News Releases



AACR Congratulates Newest Institute of Medicine Members42884810/23/2014 2:40:29 PM44 Releases/AllItems.aspx617False2014-10-23T13:00:00Z<div class="ExternalClass15BAC6E504D74D1C82D1D2259BF3355C"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) congratulates its members who have been elected to the <a href="http&#58;//" target="_blank">Institute of Medicine</a> (IOM), including President-elect and Fellow of the AACR Academy José Baselga, MD, PhD; Fellow of the AACR Academy and member of the AACR board of directors Lewis C. Cantley, PhD; Fellow of the AACR Academy and Nobel Laureate Brian K. Kobilka, MD; and member of the AACR board of directors Guillermina Lozano, PhD.</p><p>Election to the IOM is one of the highest honors in the fields of health and medicine and recognizes individuals who have demonstrated outstanding professional achievement and commitment to service. A total of 70 new members and 10 foreign associates were elected this year.</p><p>“On behalf of the American Association for Cancer Research, I wish to congratulate all of our members who were recently recognized by the Institute of Medicine,” said Margaret Foti, PhD, MD (hc), chief executive officer of the AACR. “Their dedicated efforts have significantly enhanced our understanding of cancer, paving the way for lifesaving advances in cancer prevention, detection, diagnosis, and treatment, and they truly deserve this prestigious accolade.”</p><p>The following AACR members were elected to the IOM during its 2014 annual meeting&#58;</p><ul><li><strong>José Baselga, MD, PhD</strong>, physician-in-chief and chief medical officer, Memorial Sloan Kettering Cancer Center, New York;</li><li><strong>Carol R. Bradford, MD</strong>, Charles J. Krause collegiate professor and chair, Department of Otolaryngology-Head and Neck Surgery, University of Michigan Health System, Ann Arbor;</li><li><strong>Lewis C. Cantley, PhD</strong>, director, Sandra and Edward Meyer Cancer Center, Weill Cornell Medical College/New York-Presbyterian Hospital, New York;</li><li><strong>E. Antonio Chiocca, MD, PhD</strong>, neurosurgeon-in-chief, Department of Neurosurgery and co-director, Institute for the Neurosciences, Brigham and Women’s/Faulkner Hospital; surgical director, Center for Neuro-oncology, Dana-Farber Cancer Institute; and Harvey W. Cushing professor of neurosurgery, Harvard Medical School, Boston;</li><li><strong>Joseph M. DeSimone, PhD</strong>, chancellor’s eminent professor of chemistry and William R. Kenan Jr. distinguished professor of chemistry, Departments of Chemistry and Pharmacology, University of North Carolina and North Carolina State University, Chapel Hill;</li><li><strong>James Economou, MD, PhD</strong>, vice chancellor for research and Beaumont professor of surgery, University of California, Los Angeles;</li><li><strong>Todd R. Golub, MD</strong>, investigator, Howard Hughes Medical Institute; chief scientific officer, Broad Institute of Harvard and the Massachusetts Institute of Technology; and Charles A. Dana investigator, Dana-Farber Cancer Institute, Cambridge, Massachusetts (former member of the AACR board of directors);</li><li><strong>Paul A. Khavari, MD, PhD</strong>, professor and chairman, Department of Dermatology, Stanford University, Stanford, California;</li><li><strong>Brian K. Kobilka, MD</strong>, professor of molecular and cellular physiology, Stanford University School of Medicine, Stanford, California;</li><li><strong>Guillermina Lozano, PhD</strong>, professor and chair, Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston;</li><li><strong>David R. Piwnica-Worms, MD, PhD</strong>, professor and chair, Department of Cancer Systems Imaging and deputy head, Division of Diagnostic Imaging, The University of Texas MD Anderson Cancer Center, Houston;</li><li><strong>Margaret A. Shipp, MD</strong>, chief, Division of Hematology Neoplasia, Dana-Farber Cancer Institute, Boston (former member of the AACR board of directors); and</li><li><strong>Dan Theodorescu, MD, PhD</strong>, Paul A. Bunn cancer research chair, professor of surgery and pharmacology, and director, University of Colorado Comprehensive Cancer Center, Denver.</li></ul><p>&#160;</p><p>For the entire list, please visit the <a href="http&#58;//" target="_blank">IOM website</a>.</p></div>
Genomic Sequencing More Efficient in Predicting Breast Cancer Risk Than Previously Thought42829410/23/2014 4:36:26 PM56 Releases/AllItems.aspx616False2014-10-23T04:05:00Z<div class="ExternalClassF23C3927A0E3477E95410D2AA67415C4"><p>​PHILADELPHIA — Using genomic sequencing data on all currently known genetic alterations in breast cancer, it is possible to identify a woman’s genetic risk for the disease, and this approach can bring greater gains in disease prevention than previously estimated, according to a <a href="http&#58;//" target="_blank">study</a> published in <em>Cancer Epidemiology, Biomarkers &amp; Prevention</em>, a journal of the American Association for Cancer Research.</p><p><img alt="Alice S. Whittemore, PhD" src="/PublishingImages/Whittemore_Alice_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" />Results of this study suggest that it is feasible to use genomic sequencing to identify women who would benefit most from breast cancer screening practices, such as mammography. Further, knowing one’s risk for breast cancer at birth may help women take measures to modify their nongenetic risk factors, such as diet and lifestyle, and lower their risk, according to the study.</p><p>“We need low-cost screening tools that can discriminate between women who will and won’t develop fatal breast cancer that are more effective than those currently available,” said <a href="http&#58;//" target="_blank">Alice S. Whittemore, PhD</a>, professor of epidemiology and biostatistics in the Department of Health Research and Policy at <a href="http&#58;//" target="_blank">Stanford Cancer Institute</a> in California.</p><p>“Previous studies using theoretical models have predicted that sequencing the genomes of women, ranking them by risk, and then targeting those at highest risk will provide little gain in cost-effective disease prevention,” added Whittemore. “However, our estimates suggest that preventive strategies based on genome sequencing will bring greater gains in disease prevention than previously projected. Moreover, these gains will increase with increased understanding of the genetic etiology of breast cancer,” she said.</p><p>Whittemore and colleagues used data from published literature on the frequency of 86 known breast cancer variants associated with breast cancer risk. They then developed a computational model to estimate a woman’s lifetime probability of developing breast cancer by calculating the risk score. The risk score is the sum of the breast cancer-related genetic variants a woman carries, multiplied by the effect of the variants, Whittemore explained.</p><p>The researchers estimated that the variance of the risk score based on the 86 known breast cancer susceptibility variants for the population as a whole is 0.35, which is higher than the variance of 0.07 estimated by an earlier study. “Variance is a relative measure of the heterogeneity of breast cancer risks in the population,” explained Whittemore. “The more genetic variants we discover, the more heterogeneous our genetic risks will be, and the more effective it will be to target those at highest risk.”</p><p><a href="https&#58;//" target="_blank">Weiva Sieh, MD, PhD</a>, assistant professor and epidemiologist at Stanford and first author on this study, said, “As we keep identifying additional breast cancer variants that can further explain the difference between my risk versus yours, the variance of the genetic risk score in the population will increase, and the potential utility of genomic sequencing will grow.</p><p>“Our ability to predict the probability of disease based on genetics is the starting point,” Sieh added. “If a girl knew, from birth, what her inborn risk was, she could then make more informed choices to alter her future risk by altering her modifiable factors, such as diet and lifestyle.”</p><p>This study was funded by the National Cancer Institute. Whittemore and Sieh declare no conflicts of interest.</p></div>
Stand Up To Cancer Epigenetics Dream Team Continues With $7.5 Million Funding From Van Andel Research Institute41880310/20/2014 2:03:31 PM77 Releases/AllItems.aspx615False2014-10-20T14:00:00Z<div class="ExternalClass6DDD27D10017445399585A0DA6ED65F7"><p>GRAND RAPIDS, Michigan — The work of one of the Stand Up To Cancer (SU2C) inaugural Dream Teams, launched in 2009 to focus on epigenetic therapy in cancer treatment, will continue with the commitment of $7.5 million from Van Andel Research Institute (VARI). Peter A. Jones, PhD, DSc, VARI’s research director and chief scientific officer, and Stephen Baylin, MD, deputy director of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, will serve as leaders of the Dream Team. </p><p>The VARI-SU2C Epigenetics Dream Team will include top scientists from four other leading institutions&#58;&#160;Charles Rudin, MD, PhD, Memorial Sloan Kettering Cancer Center in New York; Jean-Pierre Issa, MD, and Patricia Kropf, MD, Temple University and Fox Chase Cancer Center in Philadelphia; Kirsten Grønbæk, MD, DMSc, Rigshospitalet, University of Copenhagen; and Anthony El-Khoueiry, MD, University of Southern California Norris Comprehensive Cancer Center, part of Keck Medicine of USC in Los Angeles. </p><p>“We are extremely excited to build on the foundations already laid by the Epigenetics Dream Team by moving promising therapies into clinical trials,” Jones said. “Epigenetics provides untold opportunities to expand our knowledge of the mechanisms underlying cancer and to develop new treatments that positively affect people’s lives. By partnering with Stand Up To Cancer, the American Association for Cancer Research, and prestigious research institutions in the United States and abroad, we have the chance to do truly exceptional research that will have a significant impact on human health.”</p><p>The original Dream Team, with Baylin as leader and Jones as co-leader, has received nearly $11 million in funding from SU2C, a program of the Entertainment Industry Foundation. </p><p>“The SU2C Epigenetics Dream Team has already made significant and important progress in the treatment of cancer, finding that epigenetics can potentially ‘prime’ cancer cells, making them more receptive to chemotherapy and/or immunotherapy,” stated Nobel Laureate Phillip A. Sharp, PhD, chairman of the SU2C Scientific Advisory Committee and institute professor at the David H. Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology. “This substantial support from Van Andel Research Institute will allow their work to continue and bring hope for patients with lung and other cancers.” </p><p>As before, the team will focus on epigenetic mechanisms in cells, which help control whether genes are turned on or off without changing the DNA sequence itself. The work has involved clinical trials investigating the response of patients with lung cancer to epigenetic therapy alone, or as a way to sensitize patients to subsequent chemotherapy. VARI’s support over three years will allow the team to move forward with more extensive clinical trials in other cancer types. It will also allow the team to test additional epigenetic therapy strategies to improve upon the progress already made. </p><p>The VARI-SU2C Epigenetics Dream Team will continue within the SU2C scientific structure, a multidisciplinary, multi-institutional team engaged in accelerated translational research seeking patient benefits with rigorous scientific oversight and peer review provided by SU2C and its Scientific Partner, the American Association for Cancer Research (AACR). </p><p>Since its inception in 2008, SU2C has funded 12 Dream Teams of researchers and two translational research teams, as well as 26 early-career, innovative scientists whose high-risk, potentially high-reward projects are aimed at ending cancer’s reign as a leading cause of death worldwide.</p></div>
AACR Honors Zhu Chen for Achievements in Biomedical Research40715310/15/2014 9:06:59 PM116 Releases/AllItems.aspx614False2014-10-15T20:00:00Z<div class="ExternalClass40E844AFB5804FDC9CAE0A13E464F56C"><p>SHANGHAI — The American Association for Cancer Research (AACR) honored Zhu Chen, MD, PhD, with the 2014 AACR Award for Distinguished Public Service and Global Impact in Cancer Research in Biomedical Science at its inaugural meeting in China. </p><p>Chen, a fellow of the AACR Academy, is the vice chairman of the 12th Standing Committee of the National People’s Congress. From 2007 to 2013, he served as China’s minister of health. He received the award Oct. 9, where he delivered the opening plenary lecture at <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=24">New Horizons in Cancer Research&#58; Harnessing Breakthroughs – Targeting Cures</a>, the AACR’s inaugural meeting in China. </p><p>“Dr. Chen epitomizes the scientific work of this vast nation, and it is our honor to recognize him for his achievements. As the minister of health in China, he has been, and continues to be in his current important role, a visionary leader and proponent for cancer research, biomedical science, and improved public health,” said Carlos L. Arteaga, MD, president of the AACR.</p><p>In a career dedicated to translational research, Chen pioneered the concept of combination targeted therapies for cancer and, by combining traditional Chinese medicine with Western medicine, he provided the first successful model in the treatment of acute promyeloctyic leukemia with all-trans retinoic acid and arsenic trioxide. This treatment turned this previously fatal hematologic malignancy into a largely curable disease. </p><p>Under Chen’s leadership, the Chinese National Human Genome Center has contributed to human genome sequencing and SNP HaploMap projects; they recently completed genome sequencing of Schistosoma japonicum. The Chinese genome sequencing revealed features of a host parasite interplay that may pave the way for better control and prevention of schistomiasis japonica infection, a disease that remains a significant health problem in China. </p><p>Chen learned medicine as a “barefoot” doctor practicing traditional Chinese therapies in the countryside during the Cultural Revolution, before enrolling in formal medical school in Shanghai. His significant contributions have earned him many awards and honorary degrees as well as the recognition of his colleagues worldwide. </p></div>
In Some Men, an Increase in PSA After Prostate Cancer Surgery May Not Lead to Metastasis in Their Lifetime40604610/23/2014 4:36:55 PM145 Releases/AllItems.aspx613False2014-10-15T04:05:00Z<div class="ExternalClass1F81048FC61D4D428A76ACA4B3F51298"><p>​PHILADELPHIA — Some prostate cancer patients whose prostate-specific antigen (PSA) levels increase after a radical prostatectomy may die of causes unrelated to prostate cancer before they are diagnosed with a prostate cancer metastasis, and therefore treating them for recurrence may not be beneficial, according to a study published in <em><a href="http&#58;//" target="_blank">Clinical Cancer Research</a></em>, a journal of the American Association for Cancer Research.</p><p><img alt="Ruth Etzioni, PhD" src="/PublishingImages/Etzioni_Ruth_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" />“Previous studies have indicated that the interval from PSA recurrence to metastasis is quite long, with a median of more than eight years, even in the absence of any treatment for the recurrence,” said Ruth Etzioni, PhD, full member of the Public Health Sciences Division at <a href="http&#58;//" target="_blank">Fred Hutchinson Cancer Research Center</a> in Seattle, Washington. “Given that the majority of prostate cancer patients are older, we expect that many would die of other causes before reaching the point of metastasis.</p><p>“Much like the issues with PSA screening and overdetection of prostate cancer, overdetection of recurrence after primary treatment poses some concerns as well. We have attempted to quantify the risk associated with overdetection of recurrence,” said Etzioni.</p><p>Using prostate cancer patients’ data from different sources, the authors created a simulation model and found that at least 9.1 percent and 15.6 percent of prostate cancer patients whose PSA levels increase after five years and 10 years of initial treatment, respectively, may not have a metastatic disease in their lifetime, and therefore are overdetected for recurrence. Among those older than 70 with a PSA recurrence within 10 years of first diagnosis, the model projected that at least 31.4 percent were overdetected.</p><p>“Salvage therapy for prostate cancer patients includes radiation therapy, which has side effects such as bowel problems and urinary symptoms, and hormone therapy, which can cause hot flashes, fatigue, loss of libido, and in the long run, has been linked with osteoporosis, heart disease, and even diabetes,” said Etzioni. “Our findings are in line with treatment studies showing that immediate salvage therapy following detection of rising PSA levels is not the right thing for everyone. We need to develop ways to determine who needs salvage therapy and when to give it.” </p><p>Etzioni and colleagues used data from three sources&#58; data from 441 prostate cancer patients treated at Johns Hopkins University, data from 4,455 patients from the Cancer of the Prostate Strategic Urologic Research Endeavor database, and data from the Surveillance, Epidemiology, and End Results (SEER) registry.</p><p>Using this information, they created 1 million virtual patients with different age and disease characteristics and computed the fraction of patients with PSA recurrence for whom the time from PSA recurrence to another cause of death was less than the time from PSA recurrence to metastasis in the absence of salvage therapy.</p><p>This study was funded by the National Cancer Institute and the Centers for Disease Control and Prevention. Etzioni declares no conflicts of interest.</p></div>
Stand Up To Cancer Canada Announces Up To $22.6 Million CAD Available for Stand Up To Cancer Canada Dream Teams 40314510/14/2014 6:12:57 PM127 Releases/AllItems.aspx612False2014-10-14T18:00:00ZInaugural “Call for Ideas” Opens New Research Grant Competition for Two Dream Teams to Conduct Groundbreaking Cancer Research Focused on Breast Cancer and Cancer Stem Cells<div class="ExternalClass65C8E91AF804486AAF7B6501D20466F3"><h4>The first Stand Up To Cancer Canada Dream Teams in collaboration with the Canadian Breast Cancer Foundation, Cancer Stem Cell Consortium, Genome Canada, Canadian Institutes of Health Research and the Ontario Institute for Cancer Research will accelerate the pace of novel research</h4><p>TORONTO&#160;— Stand Up To Cancer Canada (SU2C Canada), together with Canadian Breast Cancer Foundation (CBCF) with support from CIBC, Cancer Stem Cell Consortium (CSCC), Genome Canada, Canadian Institutes of Health Research (CIHR), and the Ontario Institute for Cancer Research (OICR), is pleased to announce that up to $22.6 million CAD is available to fund two separate cancer research Dream Teams to accelerate the pace of groundbreaking research to bring new treatments from the laboratory to patients faster. Funding for this research is provided by these SU2C Canada collaborators and from the SU2C telecast which aired on September 5 and appealed to the Canadian public to pledge support for cancer research, awareness and education. </p><p>Two Dream Team funding opportunities are available, one for translational research focused on breast cancer and the other on cancer stem cells&#58;</p><ul><li>The Stand Up To Cancer Canada-Canadian Breast Cancer Foundation Breast Cancer Dream Team, will provide up to $6 million CAD over a four-year term and is funded by the Canadian Breast Cancer Foundation, with support from the CIBC, and by SU2C Canada. Ideas are invited for a translational cancer research project that will address critical problems in breast cancer patient care and include new therapeutic interventions for breast cancer that would be expected to reduce progression and improve overall survival.&#160;&#160;</li><li>The Stand Up To Cancer Canada Cancer Stem Cell Dream Team will provide approximately $10.6 million CAD over a four-year term, with funds from the CSCC (through Genome Canada and CIHR) and SU2C Canada. The Call for Ideas seeks to support a single, integrated, and cohesive pan-Canadian team bringing together key stakeholders—researchers, clinicians, industry, nongovernmental organizations, and funders—with the goal of improving the outcomes of hard-to-treat cancers by focusing on the role of cancer stem cells and stem cell programs on resistance and treatment failure in cancer. The team will employ new tools of modern biology, with an emphasis on genomics.</li><li>Additionally, the two qualifying Dream Teams may each receive supplementary funds up to $3 million over four years from OICR, to support clinical trial activities in the province of Ontario.</li></ul><p>&#160;</p><p>As the Scientific Partner of SU2C Canada, the American Association for Cancer Research International–Canada (AACR International–Canada) today issued Calls for Ideas, inviting the Canadian research community to assemble Dream Teams of the best scientists from across the country to work collaboratively in multidisciplinary, multi-institutional teams. The research proposals will be reviewed by the SU2C Canada Scientific Advisory Committee (CSAC), which will be composed of leading researchers and co-chaired by Nobel Laureate Phillip A. Sharp, PhD, institute professor at the Massachusetts Institute of Technology (MIT) and David H. Koch Institute for Integrative Cancer Research at MIT, and Alan Bernstein, OC, PhD, FRSC, president and chief executive officer of the Canadian Institute for Advanced Research. In addition, to ensure a thorough review process, each funding opportunity will also use a specialized subcommittee to contribute to the review of the submitted applications.</p><p>“Dr. Sharp and I are very pleased to launch this collaborative approach to cancer research with an emphasis on working across disciplines and institutional lines to deliver new treatments in an accelerated timeframe,” said Dr. Bernstein. “We look forward to reviewing extraordinary approaches to cancer research assembled by the best and brightest minds, and to selecting the best possible science that Canada has to offer.” </p><p>“We are thrilled to be moving swiftly, issuing the Calls for Ideas for first SU2C Canada Dream Teams, less than six weeks after the first Canada-inclusive Stand Up To Cancer fundraising telecast,” said Lisa Paulsen, EIF Canada Board Member. “These Dream Teams will quickly deliver promising treatments to benefit cancer patients throughout Canada and elsewhere.” </p><p>Letters of Intent must be submitted by noon ET, Monday, Dec. 8, 2014, using the <a href="https&#58;//" target="_blank">proposalCENTRAL website</a>. </p><p>For general information on eligibility criteria, the application process, and other details about these Dream Team grants, visit <a href="http&#58;//" target="_blank"></a>. Inquiries may be directed to the AACR International-Canada at 416-797-5366 or <a href="mailto&#58;"></a>. </p></div>
Elevated Cholesterol and Triglycerides May Increase the Risk for Prostate Cancer Recurrence39365210/23/2014 4:37:24 PM148 Releases/AllItems.aspx611False2014-10-10T04:05:00Z<div class="ExternalClass72DAADA8AE85400B8D36AD5CF85B678D"><p>PHILADELPHIA — Higher levels of total cholesterol and triglycerides, two types of fat, in the blood of men who underwent surgery for prostate cancer, were associated with increased risk for disease recurrence, according to a study published in <em><a href="http&#58;//" target="_blank">Cancer Epidemiology, Biomarkers &amp; Prevention</a></em>, a journal of the American Association for Cancer Research. </p><p><img alt="Emma Allott, PhD" src="/PublishingImages/Allott_Emma_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" />“While laboratory studies support an important role for cholesterol in prostate cancer, population-based evidence linking cholesterol and prostate cancer is mixed,” said Emma Allott, PhD, postdoctoral associate at <a href="http&#58;//" target="_blank">Duke University School of Medicine</a> in Durham, North Carolina. “Understanding associations between obesity, cholesterol, and prostate cancer is important given that cholesterol levels are readily modifiable with diet and/or statin use, and could therefore have important, practical implications for prostate cancer prevention and treatment.</p><p>“Our findings suggest that normalization, or even partial normalization, of serum lipid levels among men with dyslipidemia [abnormal lipid profile] may reduce the risk of prostate cancer recurrence,” said Allott. </p><p>Allott, Stephen Freedland, MD, associate professor of surgery at Duke University School of Medicine, and colleagues, analyzed data from 843 men who underwent radical prostatectomy after a prostate cancer diagnosis and who never took statins before surgery. They found that those who had serum triglyceride levels of 150 mg/dL or higher had a 35 percent increased risk for prostate cancer recurrence, when compared with patients who had normal levels of triglycerides. Among those with abnormal blood lipid profile, for every 10 mg/dL increase in total serum cholesterol above 200 mg/dL, there was a 9 percent increased risk for prostate cancer recurrence.</p><p>For every 10 mg/dL increase in high density lipoprotein (HDL; known as “good” cholesterol) among men with abnormal HDL (below the desirable value of 40 mg/dL), the risk for prostate cancer recurrence was lowered by 39 percent.</p><p>“Given that 45 percent of deaths worldwide can be attributed to cardiovascular disease and cancer, with prostate cancer being the second most common cause of male cancer deaths in the United States, understanding the role of dyslipidemia as a shared, modifiable risk factor for both of these common causes of mortality is of great importance,” she added.</p><p>Study subjects were identified from the Shared Equal Access Regional Cancer Hospital (SEARCH) database and treated at one of the six Veterans Affairs Medical Centers in California, North Carolina, and Georgia.</p><p>Of the 843 men studied, 343 were black, 325 had abnormal cholesterol levels, 263 had abnormal triglyceride levels, and 293 had a biochemical recurrence, defined as rising PSA levels after prostate cancer treatment, indicating the recurrence of the patient’s prostate cancer.</p><p>This study was funded by the National Institutes of Health. Allott and Freedland declare no conflicts of interest.</p></div>
Cancer Today Fall Issue Addresses Obesity-Cancer Link and Long-term Health of Childhood Cancer Survivors37292510/3/2014 3:56:18 PM180 Releases/AllItems.aspx610False2014-10-03T13:00:00Z<div class="ExternalClass50A6F8404B694C0894039F9AEE1563A6"><p>​PHILADELPHIA — The fall 2014 issue of <em><a href="http&#58;//" target="_blank">Cancer Today</a></em>, a publication of the American Association for Cancer Research (AACR), features stories on obesity’s impact on cancer risk and treatment, maintaining long-term health after childhood cancer, and the life of singer and actress Rosemary Clooney, who died of lung cancer. <img alt="Cancer Today magazine fall 2014" src="/PublishingImages/CancerToday_Fall2014_Cover_250x321.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>Published quarterly by the AACR, <em>Cancer Today</em> is an authoritative resource for cancer patients, survivors, and their family members and friends. In every issue, <em>Cancer Today</em> offers information and inspiration to help readers face the challenges of diagnosis, treatment, survivorship, and caregiving.</p><p>This issue of <em>Cancer Today</em> includes “<a href="http&#58;//" target="_blank">The Weight of Obesity on Cancer Patients</a>.” Obesity can increase risk for some types of cancer and affect treatment effectiveness and survival, but patients and survivors can take steps to help themselves. In “<a href="http&#58;//" target="_blank">Life and Health After Childhood Cancer</a>,” the impact of childhood cancer treatments on adult survivors is examined. “<a href="http&#58;//" target="_blank">More Than a Girl Singer</a>” reviews Rosemary Clooney’s troubled life and how diagnosing and treating lung cancer has improved since Clooney’s death from the disease in 2002.</p><p>Also, <em>Cancer Today</em> <a href="http&#58;//" target="_blank">tells the story</a> of Felicia Knaul, a health economist and breast cancer survivor working to reduce cancer care inequality in Mexico and other parts of the world.</p><p>To read these stories and others, go to <a href="http&#58;//" target="_blank"><em>Cancer Today</em></a>, or follow the magazine on <a href="https&#58;//" target="_blank">Facebook</a> and <a href="https&#58;//" target="_blank">Twitter</a>. </p><p><em>Cancer Today</em> also publishes a free monthly <a href="http&#58;//" target="_blank">e-newsletter</a>, which contains links to web exclusives, information about events and resources, and highlights from new issues. </p><p>Media are welcome to use information from <em>Cancer Today</em>; however, we ask that you cite the source.</p></div>
Nine-valent HPV Vaccine May Prevent Nearly 90 Percent of Cervical Cancers36664910/23/2014 4:38:45 PM172 Releases/AllItems.aspx609False2014-10-01T04:05:00Z<div class="ExternalClass8C8B96EAC9EC4E468DD9C7523F678129"><p>PHILADELPHIA — Because nine human papillomavirus (HPV) subtypes were found to cause the majority of cervical precancers, a nine-valent HPV vaccine currently being investigated may be able to prevent more cervical cancers than current vaccines, according to research published in <a href="http&#58;//" target="_blank">Cancer Epidemiology, Biomarkers &amp; Prevention</a>, a journal of the American Association for Cancer Research.</p><p><img alt="Elmar A. Joura, MD" src="/PublishingImages/Joura_Elmar_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" />“We wanted to study how many cervical precancers could potentially be prevented by an investigational nine-valent HPV vaccine that provides protection against the HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58,” said <a href="http&#58;//" target="_blank">Elmar A. Joura, MD</a> (<a href="http&#58;//" target="_blank">Adobe Reader </a>required), an associate professor of gynecology at the <a href="http&#58;//" target="_blank">Medical University of Vienna</a> in Austria. “Approximately 85 percent or more of precancerous lesions of the cervix were attributed to the nine HPV types covered in the vaccine; therefore, if nine-valent HPV vaccination programs are effectively implemented, the majority of these lesions could be prevented.</p><p>“Given the high vaccine efficacy that was observed in a large phase III clinical trial testing the nine-valent HPV vaccine, if vaccination programs with this new-generation vaccine are effectively implemented, approximately 90 percent of invasive cervical cancer cases worldwide could be prevented, in addition to the majority of precancerous lesions,” Joura added.</p><p>HPV types 16 and 18 are the predominant causative factors of cervical precancers, which are referred to as CIN 1, 2, and 3 depending on the extent of abnormality. In 2011, the International Agency for Research on Cancer (IARC) expanded the carcinogens list to include HPV types 31, 33, 35, 39, 45, 51, 52, 56, 58, and 59.</p><p>“Despite the clear safety profile of the currently disseminated HPV vaccines, uptake in the United States and other resource-rich countries has been inadequate,” said Joura. “To achieve the population-level potential of the HPV vaccine to reduce cancer, vaccine uptake must increase.”</p><p>Joura and colleagues used data from 12,514 women, ages 15 to 45, enrolled in the placebo arms of three clinical trials testing a quadrivalent HPV vaccine. Among these women, 2,507 were diagnosed with CIN1, CIN2, CIN3, or adenocarcinoma in-situ (AIS). The researchers estimated the number of precancers harboring the HPV types included in an investigational nine-valent HPV vaccine being developed by Merck and currently under review with the U.S. Food and Drug Administration.</p><p>After adjusting for the presence of multiple HPV subtypes in a single lesion, they found that seven high-risk HPV types included in the nine-valent vaccine were present in about 55 percent of CIN 1, about 78 percent of CIN 2, about 91 percent of CIN 3, and nearly 100 percent of AIS lesions.</p><p>Of the women ages 15 to 26 who had precancers, 54 percent had a single HPV infection and 32 percent were infected with more than one HPV type. Of those ages 24 to 45 with precancers, 59 percent and 19 percent were infected with one and more than one HPV types, respectively.</p><p>This study was funded by Merck and Co. Joura received grant support paid to his institution by Merck and GlaxoSmithKline PLC, advisory board fees from Merck and GlaxoSmithKline PLC, and lecture fees from Sanofi Pasteur MSD, Merck, and Roche.</p></div>
Exposure to Dim Light at Night May Make Breast Cancers Resistant to Chemotherapy3657409/30/2014 11:16:35 PM150 Releases/AllItems.aspx608False2014-09-30T23:00:00Z<div class="ExternalClassBFA002ED82814A208A5236DE9E55D583"><p>​NEW ORLEANS — For rats bearing human breast tumors, exposure to dim light at night made the tumors resistant to the standard breast cancer chemotherapy doxorubicin, but giving the rats a melatonin supplement during the dim-light exposure at night prevented resistance development and promoted tumor regression, according to data presented at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=22" target="_blank">13th Annual AACR International Conference on Frontiers in Cancer Prevention Research</a>, held Sept. 28–Oct. 1.</p><p> <img src="/PublishingImages/Hill_Steven_150x200.jpg" alt="" style="margin&#58;5px 20px;vertical-align&#58;auto;float&#58;right;" />&quot;Using our rat model of breast cancer, we recently reported [see July 25, 2014, <a href="/Newsroom/Pages/News-Release-Detail.aspx?ItemID=569" target="_blank">news release</a>] that exposure to dim light at night made human breast tumors resistant to the antihormone breast cancer drug tamoxifen,&quot; said <a href="http&#58;//" target="_blank">Steven M. Hill, PhD</a>, professor of structural and cellular biology and the Edmond and Lily Safra chair for breast cancer research at <a href="http&#58;//" target="_blank">Tulane University School of Medicine</a> in New Orleans. &quot;In this new study, we find that the same is true for doxorubicin, the most commonly used anticancer chemotherapy drug in the world.</p><p>&quot;Although our research is very promising, it is not at a point where we can make recommendations to breast cancer patients taking either tamoxifen or doxorubicin about melatonin supplementation,&quot; continued Hill, who is also director of the Tulane Center for Circadian Biology. &quot;Instead, because melatonin is produced by our bodies at a very specific time of day, exclusively during darkness at night, we can recommend that patients follow a natural light/dark cycle as much as possible, try to sleep or stay in a completely dark room during the night, and/or use a sleep mask. Taking melatonin supplements at the wrong time of day would potentially disrupt the natural melatonin cycle, which may, in itself, impair breast cancer responsiveness to tamoxifen and doxorubicin.&quot;</p><p>For the study, Hill and colleagues analyzed rats exposed to 12 hours of normal light followed by 12 hours of dim light. Half of the rats received melatonin supplementation during the dim-light period (nighttime). Tumor growth in rats that did not receive nighttime melatonin supplementation was 2.8-fold faster compared with tumor growth in rats receiving nighttime melatonin supplementation. In addition, tumors in rats that did not receive nighttime melatonin supplementation were completely resistant to doxorubicin, whereas tumors in rats given nighttime melatonin supplementation were sensitive to doxorubicin and regressed rapidly.</p><p>According to Hill, the researchers identified two potential molecular mechanisms by which exposure to dim light at night might cause the observed doxorubicin resistance. &quot;When we analyzed tumors from rats that did not receive nighttime melatonin supplementation, we detected substantially increased levels of two enzymes that break down doxorubicin to a less active form and significantly elevated levels of membrane proteins that transport doxorubicin out of cells, compared with tumors from rats receiving nighttime melatonin supplementation,&quot; said Hill.&#160;</p><p>&quot;Tumors from rats receiving nighttime melatonin supplementation had lower levels of these enzymes and transporters,&quot; Hill continued. &quot;So we think that melatonin helps maintain high levels of active doxorubicin in the cancer cells, whereas suppression of circadian melatonin production by exposure to light at night has the opposite effect.&quot;</p><p>This study was supported by funds from the National Institutes of Health and the American Association for Laboratory Animal Science. Hill declares no conflicts of interest.</p><p> <img alt="Twitter bird" src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" style="margin&#58;5px;" /> <a href="https&#58;//;q=%23AACRPrev14" target="_blank">#AACRPrev14</a></p></div>