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American Association for Cancer Research Recognizes 2015 Research Grantees at Annual Meeting11135144/22/2015 3:55:53 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx725False2015-04-22T12:00:00Z<div class="ExternalClassF2DE3F775A1340F2BB337DEA5D9AC9BF"><p class="ExternalClass6E40AD35EF11426ABCCC78380D2B3D07">​PHILADELPHIA — The American Association for Cancer Research (AACR) honored its new grantee recipients at the AACR Annual Meeting 2015, which was held in here, April 18-22. The AACR is proud to welcome this newest class of 2015 grantees to a long and distinguished list of dedicated scientists who have been selected as AACR grant recipients.&#160; </p><p class="ExternalClass6E40AD35EF11426ABCCC78380D2B3D07"><strong>Fellowships</strong>&#58; <br><span style="text-decoration&#58;underline;">2015 AACR-John and Elizabeth Leonard Family Foundation Basic Cancer Research Fellowship</span></p><div class="ExternalClass6E40AD35EF11426ABCCC78380D2B3D07"><ul><li><strong>Xiaoyang Zhang, PhD,</strong> Dana-Farber Cancer Institute, Boston<br>“To study the role of MGA loss-of-function mutations in lung adenocarcinoma”<br></li></ul></div><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 AACR Anna D. Barker Basic Cancer Research Fellowship</span></p><ul><li><strong>Aaron J. Huebner, PhD,</strong> Massachusetts General Hospital, Boston<br>“Determining the role of Sox2 in synovial sarcoma”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 AACR Basic Cancer Research Fellowships</span></p><ul><li><strong>Ling Cai, PhD,</strong> The University of Texas Southwestern Medical Center, Dallas<br>“Systematic interrogation of metabolism in non-small cell lung cancer”</li><li><strong>Chao Dai, PhD,</strong> Dana-Farber Cancer Institute, Boston<br>“Targeting the SMAD4 tumor suppressor in pancreatic cancer”</li><li><strong>Benjamin Delatte, PhD,</strong> La Jolla Institute for Allergy &amp; Immunology, San Diego <br>“Deciphering the roles of TET2 and TET3 in leukemogenesis”</li><li><strong>Laurent Fattet, PhD,</strong> University of California, San Diego<br>“Regulation of EMT and tumor invasion&#58; Twist1 mediates mechanosensing of ECM”</li><li><strong>Jennifer B. Goldstein, MD,</strong> The University of Texas MD Anderson Cancer Center, Houston <br>“Clonal evolution of glioblastoma”</li><li><strong>James P. Mahaffey, PhD,</strong> New York University School of Medicine<br>“Characterizing post-translational modifications of N-Ras”</li><li><strong>Jason J. Northey, PhD,</strong> University of California, San Francisco<br>“Tissue tension promotes stemness and breast cancer aggression”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2014 AACR-Amgen Inc. Fellowships in Clinical/Translational Cancer Research</span></p><ul><li><strong>Daria V. Babushok, MD, PhD,</strong> University of Pennsylvania, Philadelphia<br>“Clonal hematopoiesis and malignant transformation in aplastic anemia”</li><li><strong>Gangadhara Reddy Sareddy, PhD,</strong> The University of Texas Health Science Center at San Antonio<br>“KDM1 inhibition as a novel epigenetic therapy to target glioma stem cells”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2014 AACR-Bristol-Myers Squibb Oncology Fellowship in Clinical Cancer Research</span></p><span style="text-decoration&#58;underline;"></span><ul><li><strong>Frederick H. Wilson, MD, PhD,</strong> Dana-Farber Cancer Institute, Boston<br>“A genomic approach to identify drivers of resistance to ALK inhibition”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2014 AACR-Bristol-Myers Squibb Oncology Fellowship in Clinical/Translational Cancer Research</span></p><ul><li><strong>Maria Gkotzamanidou, MD,</strong> Dana-Farber Cancer Institute, Boston<br>“Modifying H3K27 methylome via UTX and JMJD3&#58; Implications in myelomagenesis”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 Colon Cancer Alliance-AACR Fellowship in Young-Onset Colorectal Cancer Research</span></p><ul><li><strong>Kent W. Mouw, MD, PhD,</strong> Dana-Farber Cancer Institute, Boston<br>“Identifying genetic vulnerabilities of hypermutated colorectal tumors”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 Colorectal Cancer-Michael’s Mission-AACR Fellowship in Young Onset, Late-Stage Colorectal Cancer Research</span></p><ul><li><strong>Noel F.C.C. de Miranda, PhD,</strong> Leiden University Medical Center, Leiden, Netherlands<br>“Neo-antigen-based therapies for young-onset, late-stage colorectal cancer”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 Conquer Cancer Foundation of ASCO/AACR Young Investigator Translational Cancer Research Award</span></p><ul><li><strong>Bob Li, MBBS, MPH,</strong> Memorial Sloan Kettering Cancer Center, New York<br>“Ado-trastuzumab emtansine for HER2 amplified or HER2 overexpressed cancers&#58; A phase 2 ‘basket’ trial”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 AACR Millennium Fellowships in Lymphoma Research</span></p><ul><li><strong>Maite Alvarez, PhD,</strong> Stanford University, Stanford, California<br>“Improving cancer therapy for lymphoma by preventing NK cell exhaustion”</li><li><strong>Katerina Hatzi, PhD,</strong> Weill Cornell Medical College, New York <br>“Therapeutic targeting of lymphoma self-renewal using LSD1 inhibitors”</li><li><strong>Yuh-Ying Yeh, PhD,</strong> The Ohio State University, Columbus<br>“Investigation of the role of exosomes in chronic lymphocytic leukemia”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 AACR-Millennium Fellowships in Multiple Myeloma Research</span></p><ul><li><strong>Hans C. Lee, MD,</strong> The University of Texas MD Anderson Cancer Center, Houston<br>“Validating novel targets against deletion 17p myeloma”</li><li><strong>Cindy Lin, PhD,</strong> Wistar Institute, Philadelphia<br>“Regulation of multiple myeloma by S100A9 protein”</li><li><strong>Bruno Paiva, PhD,</strong> Universidad de Navarra, Pamplona, Spain <br>“Defining MRD and stem myeloma clones of to understand ultra-chemoresistance”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 AACR-Ocular Melanoma Foundation Fellowship, in honor of Robert C. Allen, MD</span></p><ul><li><strong>Stefan Kurtenbach, PhD,</strong> Miller School of Medicine of the University of Miami<br>“BAP1 loss deregulates neural crest guidance cue signaling in uveal melanoma”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 Debbie’s Dream Foundation-AACR Gastric Cancer Research Fellowships</span></p><span style="text-decoration&#58;underline;"></span><ul><li><strong>Eirini Pectasides, MD, PhD,</strong> Dana-Farber Cancer Institute, Boston<br>“Enhancing the efficacy of ERBB2 inhibition in gastric cancer”</li><li><strong>Andrea Zamperone, PhD,</strong> Albert Einstein College of Medicine of Yeshiva University, Bronx, New York<br>“Mechanisms of DNA damage signaling by Helicobacter pylori”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 QuadW Foundation-AACR Fellowship for Clinical/Translational Sarcoma Research</span></p><span style="text-decoration&#58;underline;"></span><ul><li><strong>Genevieve C. Kendall, PhD,</strong> University of Texas Southwestern Medical Center, Dallas<br>“Zebrafish modeling of PAX3-FOXO1 driven rhabdomyosarcoma”</li></ul><p><br><strong>Career Development Awards&#58;</strong><br><span style="text-decoration&#58;underline;">2015 AACR-Aflac Inc. Career Development Award for Pediatric Cancer Research </span></p><span style="text-decoration&#58;underline;"></span><ul><li><strong>Branden S. Moriarity, PhD,</strong> University of Minnesota - Twin Cities, Minneapolis<br>“Validation and testing of novel therapeutic targets to treat osteosarcoma”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 Breast Cancer Research Foundation-AACR Career </span><span style="text-decoration&#58;underline;">Development Awards for Translational Breast Cancer Research</span></p><ul><li><strong>Sasha Elizabeth Stanton, MD, PhD,</strong> University of Washington, Seattle<br>“Development of a multi-antigen vaccine for breast cancer prevention”</li><li><strong>Fengtian Xue, PhD,</strong> University of Maryland, Baltimore <br>“BCL6-BTB domain inhibitors for triple-negative breast cancer”<br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 AACR-Triple Negative Breast Cancer Foundation Career Development Award for Clinical/Translational Research</span></p><ul><li><strong>Eddy S. Yang, MD, PhD,</strong> University of Alabama at Birmingham<br>“Exploiting TNBC vulnerabilities via rationally combined therapies”</li></ul><p><br><strong>Independent Investigator Awards&#58;</strong><br><span style="text-decoration&#58;underline;">2014 Breast Cancer Research Foundation-AACR Grant for Translational Breast Cancer Research</span></p><ul><li><strong>Fariba Behbod, PharmD, PhD,</strong> University of Kansas Medical Center, Kansas City<br>“Essential role of BCL9 in DCIS progression to invasive breast cancer”</li></ul><p><br><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 Caring for Carcinoid Foundation-AACR Grant for Carcinoid Tumor and Pancreatic Neuroendocrine Tumor Research</span><br style="text-decoration&#58;underline;"></p><ul><li><strong>Scott André Oakes, MD,</strong> University of California, San Francisco<br>“Unfolded protein response in neuroendocrine tumors” <br></li></ul><p><span style="text-decoration&#58;underline;"></span>&#160;</p><p><span style="text-decoration&#58;underline;">2015 Kure It-AACR Research Grant for Immunotherapy in Kidney Cancer</span></p><ul><li><strong>Eliezer Van Allen, MD,</strong> Dana-Farber Cancer Institute, Boston<br>“Response predictors to PD-1/PD-L1 inhibitors in renal cell carcinoma”</li></ul><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" />Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd">#AACR15</a></p></div>
AACR, ABC News’ Dr. Richard Besser Use Twitter’s Periscope to Live Stream “Breakthroughs in Cancer Research” From 2015 Annual Meeting11116394/22/2015 11:53:03 AMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx724False2015-04-22T11:45:00ZNew Broadcasting Platform Allows Top Cancer Researchers to Engage Hundreds of Followers<div class="ExternalClass554D2A3DF7F04BAFBDF68F44FB74D3EB"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) and Richard Besser, MD, ABC News' chief health and medical editor, joined forces Tuesday afternoon on Besser's Twitter chat to share stories, observations, and significant research from the nation's top cancer researchers in conjunction with the AACR Annual Meeting, held April 18 to 22, in Philadelphia. The chat, called &quot;<a href="https&#58;//youtu.be/JMfM8uvQMaU" target="_blank">Breakthroughs in Cancer Research</a>,&quot; drew 406 participants who sent more than 2,000 tweets in the space of an hour. It was also streamed live through Twitter's Periscope.</p><p>Periscope is Twitter's new live-streaming video app. Its live feeds can be shot through iPhones and iPads and watched through smartphones, desktops, or laptops, either through the app or on Twitter's website.</p><p>&quot;We are excited to take advantage of this new broadcasting platform to reach new audiences with the revolutionary research at this year's AACR Annual Meeting,&quot; said Rick Buck, senior director of communications and public relations for the AACR. &quot;We interacted with cancer researchers and institutions across the country, cancer patients, survivors, and caregivers in a wholly unprecedented way, and the response, combined with the efforts of the Twitter chat, was overwhelming.&quot;</p><p>A roster of the nation's most prominent leaders in cancer research participated in the Twitter chat, which was hosted by William G. Nelson, MD, PhD, director of the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University in Baltimore, and editor-in-chief of <a href="http&#58;//www.cancertodaymag.org/Pages/about-us.aspx" target="_blank"><em>Cancer Today</em></a>, the AACR's quarterly magazine for cancer patients, survivors, and their family members and friends.</p><p>Periscope participants were&#58;&#160;</p><ul><li><strong>Jose Baselga, MD, PhD</strong>, AACR president and physician-in-chief and chief medical officer at Memorial Sloan Kettering Cancer Center in New York;</li><li><strong>Carlos L. Arteaga, MD</strong>, AACR past-president and the Donna S. Hall chair in breast cancer research and director of the Center for Cancer Targeted Therapies at Vanderbilt-Ingram Cancer Center in Nashville, Tennessee;</li><li><strong>Lewis C. Cantley, PhD</strong>, AACR Annual Meeting 2015 program chair and the Meyer director of the Sandra and Edward Meyer Cancer Center, the Margaret and Herman Sokol professor in oncology research, and a professor of cancer biology in medicine at Weill Cornell Medical College in New York;</li><li><strong>Raymond DuBois, MD, PhD</strong>, executive director of The Biodesign Institute at Arizona State University in Tempe;</li><li><strong>Thomas J. Lynch, MD</strong>, Richard Sackler and Jonathan Sackler professor of medicine (medical oncology), director of Yale Cancer Center, and physician-in-chief at Smilow Cancer Hospital at Yale-New Haven;</li><li><strong>Emil Lou, MD, PhD</strong>, assistant professor of medicine at the University of Minnesota Medical School in Minneapolis;</li><li><strong>Wafik El-Deiry, MD, PhD</strong>, deputy cancer center director for translational research and the co-leader in molecular therapeutics at Fox Chase Cancer Center in Philadelphia; and</li><li><strong>AnneMarie Ciccarella</strong>, cancer survivor and founder of <a href="http&#58;//www.chemobrainfog.com/" target="_blank">Chemobrain Fog</a>, a leading blog for breast cancer advocates.</li></ul><p>The video content, which will stay on Periscope for 24 hours and is available on the AACR's <a href="https&#58;//youtu.be/JMfM8uvQMaU" target="_blank">YouTube channel</a>, featured conversations between Nelson and all the thought leaders in an interactive format. Researchers and AACR staff also called out various trending topics on the Twitter chat, and discussed them live with Nelson in front of a Periscope audience.</p><p>&quot;The 2015 Annual Meeting at AACR featured some truly groundbreaking research in immunotherapies and precision medicine, and we were proud to share some of those findings with Dr. Besser's online followers,&quot; said Dr. Nelson. &quot;It was great to leverage this new video technology in conjunction with ABC News to spread the word to our audiences in a powerful way.&quot;</p><p>Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a>.</p><p>Follow Dr. Besser's ABC News Twitter chat at <a href="https&#58;//twitter.com/search?q=%23abcDrBchat&amp;src=typd" target="_blank">#abcDrBchat</a>.</p><p>&#160;</p></div>
Olaparib–Carboplatin Combination Showed Early Signs of Clinical Activity Against Ovarian and Triple-negative Breast Cancers11005764/21/2015 3:15:54 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx722False2015-04-21T14:35:00ZThe sequence of treatment had no effect on toxicity<div class="ExternalClassB4C67C5DFE2A438DA7EDF6B87AD5507B"><p>​PHILADELPHIA — The order in which olaparib (Lynparza) and carboplatin chemotherapy were administered to patients with recurrent women’s cancers did not significantly alter the side effects experienced by the patients, and the combination therapy showed preliminary signs of clinical activity in these patients, according to data from a <a href="https&#58;//clinicaltrials.gov/ct2/show/NCT01237067?term=01237067&amp;rank=1" target="_blank">phase I clinical trial</a> presented at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25">AACR Annual Meeting 2015</a>, held here April 18-22. <img alt="Victoria L. Chiou, MD" src="/PublishingImages/Chiou_Victoria_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“The PARP [poly ADP-ribose polymerase] inhibitor olaparib was recently approved by the FDA for treating women with ovarian cancer who have a germline BRCA mutation,” said Victoria L. Chiou, MD, a medical oncology fellow in the<a href="https&#58;//ccr.cancer.gov/Womens-Malignancies-Branch" target="_blank"> Women’s Malignancies Branch </a>at the National Cancer Institute in Bethesda, Maryland. “Studies to identify treatment combinations that might increase the number of patients benefiting from olaparib are important. We asked the question&#58; What is the best way to deliver combination therapy using olaparib and carboplatin to maximize DNA damage, which likely correlates with antitumor effects, and minimize clinical toxicities.</p><p>“We found that the overall sequence of treatments did not significantly impact the side effects that patients felt,” continued Chiou. “Moreover, we identified a safe drug treatment schedule that also had preliminary activity, known as tumor shrinkage, in women with breast cancer and ovarian cancer. In fact, among women with ovarian cancer on the trial with germline BRCA mutations we saw a 60 percent overall response rate with the combination, which is higher than the approximately 30 percent reported response rate for olaparib treatment of heavily pretreated ovarian cancer patients who have a germline BRCA mutation.”</p><p>Chiou explained that the research team was concerned about their preclinical discovery that olaparib pretreatment before carboplatin led to decreased carboplatin-induced DNA damage in tumor cells carrying BRCA1 mutations and launched the phase I clinical trial to explore whether there was an optimal way to deliver the olaparib/carboplatin drug combination.</p><p>The researchers enrolled 59 patients with recurrent women’s cancers in the clinical trial. Among the patients, 47 had ovarian cancer, 10 had triple-negative breast cancer, one had a uterine carcinosarcoma, and one had endometrial cancer. Twenty-six of the ovarian cancer patients and four of the triple-negative breast cancer patients had a germline BRCA mutation.</p><p>The patients were randomized to one of two treatment arms&#58; in arm A, patients received olaparib before carboplatin in cycle one and carboplatin before olaparib in cycle two; in arm B, patients received carboplatin before olaparib in cycle one and olaparib before carboplatin in cycle two. From cycle three, patients received the same treatment regimen. Toxicity was analyzed at the end of every treatment cycle and response at the end of every two cycles.</p><p>Intra-patient and inter-cohort comparisons showed no significant differences in the frequency of grade 3/4 adverse events. The most common grade 3/4 adverse events were neutropenia and anemia.</p><p>According to Chiou, the most updated results show that olaparib given for seven days, in combination with carboplatin given once every 21 days, demonstrated preliminary clinical activity in heavily pretreated patients with breast and ovarian cancer. Among 54 patients the researchers observed one complete response, which lasted for 23 months in a woman with triple-negative breast cancer, and 24 partial responses, 20 in women with ovarian cancer and four in women with triple-negative breast cancer.</p><p>“We currently have two patients still on study,” Chiou added. “One woman has had a partial response that has persisted more than 19 months and another woman who had stable disease documented at the initial time of abstract submission has since achieved a partial response and has been on the study for more than 12 months.</p><p>“I am excited to share these findings. This clinical trial is part of a larger body of clinical trials being done by the Women’s Malignancies Branch at the National Cancer Institute,” Chiou continued. “Every day, my team is working hard to bring new ideas from the bench to the bedside for treatment of women with breast and ovarian cancer. There is more work to be done. This is just the beginning.”</p><p>This study was supported by funds from the intramural program of the National Cancer Institute, with funding to the Center for Cancer Research under an umbrella Cooperative Research and Development Agreement with AstraZeneca. Chiou was previously a recipient of the AACR-GlaxoSmithKline Outstanding Clinical Scholar award for research on PARP inhibitors in triple-negative breast cancer presented at the AACR Annual Meeting 2014. Chiou declares no conflicts of interest.</p><p><a href="/Documents/15AM_Press_Registration_Form.pdf" target="_blank">Press registration</a> for the AACR Annual Meeting 2015 is free to qualified journalists and public information officers.</p><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" />Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>
New PARP Inhibitor Combo Shows Early Promise for Cancer Patients With and Without BRCA Mutations11004684/21/2015 3:03:25 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx721False2015-04-21T14:30:00Z<div class="ExternalClassADDD005CF5C640128083962C92B2C609"><p>PHILADELPHIA — A combination of two molecularly targeted drugs, olaparib and the investigational agent AZD5363, was safe and yielded responses in patients with a variety of cancer types, including breast, ovarian, and prostate cancers, regardless of BRCA1/2 mutation status, according to data from the <a href="https&#58;//clinicaltrials.gov/ct2/show/NCT02338622?term=AZD5363&amp;rank=1" target="_blank">ComPAKT phase I clinical trial</a> presented here at the<a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25"> AACR Annual Meeting 2015</a>, April 18-22. <img alt="Timothy Yap, MD, PhD" src="/PublishingImages/Yap_Timothy_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“In this investigator-initiated clinical trial, we evaluated for the first time whether it is possible to safely combine the investigational AKT inhibitor AZD5363 with olaparib, a PARP [poly ADP-ribose polymerase] inhibitor recently approved by the FDA [U.S. Food and Drug Administration] for treating advanced ovarian cancer associated with defective BRCA genes,” said <a href="http&#58;//www.icr.ac.uk/our-research/researchers-and-teams/dr-timothy-yap" target="_blank">Timothy Yap, MD, PhD, </a>NIHR BRC clinician-scientist and consultant medical oncologist at <a href="http&#58;//www.icr.ac.uk/" target="_blank">The Institute of Cancer Research</a> and <a href="http&#58;//www.royalmarsden.nhs.uk/pages/home.aspx" target="_blank">The Royal Marsden NHS Foundation Trust</a> in London, United Kingdom.</p><p>“Here, we are reporting results from the dose-escalation portion of the trial, which showed that it was indeed possible to combine these drugs safely,” continued Yap. “We also observed that several different cancer types responded to the combination, including cancers without BRCA1/2 mutations. These early results are very exciting because preclinical data had suggested that the olaparib and AZD5363 combination had the potential to be effective in a much wider population of patients than just those harboring germline BRCA1/2 mutations.”</p><p>Yap also explained that the ComPAKT clinical trial is, to the best of his knowledge, the first phase I clinical trial using a combination of targeted agents to implement an intrapatient dose-escalation design. The design allowed individual patients to receive up to three predetermined escalating doses of AZD5363 in combination with a fixed dose of olaparib, but only if they were tolerating the drug combination well. “This design allowed us to safely complete the dose-escalation phase with at least six evaluable patients at each dose level, and in two schedules of the combination with just 20 patients in 7.5 months, which is unprecedented,” said Yap.</p><p>Of the 20 patients enrolled in the dose-escalation portion of the clinical trial, nine had germline BRCA1/2 mutations. The patients had a variety of cancer types including advanced breast, ovarian, prostate, colorectal, cervical, pancreatic, uterine, and bladder cancers; mesothelioma; and gastrointestinal stromal tumors.</p><p>According to Yap, since the abstract was submitted, there are now four confirmed <a href="http&#58;//www.eortc.org/investigators/guidelines/recist/" target="_blank">RECIST</a> partial responses, including in a patient with BRCA1/2 wild-type ovarian cancer, two patients with BRCA1/2-mutant breast cancer, and a patient with BRCA1-mutant ovarian cancer. Two patients had ongoing, prolonged RECIST disease stabilization, including a patient with BRCA1/2 unknown breast cancer at six months and a patient with peritoneal mesothelioma at one year with tumor-marker reduction, who had previously responded before developing disease progression on treatment with a PI3K/mTOR inhibitor. One patient with BRCA1/2-mutant advanced prostate cancer also continues to have a sustained response radiologically on MRI and by prostate-specific antigen <a href="http&#58;//www.ncbi.nlm.nih.gov/pmc/articles/PMC4010133/" target="_blank">Prostate Cancer Working Group 2</a> response criteria at 11 months.</p><p>Based on tolerability, the researchers established that the recommended phase II combination dose was 640 milligrams of AZD5363 twice a day for two days each week, plus 300 milligrams of olaparib twice a day. The most commonly observed side effects were nausea, vomiting, fatigue, diarrhea, and anemia. “We are currently assessing the drug combination at the recommended phase II combination dose in two different cohorts of patients within the dose-expansion phase of the trial,” said Yap.</p><p>The ComPAKT trial is part of the Combinations Alliance jointly supported by Cancer Research U.K., AstraZeneca, and the Experimental Cancer Medicine Center network. It is co-sponsored by The Institute of Cancer Research (ICR) and The Royal Marsden and received research funding from the NIHR Biomedical Research Center at The Royal Marsden and the ICR. Yap received funding for this clinical trial from AstraZeneca and is supported by the NIHR Biomedical Research Center.</p><p><a href="/Documents/15AM_Press_Registration_Form.pdf" target="_blank">Press registration</a> for the AACR Annual Meeting 2015 is free to qualified journalists and public information officers.</p><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" />Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>
Metformin Use May Not Improve Pancreatic Cancer Survival10998694/21/2015 2:12:22 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx720False2015-04-21T13:45:00Z<div class="ExternalClass218F8EFF1F574F2980003377FAAD7461"><p>PHILADELPHIA — Metformin use did not improve survival of patients with pancreatic ductal adenocarcinoma (PDAC) in a retrospective cohort study, according to data presented here at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25">AACR Annual Meeting 2015</a>, April 18-22. <img alt="Roongruedee Chaiteerakij, MD, PhD" src="/PublishingImages/Chaiteerakij_Roongruedee_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“The diabetes drug metformin is being used in some cancer treatment trials based on epidemiologic studies that have reported that use of metformin reduces the risk of death from cancer,” said Roongruedee Chaiteerakij, MD, PhD, of the <a href="http&#58;//www.mayoclinic.org/departments-centers/gastroenterology-hepatology" target="_blank">Division of Gastroenterology and Hepatology</a> at Mayo Clinic Cancer Center in Rochester, Minnesota. “This study highlights the importance of appropriate design of retrospective studies and the necessity of conducting prospective studies with solid rationale for determining the effect of diabetes drugs on cancer risk or death.”<br>According to Chaiteerakij, several epidemiological studies based on retrospective data have reported that metformin is associated with longer survival from different cancers, including pancreatic cancer. Cancer clinical trials have been opened that incorporate metformin in a treatment arm, in part based on these studies, but whether metformin has a beneficial effect on improving survival of cancer patients remains unproven.</p><p>In this retrospective study to comprehensively assess metformin use and survival, Chaiteerakij and colleagues used data from 1,360 patients with PDAC who had data available from the Mayo Clinic Specialized Programs of Research Excellence (SPORE) in pancreatic cancer database. Patients were categorized by metformin use into five groups depending on when they used metformin, from those who had never used metformin to those who started taking metformin more than 30 days after PDAC diagnosis. </p><p>The median survival for patients who did not use metformin was 308 days, compared with 292 days for patients with various metformin exposures, which was not statistically different. The longest survival, for 818 days, occurred in patients who started taking metformin more than 30 days after PDAC diagnosis. </p><p>“These patients already survived more than 30 days, suggesting that there is an inherent survival bias in this group of patients,” Chaiteerakij said. “After accounting for these unintended biases, the benefit of metformin was not confirmed in our study.”</p><p>When the researchers looked at only the 413 patients in the study with resectable disease, they did find a trend toward improved survival among metformin users, but it was not statistically significant.</p><p>“Studies of medication exposure and cancer survival warrant very careful and detailed data collection, which is not always possible in a retrospective study design,” Chaiteerakij said. “Researchers should exercise caution when initiating clinical trials based on retrospective epidemiologic studies.”</p><p>This study was supported in part by the National Cancer Institute SPORE research grant. Chaiteerakij declares no conflicts of interest. </p><p><a href="/Documents/15AM_Press_Registration_Form.pdf" target="_blank">Press registration</a> for the AACR Annual Meeting 2015 is free to qualified journalists and public information officers.</p><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" />Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>
HPV Vaccine Provides Protection at Multiple Sites, Even Among Some Previously Exposed10997824/21/2015 2:05:28 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx719False2015-04-21T13:40:00Z<div class="ExternalClass67DE7F80C0FB44828F5E97FEEA2CCB5C"><p>​PHILADELPHIA — Vaccination of women aged 18-25 with the human papillomavirus (HPV) vaccine resulted in strong protection against future infection at three anatomic sites among women without prior HPV exposure, and may still offer some protection in those with evidence of prior exposure, according to findings presented here at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25">AACR Annual Meeting 2015</a>, April 18-22. <img alt="Daniel C. Beachler, PhD" src="/PublishingImages/Beachler_Daniel_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“HPV is a local infection that can separately infect the cervical, anal, or oral sites where it can occasionally lead to cancer. This study demonstrates that the HPV16/18 vaccine provides protection at all three sites, particularly among women without evidence of HPV exposure prior to vaccination,” said Daniel C. Beachler, PhD, a postdoctoral fellow in the Infections and Immunoepidemiology Branch of the <a href="http&#58;//www.cancer.gov/" target="_blank">National Cancer Institute</a> (NCI). “And while the HPV vaccine is not therapeutic and cannot help clear current infections, we did observe that it may help protect some women previously exposed to HPV against subsequent infection at their noninfected sites.”</p><p>Beachler emphasized that the results of this study support current U.S. guidelines that recommend routine vaccination for those aged 11 to 12, and vaccination through age 26 for those not vaccinated previously. He also pointed out that this was a post-hoc analysis and that the analysis was limited to a one-time sampling of oral and anal HPV infection four years after vaccination. “Further research and better understanding of HPV infection outside of the cervix is needed,” Beachler said. </p><p>The multisite vaccine efficacy, representing protection at all three sites, was evaluated in three subgroups. This efficacy was 83 percent among women without evidence of prior HPV exposure, 58 percent among women with HPV exposure prior to vaccination, and a nonsignificant 25 percent among women with active cervical HPV16/18 infection at vaccination. In all of these women combined, the overall multisite vaccine efficacy was 65 percent and increased to 91 percent for protection of at least two of the three sites. </p><p>According to Beachler, there are three HPV vaccines on the market that protect against HPV at different anatomic sites. However, only about 50 percent of women aged younger than 18 have received the Centers for Disease Control and Prevention-recommended vaccine in the United States. With this analysis, the researchers examined the combined effect of the HPV16/18 vaccine on multiple sites among women who were aged 18-25 at vaccination.</p><p>Beachler and colleagues conducted this analysis in the Costa Rica Vaccine Trial, a randomized, controlled trial of women who were assigned to vaccination with the HPV16/18 vaccine or a control vaccine. Cervical samples were collected at each annual visit and oral and anal samples were collected at the four-year follow-up visit. There were 4,186 women who contributed samples for all three sites and were included in this analysis.</p><p>This study was funded by the intramural program of the NCI. Vaccines were provided by GlaxoSmithKline PLC. Beachler declares no conflicts of interest. </p><p><a href="/Documents/15AM_Press_Registration_Form.pdf" target="_blank">Press registration</a> for the AACR Annual Meeting 2015 is free to qualified journalists and public information officers.</p><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" />Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>
Olaparib and Investigational PI3K Inhibitor BKM120 Combination Active Against Ovarian and Breast Cancer Subtypes10996744/21/2015 1:55:37 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx718False2015-04-21T13:35:00Z<div class="ExternalClass9E3092520F604F338E9FF7224260DF00"><p>​PHILADELPHIA — Combination treatment with the poly ADP-ribose polymerase (PARP) inhibitor olaparib and the investigational phosphatidylinositol-3-kinase (PI3K) inhibitor BKM120 was safe and yielded evidence of clinical benefit for women with triple-negative breast cancer and for those with high-grade serous ovarian cancer, according to data from a <a href="https&#58;//clinicaltrials.gov/ct2/show/NCT01623349?term=01623349&amp;rank=1" target="_blank">phase I clinical trial</a> presented at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25">AACR Annual Meeting 2015</a>, held April 18-22.</p><p>“Several years ago, my colleagues on the <a href="/Funding/Pages/sutc-dream-team.aspx?ItemID=12">Stand Up To Cancer [SU2C] Targeting the PI3K Pathway in Women's Cancers Dream Team</a> found that olaparib and BKM120 were more effective in mouse models of BRCA-mutant breast cancer and BRCA-wildtype triple-negative breast cancer than either drug alone,” said <a href="http&#58;//researchers.dana-farber.org/directory/profile.asp?nxtfmt=r&amp;pict_id=0000245" target="_blank">Ursula A. Matulonis, MD,</a> director and program leader of Medical Gynecologic Oncology in the Susan F. Smith Center for Women’s Cancers at the <a href="http&#58;//www.dana-farber.org/" target="_blank">Dana-Farber Cancer Institute</a> in Boston. “Using SU2C funding, we then initiated this clinical trial to test whether the preclinical data would hold true in patients.</p><p>“We are reassured that it is possible to combine olaparib and BKM120 and that we have seen responses in women with triple-negative breast cancer as well as in women with high-grade serous ovarian cancer,” continued Matulonis who is also an <a href="http&#58;//www.dfhcc.harvard.edu/membership/profile/member/1073/0/" target="_blank">associate professor of medicine</a> at Harvard Medical School.</p><p>In the olaparib/BKM120 dose escalation phase of the clinical trial, Matulonis and colleagues have enrolled 46 patients, 12 with breast cancer and 34 with ovarian cancer. Among these patients, 35 were known to have germline BRCA gene mutations. They then enrolled patients with breast cancer and ovarian cancer in the dose expansion phase of the trial after the maximally tolerated dose had been determined.</p><p>According to Matulonis, 10 different dose level combinations of olaparib and BKM120 were tested and the maximum tolerated dose was found to be 50 milligrams once per day of BKM120 plus 300 milligrams twice per day of olaparib. The dose-limiting toxicities of a grade three depression in one patient and a grade four liver function test in another patient were concerning, Matulonis explained, and meant the researchers were able to escalate BKM120 doses to only half of the single-agent dose.</p><p>“It is important that we saw responses against both BRCA-mutant and BRCA-wildtype cancers,” said Matulonis. “We need to do further analysis to identify biomarkers that we can use to more effectively identify the patient population that will be most positively affected by the olaparib/BKM120 combination.”</p><p>Matulonis’ research is funded by the Department of Defense, the Ovarian Cancer Research Fund, and the Breast Cancer Research Foundation. The clinical trial was funded by SU2C, the Kathryn Fox Samway Foundation, and discretionary funds from the participating center. Matulonis has received research funding from AstraZeneca and remuneration for attending a speaker’s bureau; she has no Novartis disclosures. </p><p><a href="/Documents/15AM_Press_Registration_Form.pdf" target="_blank">Press registration</a> for the AACR Annual Meeting 2015 is free to qualified journalists and public information officers.</p><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" />Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>
Subgroup of Men With Metastatic Prostate Cancer Responded to Olaparib Treatment10995314/21/2015 1:41:35 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx717False2015-04-21T13:30:00Z<div class="ExternalClassCDDE340DBF254CD2A6008200F4972BBD"><p>​PHILADELPHIA — Men with metastatic, castration-resistant prostate cancer that had mutations in genes linked to repair of damaged DNA were significantly more likely to respond to treatment with olaparib compared with patients who had disease without these mutations, according to data from the first stage of the phase II <a href="https&#58;//clinicaltrials.gov/ct2/show/NCT01682772?term=TOPARP&amp;rank=1" target="_blank">TOPARP</a> clinical trial presented at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25">AACR Annual Meeting 2015</a>, held here April 18-22. <img alt="Joaquin Mateo, MD" src="/PublishingImages/Mateo_Joaquin_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“TOPARP is an investigator-initiated clinical trial designed to test the anticancer effect of the PARP [poly ADP-ribose polymerase] inhibitor olaparib in men with metastatic, castration-resistant prostate cancer and, at the same time, to identify biomarkers predictive of response to olaparib,” said Joaquin Mateo, MD, a clinical research fellow in the <a href="http&#58;//www.icr.ac.uk/our-research/research-divisions/division-of-cancer-therapeutics/prostate-cancer-team/research-projects/development-of-novel-targeted-therapeutics-for-prostate-cancer" target="_blank">Prostate Targeted Therapy Group</a> and <a href="http&#58;//www.icr.ac.uk/our-research/research-divisions/division-of-cancer-therapeutics/prostate-cancer-team/research-projects/early-anti-cancer-clinical-drug-development" target="_blank">Drug Development Unit </a>at <a href="http&#58;//www.icr.ac.uk/" target="_blank">The Institute of Cancer Research</a> and <a href="http&#58;//www.royalmarsden.nhs.uk/pages/home.aspx" target="_blank">The Royal Marsden NHS Foundation Trust</a> in the United Kingdom. </p><p>“The data from TOPARP-A show that single-agent PARP inhibition with olaparib has durable antitumor activity in men with metastatic, castration-resistant prostate cancer and identify a molecularly distinct subgroup of patients that respond to the drug,” added Mateo, who is also a doctoral candidate in the laboratory of <a href="http&#58;//www.icr.ac.uk/our-research/researchers-and-teams/professor-johann-de-bono" target="_blank">Johann S. de Bono, MD, PhD,</a> professor of experimental cancer medicine at The Institute of Cancer Research.</p><p>“These are potentially the first clinical data supporting molecular stratification of treatment in prostate cancer, and we are testing this idea in the second stage of the TOPARP trial, TOPARP-B,” continued Mateo. “For TOPARP-B, we are enrolling only patients who screen positive for the DNA repair mutations linked to response in TOPARP-A.”</p><p>Prostate cancer is projected to be the most commonly diagnosed cancer among men in the United States in 2015, and the second-leading cause of cancer-related death.</p><p>Mateo and colleagues enrolled 50 men with metastatic, castration-resistant prostate cancer in TOPARP-A. Among the 49 patients for whom there were evaluable data, 16 had a response to olaparib treatment&#58; Six patients had radiological responses, as assessed by <a href="http&#58;//www.eortc.org/investigators/guidelines/recist/" target="_blank">Response Evaluation Criteria in Solid Tumors</a> (RECIST) guidelines, version 1.1, and 11 patients had biochemical responses, as assessed by a greater than 50 percent decrease in prostate-specific antigen (PSA) levels. Four of these responses lasted more than one year.</p><p>Next-generation sequencing detected mutations in genes associated with DNA repair in tumor samples from 15 of the 49 patients evaluated. Of these patients, 13 had a response to olaparib.</p><p>The researchers calculated the specificity of the DNA repair gene panel to be 94 percent. According to Mateo, this means that 94 percent of patients without these mutations will be correctly identified as not having the mutations and this will help clinicians select the right treatment for a patient because they can be reasonably certain that olaparib will not benefit a patient testing negative for the mutations.</p><p>“The TOPARP clinical trial is being conducted in the United Kingdom but we worked with our U.S. colleagues on the <a href="/FUNDING/PAGES/sutc-dream-team.aspx?ItemID=2">Stand Up To Cancer [SU2C]-Prostate Cancer Foundation [PCF] Dream Team</a> to identify the biomarkers of response to olaparib,” said Mateo.</p><p>This study was supported by funds from the Cancer Research U.K. Clinical Trials Awards and Advisory Committee, SU2C, PCF, the Experimental Cancer Medicine Center, and the U.K. National Institute for Health Research Biomedical Research Center. Mateo has a fellowship from the Medical Research Council and Prostate Cancer U.K.–Movember Foundation. Mateo declares no conflicts of interest.</p><p><a href="/Documents/15AM_Press_Registration_Form.pdf" target="_blank">Press registration</a> for the AACR Annual Meeting 2015 is free to qualified journalists and public information officers.</p><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" />Follow the AACR Annual Meeting 2015 on Twitter&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>
Black Women Found to Have Denser Breast Tissue Than White Women10872304/20/2015 5:03:13 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx716False2015-04-20T17:00:00ZNew method could better test for density in this population with increased breast cancer risk<div class="ExternalClass6A1DE45E437247B79765FD9C6C4CB80B"><p>PHILADELPHIA — Breast density, which is associated with breast cancer risk, was found to be higher in black/African-American women than white women when measured using novel quantitative methods, according to research being presented at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25">AACR Annual Meeting 2015</a>, held here April 18-22. <img alt="Anne Marie McCarthy, PhD" src="/PublishingImages/McCarthy_AnneMarie_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Since breast density is associated with breast cancer risk, a better understanding of racial differences in breast density levels could help us identify women at the highest risk for breast cancer and target prevention strategies to those women,” said Anne Marie McCarthy, PhD, a research fellow at <a href="http&#58;//www.massgeneral.org/" target="_blank">Massachusetts General Hospital</a> in Boston.</p><p>Black women in the study had a significantly higher absolute area density of 40.1 cm2 compared with 33.1 cm2 in white women. In addition, black women had a significantly higher volumetric density of 187.2 cm3 compared with 181.6 cm3 in white women. </p><p>After adjusting for other factors associated with breast density including age, body mass index, hormone therapy, and reproductive factors, black women were found to have significantly higher breast density than white women across all measures.<br>&#160;<br>According to McCarthy, breast density refers to the amount of fibroglandular tissue in the breast when observed on a mammogram. Fibroglandular tissue appears as white on the mammogram, making it difficult to visually detect breast cancers. Research has shown that women who have the highest breast density have a four-to-six times greater risk for breast cancer compared with women with lower breast density. </p><p>Traditionally, radiologists examine mammograms and assign patients a breast density level; however, this assignment can be subjective, McCarthy said. Instead, in this study, McCarthy and colleagues used fully automated computer algorithms to produce both the conventional two-dimensional breast density measurement and a three-dimensional volumetric estimate of breast density. The study included 1,589 black/African-American women and 1,256 white women who underwent screening mammography at the University of Pennsylvania from 2010 to 2011.</p><p>“Our findings are using a new, quantitative and, perhaps, more reliable way to measure breast density,” McCarthy said. “Our next step will be to see how quantitative density measures and other imaging biomarkers are associated with cancer risk, cancer subtype, and stage of diagnosis by race.”</p><p>This study was funded by the National Institutes of Health. The computer software used for breast density estimation has been made publicly available and free for research purposes by the University of Pennsylvania. McCarthy declares no conflicts of interest.</p><p><a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank"><img alt="#AACR15" src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" style="margin&#58;5px;" /></a>&#160;<a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>
American Association for Cancer Research Inaugurates New Leadership at 2015 Annual Meeting10871294/20/2015 4:53:26 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx715False2015-04-20T16:45:00ZJosé Baselga, MD, PhD, Inaugurated as President<div class="ExternalClassFAD9033D65104064990BAADA89A91AD8"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) welcomes José Baselga, MD, PhD, as president of the organization for 2015-2016. He was inaugurated during the Annual Business Meeting, held here during the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=25" target="_blank">AACR Annual Meeting 2015</a>.</p><p><a href="http&#58;//www.mskcc.org/cancer-care/doctor/jose-baselga" target="_blank">Baselga</a>, an internationally recognized physician-scientist whose research focuses on the clinical development of novel molecularly targeted agents for the treatment of cancer, particularly breast cancer, is physician-in-chief and chief medical officer at Memorial Sloan Kettering Cancer Center in New York.</p><p>“It is an honor to serve as president of the AACR,” Baselga said. “We are currently in the midst of a revolution in cancer research, where new technologies and therapies are being developed at a record pace. The AACR is uniquely positioned to advance the promise of precision medicine initiatives. As president, I am eager to work with the AACR community as a whole to integrate basic and clinical research, improve access to clinical trials, coordinate our regulatory policies, and increase our ability to collaborate on the many breakthroughs occurring in cancer prevention, detection, and treatment.”</p><p>He is a pioneer in the development of treatments for women with HER2-positive breast cancer. He conducted the initial clinical trial that demonstrated that patients with advanced HER2-positive breast cancer benefited from treatment with the anti-HER2 monoclonal antibody trastuzumab. In addition, he led the clinical development of the second anti-HER2 monoclonal antibody to receive U.S. Food and Drug Administration approval, pertuzumab (Perjeta). His most recent focus in the laboratory and clinic is the identification of mechanisms of resistance to anti-HER2 agents and the clinical development of novel agents—including PI3-kinase inhibitors and antiestrogen therapies.</p><p>Baselga has been actively involved in the AACR for more than 20 years. Together with Lewis C. Cantley, PhD, Baselga is a founding editor-in-chief of the AACR’s high-impact scientific journal <em>Cancer Discovery</em>. He has served the AACR in many other key capacities, including&#58; Annual Meeting 2013 Program Committee chair, member of the board of directors (2009-2012), and member of the editorial boards of <em>Clinical Cancer Research</em> and <em>Cancer Prevention Research</em>. In addition, Baselga has served on numerous committees, including&#58; chair of the Clinical Trials Committee (2012-2013), chair of the Research Grant Review Committee (2009), member of the Landon Foundation-AACR INNOVATOR Award for International Collaboration in Cancer Research Committee (2006-2008), the Pezcoller Foundation-AACR International Award for Cancer Research Committee (2004-2005), and the AACR Award for Outstanding Achievement in Cancer Research Committee (2002-2003). He was inaugurated into the 2014 class of fellows of the AACR Academy. Additionally, he is a principal of the Stand Up To Cancer Dream Team, “Targeting the PI3K Pathway in Women’s Cancers.” </p><p>Baselga has received numerous awards and accolades for his work in cancer research, including the 32nd annual AACR Richard and Hinda Rosenthal Family Foundation Award in 2008 and the Queen Sofía Spanish Institute Gold Medal in 2010. He is an elected member of the American Society for Clinical Investigation, the American Association of Physicians, and the Institute of Medicine. He has also served as a past president of the European Society for Medical Oncology and on the board of directors for the American Society of Clinical Oncology and the European Cancer Organisation. </p><p>Prior to becoming physician-in-chief and chief medical officer at Memorial Sloan Kettering Cancer Center, Baselga was the chief of the Division of Hematology/Oncology and associate director of the Massachusetts General Hospital Cancer Center, and professor of medicine at Harvard Medical School in Boston. He was also the director of medical oncology, hematology, and radiation oncology and chairman of medical oncology service at Vall d’Hebron University and Hospital, in Barcelona, Spain, and professor of medicine at the Universitat Autònoma de Barcelona. He also served as a faculty member of the Breast/Gynecological Oncology Service at Memorial Sloan Kettering’s Memorial Hospital.</p><p>Baselga received his medical and doctoral degrees from the Universitat Autònoma de Barcelona and completed residencies at Vall d’Hebron University Hospital and the State University of New York Health Science Center at Brooklyn, as well as a fellowship at Memorial Sloan Kettering.</p><p>Additionally, <a href="/Newsroom/Pages/News-Release-Detail.aspx?ItemID=670">Nancy E. Davidson, MD</a>, director of the University of Pittsburgh Cancer Institute and UPMC Cancer Center, was inducted as president-elect, and <a href="/AboutUs/Pages/officers-detail.aspx?ItemID=2">Carlos L. Arteaga, MD</a>, professor of medicine and cancer biology at Vanderbilt University School of Medicine, associate director for clinical research, director of the Center for Cancer Targeted Therapies, and director of the Breast Cancer Program at Vanderbilt-Ingram Cancer Center, now serves as past-president. </p><p><a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank"><img alt="#AACR15" src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" style="margin&#58;5px;" /></a><a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACR15&amp;src=typd" target="_blank">#AACR15</a></p></div>