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Switching From Conventional to Electronic Cigarettes Reduced Toxicant Exposure, Even for Dual Users18389779/2/2015 5:56:38 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx754False2015-09-02T04:05:00Z<div class="ExternalClassB5761C6826BF49F1B7EEF0CD5D644CA5"><p>PHILADELPHIA — Among adults who wanted to stop smoking conventional cigarettes, both those who switched to using only electronic cigarettes (e-cigarettes) and those who switched to dual use of e-cigarettes and conventional cigarettes had significant reductions in exposure to carbon monoxide and the toxicant acrolein, according to a <a target="_blank" href="http&#58;//cancerpreventionresearch.aacrjournals.org/content/8/9/873.abstract">study</a> published in <em>Cancer </em><em>Prevention Research</em>, a journal of the American Association for Cancer Research.<img src="/PublishingImages/McRobbie_Hayden_150x200.jpg" alt="Hayden McRobbie, MB, PhD" style="margin&#58;10px;float&#58;right;" /></p><p>“Acrolein is a toxicant found in both tobacco smoke and e-cigarette vapor,” said <a target="_blank" href="http&#58;//www.wolfson.qmul.ac.uk/a-z-staff-profiles/hayden-mcrobbie">Hayden McRobbie, MB, PhD</a>, professor of public health interventions in the Tobacco Dependence Research Unit of the <a target="_blank" href="http&#58;//www.wolfson.qmul.ac.uk/">Wolfson Institute of Preventive Medicine</a> at Queen Mary University of London, United Kingdom. “There have been concerns about the potential for increased exposure to toxicants like acrolein that are found in both tobacco smoke and e-cigarette vapor among individuals who are both vaping and smoking, so-called ‘dual users.’</p><p>“We found that e-cigarette use significantly reduced exposure to carbon monoxide and acrolein over a four-week period,” added McRobbie. “The reduction was greatest in those who switched to e-cigarettes completely, but even those who were dual users at four weeks had reduced exposure to carbon monoxide and acrolein. These results suggest that e-cigarettes may reduce harm compared with conventional cigarettes, even in dual users, but longer-term studies are needed to confirm this.”</p><p>McRobbie and colleagues enrolled in the study 40 adults who wanted to stop smoking conventional cigarettes. All participants were provided with a brand of e-cigarettes called Green Smoke. The researchers measured carbon monoxide in participants’ breath one week before switching to the e-cigarettes, the day of switching, and once a week for the next four weeks. They also analyzed urine samples provided by participants the day of switching and four weeks after switching, looking for a biomarker of exposure to acrolein.</p><p>Four weeks after switching, 33 participants were still using e-cigarettes. Of these individuals, 16 were using only e-cigarettes and 17 were dual users. </p><p>The researchers found that from one week before switching to four weeks after switching, levels of carbon monoxide in the breath of those who were using only e-cigarettes decreased by 80 percent (from 15 parts per million [ppm] to 3 ppm). For those who were dual users, the carbon monoxide levels reduced by 52 percent (from 23 ppm to 11 ppm).</p><p>Urine levels of the biomarker of exposure to acrolein, S-(3-hydroxypropyl)mercapturic acid (3-HPMA), decreased by 79 percent (from 1,623 nanograms per milligram of creatinine [ng/mg creatinine] to 343 ng/mg creatinine) for those who were using only e-cigarettes and by 60 percent (from 2,443 ng/mg creatinine to 969 ng/mg creatinine) for dual users.</p><p>“The results are very reassuring,” said senior author <a target="_blank" href="http&#58;//archive.wolfson.qmul.ac.uk/psychology/staff/team/peter_hajek.html">Peter Hajek, PhD</a>, professor of clinical psychology and director of the Tobacco Dependence Research Unit. “Dual users did not increase their acrolein intake; on the contrary, they reduced it substantially. The reason for this is that smokers who receive nicotine from e-cigarettes have a reduced need to smoke and so smoked less.”</p><p>According to McRobbie, limitations of the study include the fact that the researchers measured levels of only two toxicants, carbon monoxide and acrolein, that the study included only people who wanted to stop smoking, and that the study was run over only four weeks.</p><p>This study was funded by the U.K. Medicines and Healthcare Products Regulatory Agency. McRobbie and Hajek have received research funds and/or consultancy fees from manufacturers of smoking cessation medications.</p></div>
Modified CAR T Cells Can Preferentially Target Cancer Cells and Spare Normal Cells18281139/1/2015 1:36:31 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx753False2015-09-01T04:05:00Z<div class="ExternalClassA2F125A865A143D5B89D4F3374FEC691"><p>PHILADELPHIA —Engineering chimeric antigen receptor (CAR) T cells to lower their affinity for the protein epithelial growth factor receptor (EGFR) made the cells preferentially recognize and eliminate tumor cells that have high amounts of EGFR while sparing normal cells that have lower amounts of the protein, according to a <a href="http&#58;//cancerres.aacrjournals.org/content/75/17/3505.abstract" target="_blank">preclinical study</a> published in <em>Cancer Research</em>, a journal of the American Association for Cancer Research. <img alt="Laurence Cooper, MD, PhD" src="/PublishingImages/Cooper_Laurence_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“The goal of the study was to make CAR-expressing T cells differentiate friend from foe,” said Laurence Cooper, MD, PhD, CEO of ZIOPHARM Oncology in Boston. “We wanted to provide CAR T cells an improved opportunity of targeting a protein that is overexpressed on a cancer cell and spare normal cells that may also have the same protein, but at lower levels.</p><p>“CAR T cells that are currently being tested to treat B-cell malignancies target a specific protein present on leukemia and lymphoma, but these immune cells cannot distinguish cancer cells from normal cells,” explained Cooper. Even though such CAR T cells attack cancer cells and normal B cells alike, the side effects are manageable, which may not be the case with solid tumors. “Many proteins that are present on solid tumors may also be present on normal cells that are vital to the body. So, while recipients of CAR T cells can tolerate the loss of normal B cells, they cannot endure damage to vital structures if the engineered T cells inappropriately damage essential tissues. Because of this, CAR T-cell-based immunotherapy may not yet be entirely safe for patients with solid tumors,” added Cooper.</p><p>To make CAR T-cell therapy applicable to solid tumors, Cooper, who conducted this study while serving as professor of pediatrics at <a href="http&#58;//www.mdanderson.org/" target="_blank">The University of Texas MD Anderson Cancer Center</a>, and his colleagues developed CAR molecules with reduced affinity for a target on solid tumors. The target they chose in this study was wild-type EGFR, a protein that is present at high levels in certain brain cancers, but is also found at low levels on some normal cells. These experiments were performed by Hillary Caruso, PhD, while a graduate student with Cooper.</p><p>First, the researchers used two monoclonal antibodies, cetuximab, which has higher affinity for EGFR, and nimotuzumab, which has lower affinity for EGFR, and from these, they engineered high-affinity cetux-CAR T cells and low-affinity nimo-CAR T cells. Next, they tested the different CAR T cells on cancer cells with high levels of EGFR and normal cells with low levels of EGFR and found that while the cetux-CAR T cells killed both cancer and normal cells, the nimo-CAR T cells were selectively activated only in response to cancer cells, but not normal cells.</p><p>The researchers then tested the CAR T cells in mice bearing human brain cancer cells expressing high levels of EGFR and found that both cetux- and nimo-CAR T cells were equally effective in inhibiting tumor growth. However, the cetux-CAR T cells caused significant toxicity to the mice, leading to death in some, whereas the infused nimo-CAR T cells were safe. The researchers further tested the new CAR T cells in mice bearing cells that had low levels of EGFR (to mimic normal human cells), and found that unlike cetux-CAR T cells, the nimo-CAR T cells did not impact the growth of these cells.</p><p>“We think this provides an advance in the field of CAR T-cell therapy because until now the focus in terms of T-cell activation was on the intracellular portion of the CAR design, which led to the development of second- and third-generation CARs with different abilities to signal T cells. Our study has shown that another possibility is to tweak the extracellular portion of the CAR that docks with the tumor by adjusting its affinity for the target protein,” said Cooper. This technology can be used to develop CAR T cells that can be fine-tuned to target other overexpressed cancer proteins besides EGFR, Cooper explained. “An important derivative of this study is that scientists can now tweak, or modulate, the affinity of a CAR T cell to meet the needs of a given tumor.”</p><p>This study was funded by multiple groups including the National Institutes of Health and private foundations. </p><p>In January 2015, the technology was licensed for commercial application to ZIOPHARM Oncology and Intrexon Corporation in exchange for equity interests in each of these companies and, as a result, Cooper and some of the authors of this study have a financial interest in ZIOPHARM Oncology Inc. and Intrexon Corporation.</p><p>For further reading&#58;<br><a href="http&#58;//www.cancer.gov/about-cancer/treatment/research/car-t-cells" target="_blank">CAR T-cell Therapy&#58; Engineering Patients’ Immune Cells to Treat Their Cancers</a></p></div>
Newly Engineered CAR T Cells Can Better Discriminate Between Cancer and Normal Cells18281249/1/2015 1:38:13 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx752False2015-09-01T04:05:00Z<div class="ExternalClass49BB888ABCE84BFA80961A27CD12E242"><p>PHILADELPHIA — A new development in engineering chimeric antigen receptor (CAR) T cells, called affinity tuning, can make the CAR T cells spare normal cells and better recognize and attack cancer cells, which may help lower the toxicity associated with this type of immunotherapy when used against solid tumors, according to a <a href="http&#58;//cancerres.aacrjournals.org/content/75/17/3596.abstract" target="_blank">preclinical study</a> published in <em>Cancer Research</em>, a journal of the American Association for Cancer Research.<img alt="Yangbing Zhao, MD, PhD" src="/PublishingImages/Zhao_Yangbing_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“CAR T-cell therapies are very promising for leukemias, with high response rates, but adapting this treatment approach to solid tumors has been a great challenge,” said <a href="http&#58;//www.med.upenn.edu/junelab/tcel/pi.html" target="_blank">Yangbing Zhao, MD, PhD</a>, director of the T-Cell Engineering Laboratory (TCEL) at the Center for Cellular Immunotherapies and an adjunct associate professor in the Department of Pathology and Laboratory Medicine at the Perelman School of Medicine at the University of Pennsylvania.</p><p>“One of the reasons for this is the lack of good targets,” said Zhao, who went on to explain that many solid cancers have high levels of certain proteins such as ErbB2 and EGFR, which make them suitable targets for anticancer therapies. However, such proteins are also present at low levels in normal cells. Because of this, CAR T cells that are developed to target one of these proteins on tumor cells also recognize and attack normal cells that have the protein, causing severe toxicity.</p><p>“I and my colleagues at the laboratory of <a href="http&#58;//www.med.upenn.edu/apps/faculty/index.php/g275/p2328" target="_blank">Carl June, MD</a>, director of the University of Pennsylvania’s Center for Cellular Immunotherapies, have been working for the past three years to optimize a system to fine-tune the affinity of single chain variable fragments (scFv)—the part of the CAR T cell that recognizes the tumor target—such that they are able to discriminate tumors that have high levels of a protein from normal tissues that have low levels of the same protein,” Zhao explained.</p><p>To develop CAR T cells that can make that distinction, Zhao and colleagues first constructed a panel of CARs with the scFvs using sequences from mutated 4D5 antibodies that had varying affinities to ErbB2, a protein present at high levels in some solid tumors, including breast cancer. Next, they incorporated different scFvs into the CAR backbone or “construct,” such that they resulted in a range of CAR T cells—from those that had high affinity to ErbB2 to those that had low affinity to ErbB2. The newly engineered CAR T cells varied in their affinity to ErbB2 by three orders of magnitude.<br>The researchers then conducted a series of experiments to test the functionality of the affinity-tuned CAR T cells and found that high-affinity CAR T cells did not discriminate tumor cells from normal cells and attacked all of them, whereas low-affinity CAR T cells were sensitive to tumor cells that had high levels of ErbB2 and not to normal cells that had low levels of the protein.</p><p>Next, they tested the engineered CAR T cells in mice that bore human cells with high levels of ErbB2 on one side of their bodies and human cells with normal levels of ErbB2 on the other side of their bodies. Here again, low-affinity CAR T cells selectively eliminated cells that had high levels of ErbB2 but had no effect on cells that had normal levels of the protein.</p><p>“Unlike the common expectation that lowering the affinity of CAR T cells might also lower their efficacy, we have shown that lowering the affinity in fact does the opposite—lower-affinity CAR T cells displayed more potent reactivity to tumor cells expressing high levels of the target than did higher-affinity CAR T cells,” Zhao said.</p><p>In order to prove that this technology can be extended to other solid tumor targets, the researchers developed low-affinity CAR T cells targeting EGFR, a protein present in high levels in some lung and colon cancers, among others, and preliminary preclinical results showed that these CAR T cells were able to discriminate between cancer cells and normal cells.</p><p>This study was funded by the National Institutes of Health and Novartis. June and Zhao have financial interests due to intellectual property and patents in the field of cell and gene therapy. Conflicts of interest are managed in accordance with University of Pennsylvania policy and oversight.</p><p>For further reading&#58;<br><a href="http&#58;//www.cancer.gov/about-cancer/treatment/research/car-t-cells" target="_blank">CAR T-cell Therapy&#58; Engineering Patients’ Immune Cells to Treat Their Cancers</a></p></div>
MicroRNA Panel Shows Early Potential as Biomarker of Pancreatic Precancers17925598/27/2015 1:11:57 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx751False2015-08-27T04:05:00Z<div class="ExternalClass0CDE1D6CA8794F63A232A5DD337916AB"><p>PHILADELPHIA — Assessing blood plasma levels of certain micro-RNAs (miRNAs) distinguished individuals with noninvasive pancreatic precancers called intraductal papillary mucinous neoplasms (IPMNs) from healthy individuals and discriminated between patients with high-risk and low-risk IPMNs, according to a preliminary, proof-of-principle <a href="http&#58;//cancerpreventionresearch.aacrjournals.org/content/early/2015/08/25/1940-6207.CAPR-15-0094.abstract" target="_blank">study</a> published in <em>Cancer Prevention Research</em>, a journal of the American Association for Cancer Research.<img alt="Jennifer Permuth-Wey, PhD" src="/PublishingImages/Wey_Jennifer_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“<a href="https&#58;//www.aacrfoundation.org/CancerTypes/Pages/Pancreatic-Cancer.aspx" target="_blank">Pancreatic cancer</a> is the fourth leading cause of cancer-related death in the United States,” said <a href="https&#58;//moffitt.org/clinical-trials-research/researchers/jenny-permuth-wey/" target="_blank">Jennifer Permuth-Wey, PhD</a>, assistant member in the Departments of Cancer Epidemiology and Gastrointestinal Oncology at the <a href="https&#58;//moffitt.org/" target="_blank">Moffitt Cancer Center</a> in Tampa, Florida. “It is typically diagnosed at a late stage because there are currently no accurate methods to diagnose pancreatic cancer early. Noninvasive tests are needed to accurately detect precancerous lesions of the pancreas so that personalized risk assessment and care can be provided.</p><p>“Our study shows that new, relatively inexpensive digital technology could reliably measure miRNAs in blood plasma from individuals newly diagnosed with pancreatic cancer precursors called IPMNs, and healthy individuals,” continued Permuth-Wey. “This is promising news and could potentially lead to a noninvasive test for early detection of pancreatic cancer. However, the results are preliminary and much more research is needed to determine if a miRNA-based blood test could help diagnose pancreatic cancer earlier or more effectively than current methods.”</p><p>Permuth-Wey explained that the main goals of the study were to measure miRNAs in the blood and determine whether a set of miRNAs could distinguish patients with IPMNs from healthy individuals, and whether a set of miRNAs could discriminate between patients with high-risk IPMNs that need to be surgically removed and those with low-risk IPMNs that can be monitored.</p><p>Using nCounter technology to measure the levels of 800 miRNAs in plasma samples obtained preoperatively from 44 patients who underwent surgery to remove IPMNs surgically and 25 healthy individuals, the researchers identified a panel of 30 miRNAs that distinguished individuals with IPMNs from those who were healthy with an area under the curve (AUC) value of 0.74. Permuth-Wey explained that AUC is a way to quantify the discriminative ability or accuracy of a diagnostic test and that a perfect diagnostic test has an AUC of 1.0 while a useless or nondiscriminating test has an AUC of 0.5, which is no better than chance alone.</p><p>The researchers also identified a panel of five miRNAs that discriminated between patients with high-risk and low-risk IPMNs with an AUC of 0.73. “To be able to distinguish between these two sets of patients is important clinically,” said senior author <a href="https&#58;//www.moffitt.org/providers/mokenge-malafa/" target="_blank">Mokenge Malafa, MD</a>, department chair and program leader for the Gastrointestinal Tumor Program at Moffitt Cancer Center. “It would help personalize care such that high-risk IPMNs that warrant resection are properly identified while individuals with low-risk IPMNs are spared the substantial risks associated with unnecessary surgery.”</p><p>According to Permuth-Wey, limitations of the study include the small number of samples analyzed and the fact that the accuracy of the 30-miRNA panel and the five-miRNA panel were 74 percent and 73 percent, respectively, when many researchers think that accuracy greater than 90 percent may be needed for a test to be clinically useful. She went on to note that large-scale, multicenter studies with rigorous designs and incorporation of other types information, such as data from imaging scans and laboratory tests offered as part of clinical care, are needed to overcome these limitations and further explore the potential for miRNAs to be utilized clinically as markers for the early detection of pancreatic cancer.</p><p>This study was funded by the American Cancer Society and the National Cancer Institute. Permuth-Wey and Malafa are among the named inventors on a provisional patent application filed on the basis of results from this study.</p><p>Further information on pancreatic cancer can be found <a href="https&#58;//www.aacrfoundation.org/CancerTypes/Pages/Pancreatic-Cancer.aspx" target="_blank">here</a> and further information on rising U.S. pancreatic cancer death rates can be found <a href="/Newsroom/Pages/News-Release-Detail.aspx?ItemID=541" target="_blank">here</a>.</p></div>
High Proportion of Women Experience Anxiety Following False-positive Screening Mammography17864128/26/2015 1:08:15 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx750False2015-08-26T04:05:00ZStudy results can help health care providers give women objective information on pros and cons of screening<div class="ExternalClassE8535118F7A446FD96BE4B5F8D947AC6"><p>PHILADELPHIA — A high proportion of women who had false-positive screening mammography reported experiencing psychosocial consequences such as anxiety, sense of dejection, and negative effects on behavior and sleeping, and for some women these consequences persisted for 12 months, according to a <a href="http&#58;//cebp.aacrjournals.org/content/early/2015/08/10/1055-9965.EPI-15-0060.abstract" target="_blank">study</a> published in <em>Cancer Epidemiology, Biomarkers &amp; Prevention</em>, a journal of the American Association for Cancer Research.<img alt="Anetta Bolejko, PhD" src="/PublishingImages/Bolejko_Anetta_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>False-positive screening mammography is a course of events that follows an abnormal mammogram, which after recall and additional diagnostic work-up—for example, clinical mammography, ultrasound, and biopsy—is considered not to be breast cancer, explained Anetta Bolejko, PhD, in the Department of Medical Imaging and Physiology at <a href="https&#58;//www.skane.se/sv/Webbplatser/Skanes-universitetssjukhus/Skane-University-Hospital/About-Us/" target="_blank">Skåne University Hospital</a> in Malmö, Sweden.</p><p>Among women who experienced false-positive screening mammography, 88 percent reported having a sense of dejection, such as being uneasy, sad, or unable to cope, before learning that the positive (suspicious) screening mammogram was not <a href="https&#58;//www.aacrfoundation.org/CancerTypes/Pages/Breast-Cancer.aspx" target="_blank">breast cancer</a>. Eighty-three percent reported anxiety, 67 percent reported experiencing an effect on behavior, such as difficulty dealing with spare time or work, and 53 percent experienced difficulty sleeping.</p><p>“Although mammographic screening leads to breast cancer mortality reduction in the population, some women experience side effects and do not benefit from the screening program,” said Bolejko. “Experiences of psychosocial distress among women who underwent diagnostic work-up following a suspicious mammogram and among which no malignancy was found [women who experienced false-positive screening mammography] are an example of adverse effects of breast cancer screening.</p><p>“Our results show that psychosocial consequences of false-positive screening mammograms are common and can persist over time, with approximately one-third of women experiencing psychosocial consequences up to one year after the diagnostic work-up,” added Bolejko. “This is important, because women invited to attend mammographic screening should be informed about the potential benefits and harm of the program, and the risk of long-term psychosocial consequences of false-positive screening mammography should be acknowledged.”</p><p>Bolejko and colleagues used the Swedish Consequences of Screening – Breast Cancer (COS-BC) questionnaire to investigate the extent of psychosocial consequences of false-positive screening mammography among 399 women who were enrolled in the study immediately after recall to the diagnostic work-up following an abnormal mammogram, and later being considered that breast cancer was not found. These women responded to the Swedish COS-BC questionnaire upon enrollment, according to how they felt before the final diagnosis (considered free from breast cancer), and then at six and 12 months later.</p><p>At all time points, women who had false-positive screening mammography were significantly more likely to report psychosocial consequences compared with women who had a negative (no breast cancer) screening mammogram. At the first time point, they were more than five times more likely to report psychosocial consequences and at six and 12 months later they were more than twice as likely to report psychosocial consequences.</p><p>In multivariate analyses, the researchers found that early recall was a predictor for experiencing psychosocial consequences, as were dissatisfaction with information at the diagnostic work-up, being foreign-born, and lack of social support.</p><p>“We were surprised to find that women who are frequently monitored by additional clinical mammography [early recall] following a false-positive screening mammogram experienced psychosocial consequences,” said Bolejko. “This means that we think that early recall should be applied cautiously because it seems to create confusion and maintain psychosocial distress.”</p><p>Bolejko explained that the limitations of the study include that the researchers investigated the extent of psychosocial consequences and not the relevance of the consequences. She noted that the Swedish COS-BC has its limitation in providing this information. To learn about the relevance of psychosocial consequences of false-positive screening mammography, the perception of the individual woman also needs to be explored.&#160; </p><p>The senior author of the study is Sophia Zackrisson, MD, associate professor in the Department of Medical Imaging and Physiology.</p><p>This study was funded by the Department of Medical Imaging and Physiology at Skåne University Hospital and through governmental funding of clinical research within the National Health Services, Lund University, in Sweden. Bolejko declares no conflicts of interest.</p></div>
Non-Hispanic Black Women Less Likely to Survive Endometrial Cancer Than Women of Other Races and Ethnicities17445648/19/2015 1:09:53 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx749False2015-08-19T04:05:00ZEndometrial cancer incidence rising across all U.S. racial and ethnic groups<div class="ExternalClass98A6226F7EFC492DAB354E21485C867A"><p>PHILADELPHIA — Non-Hispanic black women with <a href="https&#58;//www.aacrfoundation.org/CancerTypes/Pages/Endometrial-Cancer.aspx" target="_blank">endometrial cancer</a> had worse outcomes than women in other racial/ethnic groups diagnosed with the same subtype of endometrial cancer and at the same stage of disease, according to a <a href="http&#58;//cebp.aacrjournals.org/content/early/2015/08/10/1055-9965.EPI-15-0316.abstract" target="_blank">study</a> published in <em>Cancer Epidemiology, Biomarkers &amp; Prevention</em>, a journal of the American Association for Cancer Research.<img alt="Michele L. Cote, PhD" src="/PublishingImages/Cote_Michele_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Endometrial cancer is the most commonly diagnosed gynecologic cancer in the United States and incidence rates have been rising for many years,” said Michele L. Cote, PhD, an associate professor of oncology at the <a href="http&#58;//www.karmanos.org/home" target="_blank">Barbara Ann Karmanos Cancer Institute</a> and <a href="http&#58;//home.med.wayne.edu/" target="_blank">Wayne State University School of Medicine</a> in Detroit. “We set out to investigate whether the increasing incidence and mortality from endometrial cancer are equally distributed by race/ethnicity and endometrial cancer subtype.</p><p>“The most significant finding was that non-Hispanic black women had poorer outcomes compared with non-Hispanic white women diagnosed with the same subtype of endometrial cancer and at the same stage of disease, while Hispanic and Asian women had similar or better outcomes compared with their non-Hispanic white counterparts,” added Cote. “Prior studies have suggested that disparities in outcomes from endometrial cancer might be explained by differences in tumor subtype or stage at diagnosis, but our data suggest that disparities persist even when these factors are controlled for.”</p><p>Cote and colleagues analyzed endometrial cancer incidence and mortality data from the <a href="http&#58;//seer.cancer.gov/" target="_blank">Surveillance, Epidemiology, End Results </a>(SEER) database, including only the 120,513 cases diagnosed from 2000 to 2011.</p><p>Over the 12 years studied, endometrial cancer incidence rates increased among all racial and ethnic groups, with rates increasing fastest, at 2.5 percent per year, among non-Hispanic black women and Asian women. Non-Hispanic black women had higher rates of all the aggressive endometrial cancer subtypes than non-Hispanic white, Asian, and Hispanic women.</p><p>Mortality rates for the aggressive endometrial cancer subtypes were more than 1.5-fold higher among non-Hispanic black women compared with non-Hispanic white women, while mortality rates for these subtypes were similar or lower among Asian and Hispanic women compared with non-Hispanic white women.</p><p>Analysis of overall five-year survival rates showed that non-Hispanic black women had poorer survival at every stage of diagnosis, regardless of endometrial cancer subtype, compared with non-Hispanic white women, while five-year survival rates were similar or higher among Asian and Hispanic women compared with non-Hispanic white women. </p><p>“It was somewhat surprising that the endometrial cancer survival disparity we identified was limited to non-Hispanic black women because many of the challenges previously linked to worse outcomes, including low socioeconomic status and high rates of obesity and diabetes, are also experienced by Hispanic women, but that population did not have poor outcomes,” said Cote. “We are, therefore, interested in investigating whether there are molecular differences in endometrial tumors of the same subtype from women of different races or ethnicities diagnosed at the same stage of disease.”</p><p>According to Cote, a limitation of the study is that the data analyzed were from the SEER database, which meant the researchers did not have tumor samples and were, therefore, unable to perform a review of the tumor subtype to ensure they had been classified correctly. In addition, SEER does not collect information on other factors that may be associated with incidence and survival, thus potential causes for the disparities identified in this study cannot be further examined.</p><p>This study was funded by the National Institutes of Health. Cote declares no conflicts of interest.</p></div>
Nominations Open for 2016 Pezcoller Foundation-AACR International Award for Cancer Research16302377/30/2015 8:34:01 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx747False2015-07-31T13:30:00Z<div class="ExternalClassF3F8E9789F6242C98BFB79E5F68E67A9"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) is accepting nominations for the 2016 Pezcoller Foundation-AACR International Award for Cancer Research.</p><p>The <a href="/Research/Awards/Pages/Awards-Detail.aspx?ItemId=16">Pezcoller Foundation-AACR International Award for Cancer Research</a> recognizes a scientist of international renown who has made a major scientific discovery in basic cancer research or who has made significant contributions to translational cancer research; who continues to be active in cancer research and has a record of recent, noteworthy publications; and whose ongoing work holds promise for continued substantive contributions to progress in the field of cancer.</p><p>The recipient of the 19th annual award will present a 50-minute lecture at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=63">AACR Annual Meeting 2016</a>, to be held April 16-20, in New Orleans, and receive an honorarium of 75,000 euros. </p><p>The 2015 award honored the immunotherapy pioneer <a href="/Newsroom/Pages/News-Release-Detail.aspx?ItemID=685#.Va0S76RVhHw">James P. Allison</a>, PhD, professor and chair of the Department of Immunology at The University of Texas MD Anderson Cancer Center in Houston, for his discovery that blocking cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) signaling improves antitumor immune responses and his role in the development of the CTLA-4 inhibitor ipilimumab (Yervoy). His award lecture was titled, “Immune Checkpoint Blockade in Cancer Therapy&#58; New Insights, Opportunities and Prospects for a Cure.”</p><ul><li>Deadline for nominations&#58; Aug. 12, 2015</li><li><a href="/Research/Awards/Pages/Awards-Detail.aspx?ItemId=16">Review the award information</a> or&#160;contact Monique P. Eversley at <a href="mailto&#58;awards@aacr.org">awards@aacr.org</a> to learn more. </li></ul></div>
Exercise During Adolescence Linked to Lowered Risk of Death Later16333287/31/2015 1:10:59 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx748False2015-07-31T04:05:00Z<div class="ExternalClassA7DC4E8B701F47A286E19B9BF182F9AA"><p>PHILADELPHIA — Women who participated in exercise as adolescents had a reduced risk of death from cancer and all causes in their middle and older ages, according to a <a href="http&#58;//cebp.aacrjournals.org/content/early/2015/07/16/1055-9965.EPI-15-0253.abstract" target="_blank">study</a> published in <em>Cancer Epidemiology, Biomarkers &amp; Prevention</em>, a journal of the American Association for Cancer Research.<img alt="Sarah J. Nechuta, MPH, PhD" src="/PublishingImages/Nechuta_Sarah_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“In women, adolescent exercise participation, regardless of adult exercise, was associated with reduced risk of cancer and all-cause mortality,” said <a href="https&#58;//medschool.mc.vanderbilt.edu/facdb/show_faculty.php?id3=132662" target="_blank">Sarah J. Nechuta, MPH, PhD</a>, assistant professor of medicine at Vanderbilt Epidemiology Center and <a href="http&#58;//www.vicc.org/" target="_blank">Vanderbilt-Ingram Cancer Center</a> in Nashville, Tennessee. “Our results support the importance of promoting exercise participation in adolescence to reduce mortality in later life and highlight the critical need for the initiation of disease prevention early in life.”</p><p>After adjusting for socioeconomic factors in adult life, the researchers found that women who participated in exercise as adolescents for 1.33 hours a week or less had a 16 percent lowered risk for death from cancer, and a 15 percent lowered risk for death from all causes; those who participated in exercise as adolescents for more than 1.33 hours a week had a 13 percent lowered risk for death from all causes.</p><p>After adjusting for socioeconomic factors in adult life, women who participated in team sports as adolescents had a 14 percent lowered risk for death from cancer, and a 10 percent lowered risk for death from all causes. Women who participated in exercise both in their adolescent and adult lives had a 20 percent lowered risk for death from all causes.</p><p>“While we found adolescent exercise to be associated with lowered risk of death from cancer and cardiovascular disease as adults, some associations were attenuated after adjusting for adult factors that may influence mortality later in life, such as exercise, diet, body mass index [BMI], socioeconomic status, and a history of chronic diseases. However, it is important to note that adult factors, such as adult exercise, BMI, and chronic diseases are potentially influenced by adolescent exercise, and adjusting for adult factors in these types of studies may not always be the best approach, as overadjustment could be a concern,” Nechuta added.</p><p>“It is important to note that the exercise data were self-reported and potential measurement error cannot be excluded. Further, we only had data on exercise and did not have information on activities related to transportation or occupation. Future studies with more detailed adolescent physical activity assessments and studies in other populations are needed,” she noted.</p><p>Nechuta and colleagues used data from the <a href="http&#58;//www.mc.vanderbilt.edu/swhs-smhs/" target="_blank">Shanghai Women’s Health Study</a>, a large, population-based prospective cohort study of about 75,000 women ages 40 to 70, from Shanghai, China, led by Wei Zheng, MD, PhD, at the Vanderbilt Epidemiology Center. The study had detailed information on participants reported at baseline recruitment, including self-reported exercise participation between the ages of 13 and 19, adult lifestyle-related factors, and mortality outcomes. In-person interviews were conducted to collect baseline data and follow-up data every two to three years.</p><p>After an average of 12.9 years of follow-up, there were 5,282 deaths, including 2,375 from cancer and 1,620 from cardiovascular disease.</p><p>This study was funded by the National Institutes of Health. Nechuta declares no conflicts of interest.</p></div>
AACR Accepting Calls for Nominations for 2016 Team Science Award16298667/30/2015 7:52:35 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx746False2015-07-30T17:00:00Z<div class="ExternalClass95676E5A71CA4545BEF45D10CEEE8B12"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) is accepting nominations for the 2016 AACR Team Science Award.</p><p>The <a href="/Research/Awards/Pages/Awards-Detail.aspx?ItemId=8">AACR Team Science Award</a>, now in its 10th year, recognizes an outstanding interdisciplinary research team for its innovative and meritorious scientific work that has advanced, or will likely advance cancer research, detection, diagnosis, prevention, or treatment. </p><p>The winning team will be recognized at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=63">AACR Annual Meeting 2016</a>, to be held April 16-20, in New Orleans, and will collectively receive a $50,000 prize, generously supported by grants from Eli Lilly and Company.</p><p>The 2015 award recognized the <a href="/Newsroom/Pages/News-Release-Detail.aspx?ItemID=689">Designing AR Inhibitors Team</a> for their collective work in discovering and developing the novel antiandrogen enzalutamide (Xtandi) for the treatment of metastatic castration-resistant prostate cancer. The team was comprised of Charles Sawyers, MD, PhD, team leader, director of the Human Oncology and Pathogenesis Program at Memorial Sloan Kettering Cancer Center; Howard Scher, MD, chief of genitourinary oncology service at Memorial Sloan Kettering; and Michael Jung, PhD, distinguished professor in the Department of Chemistry and Biochemistry at the University of California, Los Angeles.</p><ul><li>Deadline for nominations&#58; Aug. 5, 2015</li><li><a href="/Research/Awards/Pages/Awards-Detail.aspx?ItemId=8">Review the award information</a> or&#160;contact Monique P. Eversley at <a href="mailto&#58;awards@aacr.org">awards@aacr.org</a> to learn more. </li></ul></div>
Nominations Open for 2016 AACR-CRI Lloyd J. Old Award in Cancer Immunology16292917/30/2015 6:13:49 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx745False2015-07-30T16:00:00Z<div class="ExternalClass2BF5AD0FF6EB4FC68F2B103BADB1FD5D"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) is accepting nominations for the 2016 AACR-Cancer Research Institute (CRI) Lloyd J. Old Award in Cancer Immunology.</p><p>The <a href="/Research/Awards/Pages/Awards-Detail.aspx?ItemId=2">Lloyd J. Old Award in Cancer Immunology</a> was established in 2013 to honor the memory of the late Lloyd J. Old, MD, who is considered the “Father of Modern Tumor Immunology,” and to recognize an active scientist whose outstanding and innovative research in cancer immunology has had a far-reaching impact on the cancer field.</p><p>The recipient of the fourth annual award will receive a $10,000 honorarium and present a 50-minute lecture at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=63">AACR Annual Meeting 2016</a>, to be held April 16-20, in New Orleans.</p><p>The 2015 award recognized <a href="/Newsroom/Pages/News-Release-Detail.aspx?ItemID=691">Carl H. June, MD</a>, program director of translational research at the Abramson Cancer Center of the University of Pennsylvania in Philadelphia, for his important contributions to cancer immunology, specifically his pioneering efforts related to the development of chimeric antigen receptor (CAR) T-cell therapy. June delivered his award lecture titled, “CAR T Cells&#58; Can We Move Beyond B Cells?”</p><ul><li>Deadline for nominations&#58; Aug. 5, 2015</li><li><a href="/Research/Awards/Pages/Awards-Detail.aspx?ItemId=2">Review the award information</a>&#160;or contact Monique P. Eversley at <a href="mailto&#58;awards@aacr.org">awards@aacr.org</a> to learn more.</li></ul></div>