ASCO 2013: Key Targeted Trials
An Interview with Douglas Yee, MD, Scientific Program Chair
Targeted TherapyNews (see page 24)
Personalized Medicine For the Practicing Oncology Professional
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Vol. 2 No. 3
In this issue... Prostate Cancer • Biomarkers Still Needed Ovarian Cancer • Possible Mechanism of Platinum Resistance in Ovarian Cancer Identified Genetic Research • Metabolic Gene Expression Altered in Cancer, Providing Potential Drug Targets Hematologic Malignancies • Numerous Drug Classes Studied for Use in Follicular and Other Lymphomas • Seeking a Standard in the Treatment of Elderly Patients With CLL AACR Meeting • Spotlight on Novel Agents in Early Development Breast Cancer • Trials Examine Use of T-DM1 as Combination Therapy for HER2 Breast Cancer • FDA Grants Breakthrough Therapy Designation for Palbociclib in Breast Cancer Lung Cancer • HER2-Targeted Agents May Benefit Patients With Non-Small Cell Lung Cancer
Feature
Researchers Identify How Nongenetic Mechanisms of Cancer Cell Diversity Can Affect Treatment Response By Anna Azvolinsky, PhD
A
new study suggests that even tumor cells with a common genetic background can display functional heterogeneity. The results point to nongenetic mechanisms, such as microenvironment and epigenetic differences, that contribute to tumor growth as well as tolerance to therapy. The research, led by Antonija Kreso, PhD, Catherine O’Brien, MD, and John Dick, PhD, of the Princess Margaret Cancer Centre and the University of Toronto, Canada, was published in the February 2013 issue of Science. “Genetic mutations are thought to account for tumor formation and growth, but our results indicate intra-clonal diversity with respect to functional properties also plays a role,” said Kreso. The predominant theory of solid tumor heterogeneity states that tumor cell diversity is a result of progressive mutational changes that form distinct tumor cell clones, with each type of subclone thought to be genetically similar. But how nongenetic factors contribute to tumor heterogeneity along with genetic diversity is not clear. Kreso and colleagues addressed whether these genetic clones are functionally equivalent and respond in the same manner to chemotherapy treatment by tracking individually labeled human colorectal cancer (CRC) cells in mice. They found that individual tumor cells within the same lineage had a spectrum of survival
Feature
New Developments in Oral Targeted Agents for Advanced Colorectal Cancer By Anna Azvolinsky, PhD
I
n September 2012, the FDA approved regorafenib (Stivarga) as a salvage treatment for metastatic colorectal cancer (mCRC) previously treated with chemotherapy, an anti-
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BRCA Patenting Case Reaches the Supreme Court By Ben Leach
T
he question of the validity of gene patents has reached the Supreme Court, and the impending decision could transform the current research landscape. The company on the defensive end of the case is Utah-based Myriad Genetics, a molecular diagnostic company responsible for the development of the BRACAnalysis test. In 1994, it was discovered that the BRCA1 and BRCA2 genes were linked to an increased risk of breast cancer and ovarian cancer. As the patent holder, Myriad requires that all testing for the genes be done with the company’s test only.
Peter Meldrum
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Axel Grothey, MD vascular endothelial growth factor (VEGF) therapy, or an anti-epidermal growth factor receptor (EGFR) therapy. Regorafenib had received a fast-track FDA review status and was approved after only a three-month review process. The drug is the first targeted oral therapy to receive an FDA approval for treatment of advanced CRC, and the second drug to be approved for mCRC in 2012. Although progress has been made in treating colorectal cancer, including the development of biologic agents that target EGFR and angiogenesis, the median survival in mCRC remains about two years. The five-year survival rate for a patient with stage II
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