Close
FINDING CURES TOGETHER<sup>SM</sup>

News Releases

 

 

Inhibitor of RNA Polymerase I Shows Promise as Potential Treatment for Acute Myeloid Leukemia and Multiple Myeloma3424889/22/2014 8:24:52 PMhttp://www.aacr.org/Newsroom/Lists/News 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;//www.petermac.org/search/expert?search=Professor%2BRoss%2BHannan" 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;//www.petermac.org/" 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;//twitter.com/search?f=realtime&amp;q=%23AACRHeme14" target="_blank">#AACRHeme14</a></p></div>
Study Finds a New Approach to Tackle Drug Resistance in Hematologic Malignancies3425719/22/2014 2:44:54 PMhttp://www.aacr.org/Newsroom/Lists/News 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;//be.mit.edu/directory/douglas-a-lauffenburger" target="_blank">Douglas Lauffenburger, PhD</a>, professor in the Department of Biological Engineering and <a href="http&#58;//ki.mit.edu/" 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 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;//twitter.com/search?f=realtime&amp;q=%23AACRHeme14" target="_blank">#AACRHeme14</a></p></div>
Drugs Approved to Treat Other Cancer Types May Improve Treatment Outcome for a Type of Childhood Leukemia3426119/22/2014 2:45:11 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx600False2014-09-22T14:00:00Z<div class="ExternalClass2A7C12A1634C4DC5AC1FE7917B65A46D"><p>PHILADELPHIA —Tyrosine kinase inhibitors (TKIs) may improve treatment outcome for children and young adults with Ph-like acute lymphoblastic leukemia (Ph-like ALL), a disease with dismal prognosis, 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="Kathryn Roberts, PhD" src="/PublishingImages/Roberts_Kathryn_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“We recently described a subtype of B-cell acute lymphoblastic leukemia with very poor outcome that is characterized by genetic alterations involving tyrosine kinases, termed Ph-like ALL,” said Kathryn Roberts, PhD, postdoctoral research associate in the Department of Pathology at <a href="http&#58;//www.stjude.org/stjude/v/index.jsp?vgnextoid=7b22b46b476a7410VgnVCM100000290115acRCRD" target="_blank">St. Jude Children’s Research Hospital</a> in Memphis, Tennessee. “We wanted to examine whether these alterations contribute to the development of Ph-like ALL, and determine if they could be targeted with tyrosine kinase inhibitors.</p><p>“We showed for the first time that the kinase alterations we tested contribute to the development of Ph-like ALL, and that Ph-like ALL can be treated effectively with tyrosine kinase inhibitors in animal models,” added Roberts. “These findings provide a strong rationale for treating Ph-like ALL patients with targeted therapies to improve their survival.”</p><p>Roberts and colleagues conducted experiments in the laboratory using normal mouse blood cells and found that introduction of genetic alterations to tyrosine kinases, enzymes that play an important role in cellular functions, caused the development of Ph-like ALL. With further experiments, they found that the different types of kinase alterations triggered different cell signaling pathways.</p><p>Next, they grew human Ph-like ALL tumors in mice, treated them with the TKI dasatinib, and found that the tumor burden reduced with treatment. As proof of principle, the STAT signaling pathway associated with the specific kinase alteration in the tumors was suppressed. The animal models used in these studies were newly developed by Roberts and colleagues.</p><p>“Our studies show that different FDA-approved TKIs such as imatinib, dasatinib, ruxolitinib, or crizotinib could potentially be used to treat Ph-like ALL patients, depending on the type of kinase alterations their tumors bear,” said Roberts.</p><p>“We were able to gain a better understanding of the genetics underlying Ph-like ALL, and our studies could help identify patients who will not respond optimally to current therapy,” added Roberts. “By knowing the exact genetic alteration upfront, we may be able to implement different therapeutic strategies to improve the survival rate of future patients with ALL.”</p><p>This study was funded by the ALSAC of St. Jude Children’s Research Hospital, the National Cancer Institute, Stand Up To Cancer, the St. Baldrick’s Foundation, the Leukemia and Lymphoma Society, and Alex’s Lemonade Stand Foundation. Roberts 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;//twitter.com/search?f=realtime&amp;q=%23AACRHeme14" target="_blank">#AACRHeme14</a></p></div>
New Type of Targeted Therapy Shows Promise in Preclinical Models of B-cell Malignancy3426619/22/2014 2:43:40 PMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx601False2014-09-22T14:00:00Z<div class="ExternalClassA492A790AEB444C98138B4B9DC3D2ECC"><p>PHILADELPHIA — An investigational, bacterial toxin-based therapy targeted to the protein CD38, which is found on the surface of many human blood cancer cells, including multiple myeloma cells, dramatically increased survival in mice bearing human tumor cells, 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="Erin K. Willert, PhD" src="/PublishingImages/Willert_Erin_150x200.jpg" style="margin&#58;10px;vertical-align&#58;auto;float&#58;right;" /></p><p>“Although there are treatment options for patients with multiple myeloma, there is currently no cure, and many patients receive multiple treatments to manage the disease,” said Erin K. Willert, PhD, executive vice president of research and development at Molecular Templates Inc. in Georgetown, Texas. “In this study, we found that the growth of human cancer cells in mice was substantially decreased, or the cells were even eliminated, following treatment with our investigational CD38-targeted therapy.</p><p>“Our results give us confidence in moving the drug forward toward clinical trials for CD38-positive B-cell malignancies such as multiple myeloma,” continued Willert. “Moreover, since our CD38-targeted engineered toxin body works differently than current therapeutics, we think that our investigational therapy has the opportunity to be effective in cases of relapsed or refractory multiple myeloma and other CD38-positive B-cell malignancies.”</p><p>The investigational therapy studied by Willert and colleagues is a CD38-targeted engineered toxin body. According to Willert, engineered toxin bodies recognize a specific protein on the surface of a cancer cell, CD38 in the case of this investigational therapy, and deliver a modified bacterial toxin that enters the cancer cell and then shuts down protein production and kills the cell.</p><p>In mice bearing human cancer cells, the lowest dose of the investigational CD38-targeted engineered toxin body (0.05 mg/kg body weight) significantly reduced tumor burden&#58; Mean tumor burden was 29 percent of the burden in control mice. Treatment with higher doses, 0.5 and 2 mg/kg, resulted in mean tumor burden of less than 1 percent of control.</p><p>The investigational CD38-targeted engineered toxin body increased median survival. Control mice had a median survival of 34 days compared with 59.5 days for mice treated with the lowest dose of the investigational therapy. Among mice who received 0.5 or 2 mg/kg of the investigational therapy, 90 percent and 100 percent were alive at day 60 of the study, respectively.</p><p>“Based on comparisons with another engineered toxin body therapy that is entering clinical testing, we believe the concentrations of the investigational CD38-targeted engineered toxin body we used in the mice in this study will be relevant to the doses used in humans,” said Willert. “However, more preclinical studies are needed before we can test the therapy in the clinic.”</p><p>This study was funded by Molecular Templates Inc. Willert is an employee of Molecular Templates Inc. and has stock options in the company.</p><p><img alt="Twitter bird" src="/PublishingImages/Twitter-bird-blue-on-white_50x50.jpg" style="margin&#58;5px;" /><a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23AACRHeme14" target="_blank">#AACRHeme14</a></p></div>
Study Identifies Potential Drug Combination for Mantle Cell Lymphoma and Chronic Lymphocytic Leukemia3449709/23/2014 1:36:00 AMhttp://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx602False2014-09-22T04:00:00Z<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. <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;//www.medicine.virginia.edu/research/research-centers/cancer-center/cancer-research/membership/members/weber.html" target="_blank">Michael J. Weber, PhD</a>, professor of microbiology, immunology, and cancer biology at the <a href="http&#58;//www.medicine.virginia.edu/" 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;//twitter.com/search?f=realtime&amp;q=%23AACRHeme14">#AACRHeme14</a><br></p></div>
American Association for Cancer Research to Participate in Upcoming Twitter Chat on Proton Therapy3325569/22/2014 9:21:45 PM49http://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx597False2014-09-19T13:00:00Z<div class="ExternalClassE9082EC942154243A270AAABACD43D8A"><p>The American Association for Cancer Research (AACR) will partner with the Mayo Clinic Cancer Center and TIME magazine for a Twitter chat titled “The Role of Proton Beam Therapy in Cancer Care,” Sept. 23, 1-2 p.m. ET. The chat will be moderated by TIME's senior health reporter, Alice Park.</p><p>Dennis Hallahan, MD, and Jeffrey Bradley, MD, will represent the AACR on this Twitter chat. Hallahan is a member of the AACR’s Radiation Oncology Task Force; chairman of the Radiation Oncology Department and the Elizabeth H. and James S. McDonnell III distinguished professor in medicine at Washington University School of Medicine in St. Louis; and is part of the senior leadership at the Siteman Cancer Center. Bradley is director of the S. Lee Kling Center for Proton Therapy, S. Lee Kling professor of radiation oncology, and chief of thoracic service at Washington University.</p><p>Follow the conversation on Twitter and join us&#58; <a href="https&#58;//twitter.com/search?f=realtime&amp;q=%23protonbeam&amp;src=typd" target="_blank">#ProtonBeam</a></p><p>Follow the AACR on Twitter&#58; <a href="http&#58;//www.twitter.com/aacr" target="_blank">@AACR</a></p><p>For more information, please contact Jeremy Moore at <a href="mailto&#58;jeremy.moore@aacr.org">jeremy.moore@aacr.org</a> or 215-446-7109, or Lauren Riley at <a href="mailto&#58;lauren.riley@aacr.org">lauren.riley@aacr.org</a> or 215-446-7155.</p></div>
Call for Ideas Open for the Stand Up To Cancer-American Cancer Society Lung Cancer Translational Research Dream Team Grant3272309/18/2014 2:20:40 PM78http://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx595False2014-09-18T14:00:00Z<div class="ExternalClassEAA231E9C6604D9A98C567093BBC662C"><p>​PHILADELPHIA — The American Association for Cancer Research (AACR) is now accepting submissions of ideas for the Stand Up To Cancer (SU2C)-American Cancer Society Lung Cancer Translational Research Dream Team Grant that will offer up to $20 million in research funding, with the Society and SU2C each providing half the funds over a three-year period. Bristol-Myers Squibb will provide funding in the amount of $5 million to SU2C that will support this Dream Team.</p><p>The grant provides funding for research projects that must include therapeutic interventions for lung cancer and deliver near-term patient benefit through investigation by a multidisciplinary, multi-institutional Dream Team of experts. The research will be expected to involve new immunological approaches. Proposals for the grant must describe plans indicating how the group will use a transformative and synergistic approach, and how the work will be translated into the clinic. To maximize creativity, innovation, and collaboration, the projects should span multiple disciplines and use modern scientific tools to attack research questions in a coordinated effort. </p><p>A SU2C-American Cancer Society Joint Scientific Advisory Committee (JSAC) will conduct a unique, interactive, rapid, and rigorous evaluation of the applications via a multistep scientific review process. The JSAC is comprised of highly accomplished senior laboratory researchers and physician-scientists, as well as advocates. </p><p>The committee is chaired by Nobel Laureate Phillip A. Sharp, PhD, institute professor at the David H. Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology in Cambridge. Arnold J. Levine, PhD, professor at the Institute for Advanced Study in Princeton, New Jersey, and at the Cancer Institute of New Jersey in New Brunswick, and William H. Chambers, PhD, national vice president, extramural research, at the American Cancer Society will serve as vice-chairs.</p><p>Letters of Intent for the SU2C-American Cancer Society Lung Cancer Translational Research Dream Team Grant are due by noon ET, Nov. 5, 2014, via <a href="https&#58;//proposalcentral.altum.com/default.asp?GMID=39" target="_blank">proposalCENTRAL</a>.</p><p><a href="/funding/Pages/funding-listing.aspx#Default=%7b%22k%22%3a%22%22%2c%22r%22%3a%5b%7b%22n%22%3a%22RefinableString09%22%2c%22t%22%3a%5b%22%5c%22%C7%82%C7%82447265616d205465616d%5c%22%22%5d%2c%22o%22%3a%22AND%22%2c%22k%22%3afalse%2c%22m%22%3anull%7d%5d%7d">Learn more</a> about general information on eligibility criteria, the application process, and other details about Dream Team grants<a href="/su2cfunding/dreamteam.">.</a> </p><p>Inquiries may be directed to the AACR Scientific Review and Grants Administration Department at 267-765-1049 or <a href="mailto&#58;su2c@aacr.org">su2c@aacr.org</a>. </p><p>The SU2C-American Cancer Society Lung Cancer Translational Research Dream Team Grant recipients are scheduled to be announced in spring 2015. </p></div>
​Call for Ideas Now Open for the Ovarian Cancer Translational Research Dream Team Grant3272439/18/2014 2:24:50 PM63http://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx596False2014-09-18T14:00:00ZA Collaboration of Stand Up To Cancer, Ovarian Cancer Research Fund, Ovarian Cancer National Alliance and National Ovarian Cancer Coalition<div class="ExternalClass4B37BD1B3C5049C8B049E6D2DDB36E34"><p>PHILADELPHIA — The American Association for Cancer Research (AACR) is now accepting submissions of ideas for the Stand Up To Cancer (SU2C)-Ovarian Cancer Research Fund (OCRF)-Ovarian Cancer National Alliance (OCNA)-National Ovarian Cancer Coalition (NOCC) Translational Research Dream Team Grant that will offer up to $6 million in research funding. </p><p>The SU2C-OCRF-OCNA-NOCC Translational Research Dream Team grant provides three years of funding for research projects that must include therapeutic interventions for ovarian cancer and deliver near-term patient benefit through investigation by a multidisciplinary, multi-institutional Dream Team of experts. Proposals for the grant must describe plans indicating how the group will use a transformative and synergistic approach, and how the work will be translated into the clinic. To maximize creativity, innovation, and collaboration, the projects should span multiple disciplines and use modern scientific tools to attack research questions in a coordinated effort. </p><p>A Joint Scientific Advisory Committee (JSAC) appointed by SU2C, OCRF, OCNA, and NOCC will conduct a unique, interactive, rapid, and rigorous evaluation of the applications via a multistep scientific review process. The JSAC is comprised of highly accomplished senior laboratory researchers and physician-scientists, as well as advocates. </p><p>The committee is chaired by Arnold J. Levine, PhD, professor at the Institute for Advanced Study in Princeton, New Jersey, and at the Cancer Institute of New Jersey in New Brunswick. William G. Nelson, MD, PhD, director of the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center in Baltimore, and Jeff Boyd, PhD, senior vice president at the Fox Chase Cancer Center in Philadelphia and chair of OCRF’s Scientific Advisory Committee, will serve as vice-chairs.</p><p>Letters of Intent for SU2C-OCRF-OCNA-NOCC Translational Research Dream Team Grant are due by noon ET, Nov. 7, 2014, via <a href="https&#58;//proposalcentral.altum.com/default.asp?GMID=39" target="_blank">proposalCENTRAL.</a> </p><p><a href="/FUNDING/PAGES/FUNDING-LISTING.ASPX#Default=%7b%22k%22%3a%22%22%2c%22r%22%3a%5b%7b%22n%22%3a%22RefinableString09%22%2c%22t%22%3a%5b%22%5c%22%C7%82%C7%82447265616d205465616d%5c%22%22%5d%2c%22o%22%3a%22AND%22%2c%22k%22%3afalse%2c%22m%22%3anull%7d%5d%7d">Learn more</a> about general information on eligibility criteria, the application process, and other details about this Dream Team grant. Inquiries may be directed to the AACR Scientific Review and Grants Administration Department at 267-765-1049 or <a href="mailto&#58;su2c@aacr.org">su2c@aacr.org</a>. </p><p>The SU2C-OCRF-OCNA-NOCC Translational Research Dream Team Grant recipients are scheduled to be announced in spring 2015. </p></div>
American Association for Cancer Research Releases 2014 Cancer Progress Report: Research is Transforming Lives3178999/16/2014 2:16:03 PM86http://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx593False2014-09-16T14:00:00ZNow is the time to invest in the NIH<div class="ExternalClassA5C35EE6D23B4C24A6D968569DA700AA"><p>​PHILADELPHIA — Research continues to fuel significant advances against cancer. This progress has been spurred by federal investments in the National Institutes of Health (NIH) and National Cancer Institute (NCI), according to the American Association for Cancer Research's (AACR) fourth annual Cancer Progress Report, released today.</p><p>Thanks to research, Americans today are more likely to survive a cancer diagnosis and enjoy a higher quality of life than at any other time in history.</p><p>&quot;While we are continuing to make impressive progress against cancer, the pace of that progress is being slowed due to years of declining budgets at the NIH and NCI,&quot; said <a href="http&#58;//www.vicc.org/dd/display.php?person=carlos.arteaga">Carlos L. Arteaga, MD</a>, president of the AACR and professor of medicine and cancer biology at <a href="http&#58;//www.vicc.org/">Vanderbilt-Ingram Cancer Center</a>, Vanderbilt University, Nashville, Tennessee. &quot;If we are to fully realize the promise of science to transform cancer care, it will require leadership in Congress and within the administration to ensure that biomedical research in cancer becomes a major priority for our nation.&quot;</p><p>The <em><a href="http&#58;//cancerprogressreport.org/Pages/default.aspx" target="_blank">AACR Cancer Progress Report 2014</a></em> is a comprehensive educational tool that chronicles the progress that has been made against cancer; details how federal investment in the NIH and NCI is transforming lives, such as the lives of the 12 individuals who shared their experiences with cancer in the report; and calls on the administration and Congress to prioritize the growth of the NIH and NCI budgets at a predictable, robust pace by providing annual budget increases at least comparable to the biomedical inflation rate.</p><p>According to the report&#58;</p><ul><li>There are estimated to be nearly 14.5 million cancer survivors alive today in the United States, and almost 380,000 of these individuals received their cancer diagnoses as children or adolescents.</li><li>Between Aug. 1, 2013, and July 31, 2014, the U.S. Food and Drug Administration (FDA) approved six new anticancer therapeutics and new uses for five previously approved anticancer therapeutics.</li><li>During the same period, two imaging agents received new cancer-related FDA approvals, as did a previously approved screening test.</li><li>Research discoveries continue to advance precision medicine&#58; Five of the six new anticancer therapeutics are molecularly targeted agents.</li><li>Patients with some types of cancer have three or more molecularly targeted treatment options, should their cancer recur or become resistant to the primary therapy.</li><li>Cancer genomics research is the foundation for novel clinical trials designed to accelerate the pace at which new therapeutics are approved for patient care.</li><li>Cancer immunotherapeutics are continuing to yield remarkable, long-lasting patient responses in several types of cancer.</li></ul><p><strong><br>Cancer&#58; An Ongoing Challenge; Research&#58; A Vital Investment</strong><br>The report states that although extraordinary advances are being made against cancer, the disease remains a major health care challenge and a huge financial burden, both nationally and internationally.</p><p>Moreover, because most cancer diagnoses occur in those who are 65 years of age and older, a segment of the U.S. population that is expected to double by 2060, it is predicted that the number of cancer diagnoses will increase dramatically in the future.</p><p>The report emphasizes that the rising economic and personal burden of cancer underscores the urgent need for more research to develop new prevention and treatment approaches.</p><p>&quot;Research has transformed the lives of millions of individuals,&quot; said Margaret Foti, PhD, MD (hc), chief executive officer of the AACR. &quot;However, we need more progress because it is unacceptable that one American will die of cancer every minute of every day this year. Cancer survivors like the 12 courageous individuals who shared their stories in this report, as well as those who are projected to receive a cancer diagnosis in the future, are depending on our nation's policymakers to make funding for biomedical research a national priority.&quot;</p></div>
Identification of Novel Mutations Causing Lung Cancer Resistance Leads to New Treatment Strategies3193629/16/2014 8:13:55 PM116http://www.aacr.org/Newsroom/Lists/News Releases/AllItems.aspx594False2014-09-16T04:00:00Z<div class="ExternalClassA9CA5A4EA7434C05985DCFB456E0C6A5"><p>​PHILADELPHIA — Two mutations that cause lung cancer resistance to the investigational ALK inhibitor alectinib were identified, and this information may help design new treatment regimens for patients with ALK-positive lung cancer, according to a study published in <em><a href="http&#58;//clincancerres.aacrjournals.org/" target="_blank">Clinical Cancer Research</a></em>, a journal of the American <span><span>Association for Cancer Research. </span></span></p><p>In 2014, more than 159,000 men and women are expected to die of lung cancer in the United States. About 84 percent of lung cancers are non-small cell lung cancers (NSCLC), and 3 to 5 percent of NSCLCs have mutations in the gene ALK.<br><br>“The goal of our study was to determine why ALK-positive lung cancers become resistant to alectinib, and we looked at this in two different ways,” said <a href="http&#58;//www.massgeneral.org/doctors/doctor.aspx?ID=17279" target="_blank" title="Alice T. Shaw, MD, PhD">Alice T. Shaw, MD, PhD</a>, a thoracic oncologist at the <a href="http&#58;//www.massgeneral.org/cancer/" target="_blank">Massachusetts General Hospital Cancer Center</a>. “We studied a resistant cell line model that we generated in the lab, and we also studied a tumor sample from a patient with NSCLC who had been treated with alectinib and then became resistant.<br><br>“We discovered two novel mutations that have not been described before in patients with NSCLC, and these mutations conferred high-level resistance to alectinib,” Shaw added. “Another equally important finding from this study is that we were able find a way to overcome this type of resistance, in our laboratory experiments as well as in a patient, using another next-generation ALK inhibitor, ceritinib, previously known as LDK378.”<br><br>A drug that targets ALK, crizotinib, was approved in 2011 by the United States Food and Drug Administration (FDA) but patients develop resistance to this drug within a year. As a result, next-generation ALK inhibitors, such as alectinib, are being developed. Alectinib was recently approved in Japan and has “breakthrough therapy” designation from the FDA. <br><br>“Our studies suggest that ceritinib may be effective against ALK-positive lung cancers that have become resistant to alectinib due to the mutations we have identified,” said Shaw. “There are eight next-generation ALK inhibitors that have entered the clinic and our results show that ALK-positive lung cancer patients may benefit from multiple, sequential ALK-inhibitor therapies depending on the underlying resistance mechanism.”<br><br>Using a computational model, Shaw and colleagues found that the two newly identified mutations decreased the binding affinity of alectinib to its target in the tumor, thereby enabling the tumor to become resistant to the drug. They conducted more laboratory experiments and identified two more-potent, next-generation ALK inhibitors, ceritinib and AP26113, to be effective in tumors that developed resistance to alectinib.<br><br>Shaw and colleagues treated a lung cancer patient who developed resistance to alectinib with ceritinib and this patient had a marked response to ceritinib, which lasted for seven months.<br><br>“These studies have been invaluable in learning how ALK-positive cancers become resistant to different ALK inhibitors and in identifying the best therapeutic strategies that will reinduce remissions,” said <a href="http&#58;//www.massgeneral.org/research/researchlab.aspx?id=1169">Jeffrey A. Engelman, MD, PhD</a>, director of the <a href="http&#58;//www.massgeneral.org/cancer/services/centers/thoracic.aspx">Center for Thoracic Cancers</a> at the Massachusetts General Hospital Cancer Center, and a co-investigator of this study.<br><br>This study was funded by the National Cancer Institute and the Japan Society for the Promotion of Science KAKENHI grants. Shaw is a consultant for Pfizer, Novartis, Chugai Pharmaceutical Co., Ariad Pharmaceuticals Inc., Ignyta Inc., Daiichi-Sankyo, and Genentech. Engelman is a consultant for Genentech, Chugai, and Novartis.<br></p></div>