The Personalized Oncology Pipeline:
Solid tumors and hematologic malignancies: Phase III trials
Targeted TherapyNews (see page 35)
For the Practicing Oncology Professional
Bevacizumab
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In this issue... Melanoma • Nab-paclitaxel extends PFS vs standard chemotherapy Prostate Cancer • Enzalutamide delays first SRE, improves pain and QoL • FDA approves earlier use of abiraterone acetate
Feature
Innovations in Precision Medicine
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s 2012 drew to a close, several key oncology conferences highlighted the most important innovations in targeted oncology therapy—an area often termed “precision medicine” based on our increasing ability to precisely target and treat specific oncogeneic mutations and pathways. The Chemotherapy Foundation Symposium, held November 7 to 9, and the 35th Annual CTRC-AACR San Antonio Breast Cancer Symposium (SABCS), held December 4 to 8, were two such conferences, both focusing on recent rapid developments in targeted therapies. In this issue, we highlight key data and presentations from the two conferences.
Lung Cancer • EGFR mutation status and sorafenib in NSCLC
Thyroid Cancer • FDA approves cabozantinib to treat medullary thyroid cancer
© SABCS/Todd Buchanan 2012
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Targeted Oncology Therapy in 2012 and 2013: Where Have We Been, Where Are We Going? By Anna Azvolinsky, PhD
T © SABCS/Todd Buchanan 2012
Feature
Researchers Determine How PARP Inhibitors Work By Ben Leach
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Hematologic Malignancies • Ponatinib approved for CML and ALL
Colorectal Cancer • Biomarker may predict response to bevacizumab in mCRC
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wenty new cancer drugs were approved in 2012, and thousands of new targeted and immunotherapeutic oncology agents, including some that will emerge in 2013, are in development. Here we look back at the most important advances in oncology targeted therapy in 2012, and ahead to what to expect for 2013 in key therapeutic areas.
Breast Cancer It has been a productive year for breast cancer trial results and approvals. Two new drugs were
Sara Hurvitz, MD
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esearchers from the National Institutes of Health Yves Pommier, MD, PhD (NIH) have discovered a new mechanism of action utilized by poly (ADP-ribose) polymerase (PARP) inhibitors in an effort to promote antitumor activity, suggesting that existing and in-development PARP inhibitors differ in how they are able to treat cancer. The results of the study were published in the journal Cancer Research. PARP1 and PARP2 belong to a family of proteins associated with cellular processes such as chromosome stability, regulation of apoptosis, cell division, and transcriptional regulation and differentiation. PARP enzymes are responsible for repairing DNA damage caused by environmental stresses and DNA replication errors, including single-strand breaks, by enlisting other proteins to actually repair the damage. These single-strand breaks can become double-strand breaks that are then repaired by a complex that contains BRCA1 and BRCA2, mutations closely linked to breast cancer and ovarian cancer. Prior to the study, researchers understood that PARP inhibitors—including drugs such as olaparib and veliparib—worked by blocking PARP enzyme activity, thus preventing the repair of DNA damage and ultimately initiating apoptosis, or cell death, by selectively killing cells with genetic abnormalities.
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