News Releases



Nine-valent HPV Vaccine May Prevent Nearly 90 Percent of Cervical Cancers36664910/1/2014 1:07:55 PM40 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.<img alt="Elmar A. Joura, MD" src="/PublishingImages/Joura_Elmar_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“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 PM61 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>
Obesity and High Inflammation in Adolescence Associated with Increased Risk for Colorectal Cancer 3622369/30/2014 11:15:43 PM82 Releases/AllItems.aspx606False2014-09-29T17:00:00Z<div class="ExternalClass45E8EDEDD55047E78D69348D3C970F29"><p>​NEW ORLEANS — Among a large cohort of Swedish adolescent males, ages 16–20, those who were obese or had blood markers indicating high levels of inflammation were at increased risk for developing colorectal cancer later in life, according to data presented at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=22">13th Annual AACR International Conference on Frontiers in Cancer Prevention Research</a>, held Sept. 28–Oct. 1.&#160;&#160;&#160;&#160;&#160;&#160; </p><p> <img src="/PublishingImages/Kantor_Elizabeth_150x200.jpg" alt="" style="margin&#58;10px;float&#58;right;" />During an average of 35 years of follow-up, those who were obese (as measured by body mass index) as adolescents were 2.37 times more likely to develop colorectal cancer compared with those who were normal weight as adolescents. Adolescents who had high levels of inflammation, as measured by erythrocyte sedimentation rate, experienced a 63 percent higher risk of the disease compared with whose who had low levels of inflammation.</p><p>“Obesity and inflammation in adulthood have been implicated in colorectal cancer for a number of years,” said Elizabeth Kantor, PhD, a postdoctoral research fellow in the <a href="http&#58;//" target="_blank">Department of Epidemiology at the Harvard School of Public Health</a> in Boston, Massachusetts. “But little is known about the role of adolescent obesity and inflammation in the development of colorectal cancer.</p><p>“Our results suggest that early-life body mass index and inflammation may independently play a role in the development of cancer later in life,” continued Kantor. “These results are important because understanding how life-course exposure to high body mass index and inflammation relates to colorectal cancer risk may improve our understanding of this disease and may help guide prevention strategies. However, further research is needed to better understand these relationships.”</p><p>Kantor and colleagues analyzed data collected from 239,464 Swedish men who were conscribed in the military in late adolescence (ages 16–20) from 1969 to 1976. At the time of conscription, erythrocyte sedimentation rate was measured as a marker of inflammation and height and weight were recorded. Colorectal cancer diagnosis was determined through Jan. 1, 2010, by linking the conscription registry with the national cancer registry. During the follow-up period, 885 cases of colorectal cancer were recorded.</p><p>According to Kantor, the registries the researchers used to obtain the data do not contain information on all variables, such as adolescent diet, that may influence the observed associations. “Obesity was relatively uncommon among adolescents in Sweden at the time the cohort of men enlisted, and it is possible that ‘obesity’ in this study represents something different from what is represented by ‘obesity’ in populations in which this exposure is more ubiquitous,” she added. “As a result, the association between obesity and colorectal cancer risk needs to be investigated in large cohorts from different populations, and further research is needed to disentangle body mass index and inflammation from associated exposures, and similarly, from exposure at other points in the life-course.”</p><p>This work was supported by funds from the National Institutes of Health (T32CA009001), the Harvard School of Public Health (Rose Traveling Fellowship), Örebro University Strategic Funding, and the UK Economic and Social Research Council (ESRC) as grants to the International Centre for Life Course Studies (grants RES-596-28-0001 and ES/JO19119/1). Kantor 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>
Study Identifies Low-dose Aspirin’s Mechanisms of Action in Reducing Cancer Mortality3615309/29/2014 12:23:11 PM98 Releases/AllItems.aspx605False2014-09-29T12:15:00Z<div class="ExternalClassF2F08D5C4C2F4459B18C0566DF9188DC"><p>NEW ORLEANS —Low-dose aspirin may lower the risk for cancer metastasis and mortality by inhibiting both COX-1 and COX-2 pathways, 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.&#160;</p><p>The involvement of the COX-2 pathway is new, as prior studies suggested that low-dose aspirin lowers cancer risk only by inhibiting the COX-1 pathway.</p><p>&quot;Studies have shown that aspirin administration for five or more years reduces the incidence of all cancers by 38 percent. This benefit is seen even at the low doses of aspirin [e.g., 81 mg daily] required to inhibit platelet aggregation via inhibiting the COX-1 pathway, a finding consistent with the known participation of platelets in the metastatic process,&quot; said <a href="https&#58;//" target="_blank">Pierre Massion, MD</a>, professor of medicine and cancer biology in the Division of Allergy, Pulmonary and Critical Care Medicine at <a href="https&#58;//" target="_blank">Vanderbilt University School of Medicine</a> in Nashville, Tennessee.&#160;</p><p>In this study, Massion and his colleagues Oates and Boutaud, sought to determine whether low-dose aspirin, in addition to blocking platelet function by inhibiting the COX-1 pathway, also reduced levels of the pro-metastatic molecule prostaglandin E2 (PGE2) through inhibition of the COX-2 pathway.</p><p>&quot;We found that the potency of low-dose aspirin in inhibiting COX-2 in the tumor cells is as great or greater than its potency as an inhibitor of COX-1 in the platelet,&quot; Massion said. &quot;This indicates that at a cellular level, aspirin is not selective for the platelet, but could also block COX-2 in cancers.</p><p>&quot;The conventional wisdom held that at low doses, aspirin is selective for the platelet and that it does not block extra-platelet COXs. Thus, the finding that it blocked PGE2 production is likely surprising to most investigators in the field,&quot; said Massion. &quot;Our findings may explain how even a very low dose of aspirin taken daily can produce such a substantial reduction in cancer deaths and metastasis.&quot;</p><p>Using three lung adenocarcinoma cell lines, the researchers first found that the doses of aspirin required to inhibit COX-2-dependent PGE2 production were equal to or less than the doses required for the inhibition of COX-1-dependent platelet aggregation.</p><p>Next, using urine samples of 54 subjects who took the low-dose 81 mg aspirin tablets for two weeks, the researchers demonstrated that aspirin inhibited PGE2 production by 45 percent and reduced the levels of a metabolite of PGE2, prostacyclin, by 37 percent.</p><p>The researchers also found that by blocking platelet COX-1, aspirin inhibits the adherence of platelets to the cancer cells to prevent metastasis, suggesting that the two mechanisms described act in concert to reduce the risk for cancer mortality.&#160;</p><p>This study was supported by the National Institutes of Health. Massion 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>
Aspirin May Lower the Risk for Aggressive Prostate Cancer3615329/29/2014 12:23:47 PM80 Releases/AllItems.aspx604False2014-09-29T12:15:00Z<div class="ExternalClassD56A37587D7F4742AA3D9EAE82D02F40"><p>​NEW ORLEANS — Use of aspirin and/or other non-steroidal anti-inflammatory drugs (NSAIDs) was associated with a reduced risk for aggressive prostate cancer in men who had elevated prostate specific antigen (PSA) and a negative biopsy prior to study commencement, according to data presented at the <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=22" target="_blank">13th Annual American Association for Cancer Research International Conference on Frontiers in Cancer Prevention Research</a>, held Sept. 28-Oct. 1.</p><p> <img alt="Adriana Vidal, PhD" src="/PublishingImages/Vidal_Adriana_150x200.jpg" style="margin&#58;5px 20px;vertical-align&#58;auto;float&#58;right;" />&quot;Our purpose was to examine the effects of anti-inflammatory medication use on prostate cancer diagnosis in a study where biopsies were performed largely independent of PSA screening, because anti-inflammatory drugs can lower PSA levels and thus could cloud the real effects of these drugs on prostate cancer detection,&quot; said Adriana Vidal, PhD, assistant professor of surgery in the <a href="http&#58;//" target="_blank">Division of Urology at Duke University School of Medicine</a> in Durham, North Carolina.&#160;</p><p>&quot;Our data support the hypothesis that anti-inflammatory drugs may have a biological role in arresting prostate cancer development, but this requires formal prospective testing in randomized trials,&quot; said Vidal. &quot;In the meantime, men should discuss with their doctors the benefits and risks of taking these medicines to potentially lower prostate cancer risk.</p><p>&quot;Given that aspirin inhibits enzymes in the inflammation pathway, any decrease in inflammatory infiltration in the prostate epithelium would be enough to lower PSA levels,&quot; explained Vidal. &quot;Therefore, it is key to note that nearly all the men in our study had a prostate biopsy regardless of PSA values. Importantly, we found anti-inflammatory drugs were associated with lowered prostate cancer risk, which is consistent with the hypothesis that these agents reduce prostate cancer risk supporting future clinical trials of anti-inflammatory drugs for prostate cancer prevention.</p><p>&quot;Further, we found that NSAIDs only lower PSA by a small amount, and we predict this would have no effect on PSA's ability to predict prostate cancer in these men,&quot; added Vidal.</p><p>Participants were from the REDUCE study that tested if dutasteride reduces the risk of incident prostate cancer. All men had a PSA between 2.5 ng/mL and10 ng/mL, and a biopsy with negative results for prostate cancer prior to the start of the study.</p><p>Of the 6,390 men, 50 percent never used aspirin and/or other NSAIDs, 21 percent were aspirin users, 18 percent were users of other NSAIDs, and 11 percent used both aspirin and other NSAIDs.</p><p>The researchers found that aspirin and/or NSAIDs use lowered the risk for prostate cancer by 14 percent. After adjusting for confounding factors, the researchers found that the use of aspirin and/or other NSAIDs reduced the risk for overall prostate cancer by 13 percent and the risk of&#160; high-grade prostate cancer by 17 percent, but no association was found with low-grade prostate cancer alone.&#160;</p><p>The benefit from aspirin and/or other NSAIDs was found to be similar between participants from Europe and North America. The results were also similar between those who were in the dutasteride arm and those in the placebo arm.</p><p>This study was funded by GlaxoSmithKline PLC and the National Institutes of Health. Vidal 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>
Dr. Graham Colditz Honored With 2014 AACR Award for Outstanding Achievement in Cancer Prevention Research3655499/30/2014 9:11:27 PM50 Releases/AllItems.aspx607False2014-09-24T13:00:00Z<div class="ExternalClass5D3C636FF2BB4550BB4DAC96D4DAEE98"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) congratulates Graham A. Colditz, MD, DrPH, on receiving the <a href="/Research/Awards/Pages/Awards-Detail.aspx?ItemId=17">2014 AACR Award for Outstanding Achievement in Cancer Prevention Research</a>. As an epidemiologist and public health expert, Colditz is being honored for his longstanding commitment to the prevention and control of chronic diseases, including cancer.</p><p>Colditz, Niess-Gain professor of surgery, professor of medicine, and associate director of prevention and control at the Alvin J. Siteman Cancer Center at the Barnes-Jewish Hospital and Washington University School of Medicine in St. Louis, will receive the award at the 13th Annual AACR International Conference on <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=22">Frontiers in Cancer Prevention Research</a>, held Sept. 28-Oct. 1, in New Orleans.</p><p>Colditz, who is also chief of the Division of Public Health Sciences and deputy director of the Institute for Public Health at Washington University School of Medicine, will present his lecture, “Challenges and Opportunities in Breast Cancer Prevention,” 4&#58;25 p.m. CT, Sept. 29, in Grand Ballroom C of the Sheraton New Orleans Hotel.</p><p>The award is given annually to a scientist residing in any country in the world for his or her seminal contributions to the field of cancer prevention. Such investigations must have been conducted in basic, translational, clinical, epidemiological, or behavioral science in cancer prevention research. Further, these studies must have had not only a major impact on the field, but must also have stimulated new directions in this important area.</p><p>Colditz is an internationally recognized leader in cancer prevention. Colditz’s research includes developing statistical models to more accurately classify levels of risk for several cancers, and to clarify the importance of adolescent lifestyle in the prevention of breast cancer. </p><p>“It is an honor to receive this recognition for cancer prevention research that would not be possible without a team of outstanding collaborators and strong institutional support from Siteman,” Colditz said. “The global burden of breast cancer – one in four cancers diagnosed among women worldwide – and the emerging evidence on childhood and adolescent lifestyle means we must shift our focus to earlier life to stand a chance of significantly reducing the burden of breast cancer now and for future generations.”</p><p>Other areas of interest for Colditz include tobacco and obesity in relation to cancer. His work has also shown that smoking increases the risk of stroke and total mortality among women and that weight gain increases the risk of diabetes. Colditz’s work has also demonstrated the validity of self-report methods for use in large-scale epidemiologic studies and refined diet assessment tools for use in public health settings such as the Women, Infants, and Children Program. Colditz developed the award-winning <a href="http&#58;//" target="_blank">Your Disease Risk</a> website, which shares tailored prevention messages with the public. </p><p>Colditz has been an active AACR member since 1996, serving on several research grant and awards committees and as a mentor in a grant-writing workshop. He was also honored with the AACR-American Cancer Society (ACS) Award for Research Excellence in Cancer Epidemiology and Prevention in 2012. He has been recognized with the ACS Medal of Honor, the American Society of Clinical Oncology-ACS Award and Lecture, membership in the Institute of Medicine, and appointment to the National Institute of Health Board of Scientific Directors.</p><p>Prior to his tenure at Washington University in St. Louis, Colditz had served on the faculties at Harvard Medical School in Boston, and the University of Michigan in Ann Arbor. He is currently honorary professor of population at the University of Queensland in Brisbane, Australia.</p><p>Colditz received his medical degree from the University of Queensland and his doctorate of public health from Harvard University School of Public Health. He was an intern at the Royal Brisbane Hospital and a resident at the Internal Medicine Royal Brisbane Hospital, and then completed research fellowships at Harvard as a Fulbright Scholar and Knox Fellow.</p></div>
American Association for Cancer Research CEO Margaret Foti to Receive Ellen V. Sigal Advocacy Leadership Award3462679/23/2014 3:17:40 PM142 Releases/AllItems.aspx603False2014-09-23T04:00:00Z<div class="ExternalClass9AA318A10EC24D9593B97057C9306CBA"><p>​PHILADELPHIA — Margaret Foti, PhD, MD (hc), chief executive officer of the American Association for Cancer Research (AACR), will receive the Ellen V. Sigal Advocacy Leadership Award from the prestigious national advocacy organization <a href="http&#58;//" target="_blank">Friends of Cancer Research</a> (Friends) tonight at its 18th Annual Cancer Leadership Awards Reception in Washington, D.C. <img alt="Margaret Foti, PhD, MD (hc)" src="/PublishingImages/Foti_Margaret_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>This is the second year Friends of Cancer Research has awarded the Ellen V. Sigal Advocacy Leadership Award, named for the chairperson and founder of <em>Friends</em> to celebrate her lifelong commitment to science, research, and patient advocacy. The first Ellen V. Sigal Advocacy Leadership Award was given to Sherry Lansing, chief executive officer of The Sherry Lansing Foundation, co-founder of Stand Up To Cancer, and former president of Paramount Pictures in Los Angeles. </p><p>“Friends of Cancer Research is truly honored to recognize Margaret Foti as the second recipient of the Sigal Advocacy Leadership Award,” said Ellen Sigal, PhD, chairperson and founder of <em>Friends</em>. “Her dedication to cancer research, trailblazing work as CEO of the AACR, and steadfast advocacy for science and patients is unparalleled and invaluable to all in the community.” </p><p>The award honors advocates who have made unprecedented contributions to the cancer research community. Foti serves as chief executive officer of the AACR, the world’s first and largest professional organization dedicated to advancing cancer research. During her long tenure, AACR membership has grown from 3,000 to more than 35,000 laboratory, translational, clinical, and population scientists; other health care professionals; and cancer advocates residing in 97 countries. Under Foti’s leadership, the organization’s scientific meetings, peer-reviewed journals, and science and public policy work have flourished, furthering progress against cancer through research, education, communication, and collaboration. </p><p>“Ellen Sigal is a true visionary, an advocate, a collaborator, and a dear friend. She has made an enormous impact by fostering groundbreaking partnerships in the cancer field to discuss national policies and solutions that will accelerate the development of effective treatments for patients,”&#160;&#160; Foti said. “I am deeply honored to receive this award bearing her name. </p><p>“I am immensely proud of AACR’s accomplishments in the battle against cancer over the years, but there is much more work to be done,” she continued. “We will continue to provide support and opportunities for professional development to basic researchers and physician-scientists at all stages of their careers, so that they can continue to make the advances that lead to more cures. And we will continue to advocate strongly for increased federal funding for cancer research and biomedical sciences, which must be a national priority if we are to improve public health, spur more progress, inspire more hope, and save more lives.” </p><p>During Foti’s tenure, the AACR has become an outspoken proponent of policies that support all aspects of cancer research and prevention. The organization engages with policymakers through its Science Policy and Government Affairs Committee and Washington, D.C. office, which opened in 2007 to amplify the voice of cancer researchers, patients, survivors, and caregivers on Capitol Hill. The AACR’s commitment to advocacy was evident in April 2013, when under Foti’s direction, the organization spearheaded a Rally for Medical Research in downtown Washington, D.C. That event brought more than 200 organizations and 10,000 people to the streets to call for increased investment in the National Institutes of Health. The momentum from that day has continued in the form of a Rally for Medical Research Hill Day held last week with nearly 300 supporting organizations and also in September 2013.</p><p>In addition to her leadership at the AACR, Foti has been elected president of three professional societies in scholarly publishing and cancer research. She has also served as a board member, committee member, and consultant to a number of other nonprofit, scientific, and cancer-related organizations, and is a founding board member and member of the Executive Committee of <em>Friends</em>. Foti has received numerous accolades for her leadership, including honorary degrees in medicine and surgery from three universities in Italy and Spain and, most recently, the 2014 Morton M. Kligerman Visiting Professorship Award from the University of Pennsylvania.<br><br>The awards reception this evening will take place at the Hays-Adam Hotel. <em>Friends</em> will also honor Louisiana Governor Bobby Jindal and Massachusetts Governor Deval Patrick. For more information about <em>Friends</em> and the Ellen V. Sigal Advocacy Leadership Award, visit the organization’s <a href="http&#58;//" target="_blank">website</a>.</p></div>
Study Identifies Potential Drug Combination for Mantle Cell Lymphoma and Chronic Lymphocytic Leukemia3449709/23/2014 3:20:11 PM176 Releases/AllItems.aspx602False2014-09-23T00:00:00Z<div class="ExternalClass7776CC5BC2A9444D9AC4174BC8893539"><p>​PHILADELPHIA — Using the molecularly targeted drug ibrutinib (Imbruvica) together with the investigational anticancer agent ABT-199 may improve outcomes for patients with mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL), according to preclinical data presented at the American Association for Cancer Research special conference, <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=20" target="_blank">Hematologic Malignancies&#58; Translating Discoveries to Novel Therapies</a>, held Sept. 20-23. <img alt="Michael J. Weber, PhD" src="/PublishingImages/Weber_Michael_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /><br><br>“Ibrutinib was recently approved by the FDA [U.S. Food and Drug Administration] for the treatment of both mantle cell lymphoma and chronic lymphocytic leukemia,” said <a href="http&#58;//" target="_blank">Michael J. Weber, PhD</a>, professor of microbiology, immunology, and cancer biology at the <a href="http&#58;//" target="_blank">University of Virginia School of Medicine</a> in Charlottesville. “Unfortunately, about one-third of patients have disease that is resistant to ibrutinib, and even for those who have disease that responds, in very few cases is it a complete response. This problem of treatment resistance is one of the biggest challenges in cancer treatment at the moment.<br><br>“We took an empirical but systematic approach to identify combinations of drugs that might improve the ability of ibrutinib to kill cancer cells,” continued Weber. “The combination of ibrutinib and ABT-199 was by far the most effective in our assays, and we are in the very earliest stages of planning a clinical trial to test this combination in the clinic.”<br><br>In previously reported studies, Weber and colleagues found that ibrutinib and ABT-199 synergized to kill, by a process called apoptosis, MCL cell lines. In this study, they assessed the effects of exposure to the combination on blood samples from 16 patients who had MCL or CLL cells detectable in the blood. The percentage of cells undergoing apoptosis was sixfold higher in samples exposed to the combination compared with samples exposed to either drug alone&#58; 23 percent of cells exposed to the combination underwent apoptosis compared with 3.8 and 3 percent of cells exposed to ibrutinib and ABT-199, respectively.<br><br>Further analysis showed that the combination of ibrutinib and ABT-199 worked synergistically to cause apoptosis in leukemic cells from five of nine patients with CLL. According to Weber, the variable response to this combination points to the importance of understanding how these combinations work, so that we can match the treatments with the most appropriate patients.<br><br>“Ibrutinib and ABT-199 target different pathways involved in promoting cancer cell survival and growth,” said Weber. “This is very intriguing because in most instances where cancer cells are resistant to a particular molecularly targeted drug, we find that cancer cells adapt and find new ways to reactivate the pathway being targeted by the drug and that combinations of drugs targeting this pathway in different ways can improve outcomes. Here, we found that targeting a pathway outside the primary pathway was effective.”<br><br>This study was funded by the University of Virginia Cancer Center. Weber declares no conflicts of interest.</p><p><img src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" alt="" style="margin&#58;5px;" /><a href="https&#58;//;q=%23AACRHeme14">#AACRHeme14</a><br></p></div>
Inhibitor of RNA Polymerase I Shows Promise as Potential Treatment for Acute Myeloid Leukemia and Multiple Myeloma3424889/22/2014 8:24:52 PM130 Releases/AllItems.aspx598False2014-09-22T14:00:00Z<div class="ExternalClass48DF939D44904B369DA569E9C98DF5D7"><p>PHILADELPHIA — The investigational drug CX-5461, which blocks the protein RNA polymerase I (Pol I), prolonged survival in mouse models of highly aggressive acute myeloid leukemia (AML) and multiple myeloma, according to data presented at the American Association for Cancer Research special conference <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=20">Hematologic Malignancies&#58; Translating Discoveries to Novel Therapies</a>, held Sept. 20-23.<img alt="Ross D. Hannan, PhD" src="/PublishingImages/Hannan_Ross_150x200.jpg" style="margin&#58;10px;width&#58;150px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Some forms of AML and multiple myeloma are highly refractive to standard therapies,” said <a href="http&#58;//" target="_blank">Ross D. Hannan, PhD</a>, head of the Oncogenic Signalling and Growth Control Program and a professor at the <a href="http&#58;//" target="_blank">Peter MacCallum Cancer Centre</a>, Melbourne, Australia. “There is an urgent need for new drugs that can treat patients with these cancers that have relapsed on standard therapy, which is why we chose to study the effects of CX-5461 in mouse models of these diseases.</p><p>“Our results show that CX-5461 was effective in preclinical models of MLL-AML and multiple myeloma refractory to standard therapy and that therapeutic efficacy was independent of p53 status,” continued Hannan. “These results provide further rationale for the first-in-human phase I clinical trial that we initiated in July 2013 testing CX-5464 for patients with advanced hematological malignancies, including AML and multiple myeloma.”</p><p>According to Hannan, Pol I levels are consistently found to be upregulated in cancers, in particular hematologic malignancies, suggesting it might be a good therapeutic target. He and his colleagues found that CX-5461 significantly extended overall survival in a mouse model of highly aggressive AML, the MLL/ENL + Nras model. Median survival was 17 days for mice treated with vehicle with no drug, compared with 21 days for mice treated with the standard chemotherapy combination of cytarabine and doxorubicin and 36 days for mice treated with CX-5461.</p><p>In the V-kappa-MYC driven model of multiple myeloma, CX-5461 significantly prolonged overall survival&#58; median survival was 103.5 days for mice receiving vehicle with no drug and 175 days for mice receiving CX-5461.</p><p>Pol I is a protein involved in a cellular process central to cell proliferation and survival; as such, it is referred to as a house-keeping protein. “We were excited to find that therapeutic doses of CX-5461 had little effect on normal cells in our experiments,” said Hannan. “Prior to these studies, few people would have guessed that such a therapeutic window could be obtained by targeting a so-called house-keeping protein that is essential to all cells for survival.”</p><p>This study was funded by the National Health and Medical Research Council, Australia; the Leukaemia Foundation of Australia; and Cancer Council Victoria, Melbourne, Australia. Senhwa Biosciences provided CX-5461. Hannan declares no conflicts of interest.</p><p><img alt="Twitter bird" src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" style="margin&#58;5px;" />&#160;<a href="https&#58;//;q=%23AACRHeme14" target="_blank">#AACRHeme14</a></p></div>
Study Finds a New Approach to Tackle Drug Resistance in Hematologic Malignancies3425719/24/2014 7:23:35 PM148 Releases/AllItems.aspx599False2014-09-22T14:00:00Z<div class="ExternalClassE5F9C9DDD4E14926AFFCF3F027A384F1"><p>PHILADELPHIA — Treating hematologic malignancies upfront with a combination of drugs based on the vulnerabilities of tumors as they evolve may be a viable strategy to avoid drug resistance, according to data presented at the American Association for Cancer Research (AACR) special conference <a href="/Meetings/Pages/MeetingDetail.aspx?EventItemID=20">Hematologic Malignancies&#58; Translating Discoveries to Novel Therapies</a>, held Sept. 20-23.<img alt="Douglas Lauffenburger, PhD" src="/PublishingImages/Lauffenburger_Douglas_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Our goal is to identify vulnerabilities in cancer across stages of tumor evolution while it is developing resistance to initial treatment, to help guide the design of drug combination strategies,” said <a href="http&#58;//" target="_blank">Douglas Lauffenburger, PhD</a>, professor in the Department of Biological Engineering and <a href="http&#58;//" target="_blank">Koch Institute for Integrative Cancer Research</a> at MIT in Boston.</p><p>“There may be many stages in a tumor evolution while under treatment that may make them vulnerable to already existing therapies,” Lauffenburger continued. “Rather than waiting for the tumor to become resistant to the first treatment and then thinking about a second-line drug to use, we can capitalize on opportunities that exploit vulnerabilities at different early stages, as the tumor is evolving to become resistant to the first drug.”</p><p>In an initial screening experiment using a combination of computational and experimental approaches, Lauffenburger and colleagues Boyang Zhao and Michael Hemann identified drugs that are likely to be effective against a murine acute lymphoblastic leukemia (ALL) cell line as the cells evolve. These drugs were effective against certain human chronic myelogenous leukemia (CML) cell lines as well.</p><p>Next, to develop drug combinations based on the characteristics of evolving tumors, the researchers used escalating doses of the drugs imatinib, dasatinib, nilotinib, foretinib, and crizotinib on ALL cells. As some cells exhibited resistance to a particular drug, the research team treated the resistant cells with other drugs to check for cross-resistance. They found that resistant cells surviving at low multiples of the original drug dose actually demonstrated sensitization to certain other drugs, with the sensitization abrogated at higher doses.</p><p>“Instead of only looking for the most resistant population of ALL cells at the end of this selection process, we monitored for drug sensitivity of the cells at each stage of the dose escalation,” explained Lauffenburger. “This led us to discover the vulnerabilities of a tumor at different stages of clonal evolution, a phenomenon we would have missed if we only analyzed for drug sensitivity at the last stage of this process, which is equivalent to when a patient has relapsed.</p><p>“From our studies, we found that, for example, it would be ideal to treat an ALL patient with dasatinib followed by crizotinib/foretinib for synergy during the early stages of clonal evolution of the patient’s tumor, rather than treating only with dasatinib and waiting until the patient has relapsed,” said Lauffenburger.</p><p>This study was funded by the National Institutes of Health and the MIT Ludwig Center for Molecular Oncology. Lauffenburger is a consultant for Genentech Inc., Merrimack Pharmaceuticals Inc., and Pfizer Inc., and receives research funding from Janssen.</p><p><img alt="Twitter bird" src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" style="margin&#58;5px;" /><a href="https&#58;//;q=%23AACRHeme14" target="_blank">#AACRHeme14</a></p></div>