&#58;//" target="_blank">Robert S. Langer, ScD</a>, the David H. Koch Institute Professor, and <a href="http&#58;//" target="_blank">Michael Cima, PhD</a>, a David H. Koch Professor of Engineering, at <a href="http&#58;//" target="_blank">Massachusetts Institute of Technology</a>. </p><p>“Being able to identify the right therapy that will work optimally for every patient will be a major advance,” he added.</p><p>Jonas and colleagues engineered a small implantable microdevice that is less than a millimeter in diameter and about 4 millimeters in length, which has multiple reservoirs to hold single agents and combination therapies. The device is implanted into the tumor through a small biopsy needle and left there for about 24 hours. The implant is then extracted along with a layer of surrounding tumor tissue, and the tumor tissue is analyzed to determine the effect of each of these drugs and combinations on the tumor.</p><p>“We <a href="http&#58;//" target="_blank">published</a> a study last year in <em>Science Translational Medicine</em>, in which we demonstrated that we can implant this microdevice into mouse tumors and that we can test 16 different therapies. We've increased that number to 100 since then,” Jonas said. “We showed that the local readout that we can get from many agents in a single tumor is actually predictive of the drug sensitivity.”</p><p>The researchers engineered the cylindrical microdevice, using biocompatible plastics. When implanted in a mouse tumor, the therapeutics, loaded in specific reservoirs within the device, were released in such a way that crosstalk between the different drugs was eliminated by taking into account the chemistry of drug and formulating the drugs appropriately to separate the reservoirs from each other. The researchers can also adjust the drug-release rates to mimic the concentration of the drug achieved by standard systemic delivery, Jonas explained.</p><p>In addition to further developing the device to hold up to 100 different drugs and combinations, they are now able to study the tumor at different time points while the device is still in place, by real-time imaging using optical fibers attached to each reservoir, Jonas added. “We are now able to measure how tumors adapt and change when they are treated locally or systemically, and how their sensitivity to different drugs changes when switched from standard-of-care therapy,” Jonas said.</p><p>“Our study points to two important aspects,” Jonas said. </p><p>He explained that traditionally, there are two approaches to systems biology; one approach is to study the effects of multiple drugs on one type of cells in the laboratory, and the other is to conduct whole mouse studies where one could only test one or two agents at a time, which takes a long time and comes at a high cost. “We are showing that there is a middle ground where one can work in vivo, so that we take into account the effects of the microenvironment, but can also screen 100 or more compounds efficiently and rapidly in a single tumor, such that we can prioritize therapy to a patient, in addition to being able to understand the cancer in a functional way that we haven't been able to do before,” Jonas said.</p><p>As proof of principle, Jonas and his colleagues at MIT’s <a href="http&#58;//" target="_blank">Koch Institute for Integrative Cancer Research</a> have so far tested the effects of many drugs in patient-derived xenograft (PDX) mouse models of melanoma, and prostate and breast cancer. In recent studies, they tested the sensitivity of estrogen receptor-positive breast cancer to single agents and combinations that target the ER, CDK4/6, PI3K, and other pathways.</p><p>“This microdevice also enables us to investigate the mechanisms behind drug resistance. Our results demonstrate new patterns of therapy evasion by cancer cells and adaptive signaling mechanisms, which offer clues for effective combination therapy,” Jonas said.</p><p>This study was funded by the National Institutes of Health and the Koch Institute Frontier Research Program. Jonas declares no conflict of interest.<br></p></div>
Nivolumab Improved Survival For Patients With Head and Neck Squamous Cell Carcinoma161464/19/2016 1:15:15 PM Releases/AllItems.aspx882False2016-04-19T13:30:00Z<div class="ExternalClassDDE5F2B36C444368864EF4D4F39D6BD9"><p>​NEW ORLEANS — Treatment with the immunotherapeutic nivolumab (Opdivo) improved survival for patients with recurrent or metastatic <a href="https&#58;//">head and neck squamous cell carcinoma </a>that progressed after platinum-based chemotherapy compared with single-agent chemotherapy of the investigator’s choice, according to results from the <a href="https&#58;//" target="_blank">CheckMate-141 </a>phase III clinical trial presented here at the AACR Annual Meeting 2016, April 16-20.<img alt="Maura Gillison" src="/PublishingImages/Gillison_Maura_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Recurrent or metastatic head and neck squamous cell carcinoma that is not responsive to platinum-based chemotherapy progresses very rapidly, and patients have a very poor prognosis,” said <a href="http&#58;//" target="_blank">Maura L. Gillison, MD, PhD</a>, a professor in the Department of Internal Medicine at <a href="http&#58;//" target="_blank">The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute</a>. “Treatment usually involves single-agent chemotherapy. However, no therapy has been shown to improve survival for this patient population. New treatment options are desperately needed.</p><p>“This study is the first randomized clinical trial to clearly demonstrate improved overall survival for patients with platinum-refractory recurrent or metastatic head and neck squamous cell carcinoma,” continued Gillison. “We hope that the results will establish nivolumab as a new standard of care option for this patient population and thereby fulfill a huge unmet need.”</p><p>CheckMate-141 was a randomized, phase III clinical trial designed to determine whether the PD-1 inhibitor nivolumab could extend overall survival for patients with platinum-refractory recurrent or metastatic head and neck squamous cell carcinoma compared with treatment of the investigator’s choice, which was any of the commonly used therapeutics docetaxel, methotrexate, or cetuximab.</p><p>Of the 361 patients enrolled in the clinical trial, 240 were randomly assigned to nivolumab and 121 to single-agent chemotherapy of investigator’s choice.</p><p>At the interim analysis, which was conducted after 218 events, patients assigned to nivolumab were found to have a 30 percent reduction in risk of death compared with those assigned therapy of investigator’s choice. Median overall survival was 7.5 months for those assigned nivolumab versus 5.1 months for those assigned therapy of investigator’s choice. At 12 months, 36 percent of the patients treated with nivolumab were alive compared with 17 percent of those assigned therapy of investigator’s choice.</p><p>Because certain types of head and neck squamous cell carcinoma, particularly those arising in the oropharynx (back of the throat, including the base of the tongue and tonsils), have been linked with human papillomavirus (HPV) infection, the investigators also evaluated the data based on the HPV status of the patients’ tumors.</p><p>The effect of nivolumab on overall survival was seen for both patients with HPV-positive disease and those with HPV-negative disease. Among patients with HPV-positive disease, median overall survival was 9.1 months for those assigned nivolumab versus 4.4 months for those assigned therapy of investigator’s choice, and among patients with HPV-negative disease, median overall survival was 7.5 months for those assigned nivolumab versus 5.8 months for those assigned therapy of investigator’s choice.</p><p>A survival benefit in patients treated with nivolumab was observed for the overall study population. Exploratory analysis suggested that the benefit was greater for patients treated with nivolumab whose tumors had PD-L1 expression (of 1 percent or greater) or were HPV-positive.</p><p>“Overall, our data are extremely exciting. This clinical trial has established head and neck squamous cell carcinoma as responsive to immunotherapy. We are hopeful that this represents the tip of the iceberg with regard to future benefit of immunotherapy for patients with head and neck squamous cell carcinoma,” added Gillison. </p><p>This study was funded by Bristol-Myers Squibb. Gillison’s role in the study was funded in part by the Oral Cancer Foundation. Gillison has consulted for Bristol-Myers Squibb, Eli Lilly and Company, and Merck in the past year. <br></p></div>