SEP 16, 2014 10:00 AM PDT

Expanded clinical research opportunities for Crizotinib identified from an analysis of over 5,000 exomes

Speaker
  • Staff Scientist, Bioinformatics, Thermo Fisher Scientific
    Biography
      Dr. Eddy joined the Compendia Bioscience™ Translational Bioinformatics Services team, now part of Thermo Fisher Scientific, in July 2010. In his current position, Dr. Eddy provides oncology genomic solutions including but not limited to: identification and cataloging of actionable cancer driving genetic variants, assisting pharmaceutical partners in the identification/validation of novel drug targets, and the identification of potentially clinically relevant biomarkers using the Oncomine® Platform.  Prior to joining Thermo Fisher Scientific, he was employed as a scientist at Genstruct, Inc. in Cambridge, Massachusettes where he interrogated transcriptional regulatory networks to identify mechanisms of cancer progression, disease recurrence, drug-induced toxicity and drug resistance. He earned his doctorate from Carleton University in 1998 by characterizing the role that the PI3K/AKT and PPAR-gamma pathways in stress adaptation. He subsequently completed his postdoctoral studies at Boston University School of Medicine characterizing kinase signaling networks in breast cancer, and implicated IKBKE as having an oncogenic role in progression of the disease.

    Abstract
    Patients with chromosomal rearrangements resulting in fusion proteins are among the most responsive to published targeted therapy. For example, targeting of the EML4-ALK fusion in non-small cell lung cancer (NSCLC) with crizotinib has led to dramatic responses. While crizotinib is approved for use in EML4-ALK positive NSCLC for targeted inhibition of ALK, the drug also inhibits MET, MST1R (RON), ROS1, and more recently, has been reported to inhibit the ALK homolog LTK. To further understand the expanded therapeutic potential of crizotinib, a genomic survey to identify aberrations in ALK, MET, MST1R (RON), ROS1 and LTK was performed across >90,000 samples in the Oncomine Knowledgebase, including >7,000 samples subjected to full exome sequencing to identify known and novel fusion events. In this session, Dr. Eddy will reveal novel findings identified in this analysis including recurrent ALK fusions in colorectal adenocarcinoma, papillary renal cell carcinoma, thyroid gland carcinoma and sarcoma, as well as confirmation of the EML4-ALK fusion in lung adenocarcinoma. In this session, Dr. Eddy will highlight key findings of the analysis and provide an overall breakdown of molecular aberrations by cancer type.

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