Genomics of lung cancer

Published on January 31, 2016   39 min

Other Talks in the Series: Cancer Genetics

Please wait while the transcript is being prepared...
0:00
Hello, I am Ramaswamy Govindan, a medical oncologist at the Washington University School of Medicine in St. Louis. I'm an expert in lung cancer and cancer genomics. Today we are going to talk about the genomics of lung cancer.
0:17
I have no conflicts relevant to this presentation. I'm a consultant for BMS, BI, Pfizer, Mallinckrodt Medical, Genentech, Novartis, and GlaxoSmithKline.
0:30
I want to acknowledge the investigators from the Cancer Genome Atlas project. I specifically want to thank Dr. Matthew Meyerson and Dr. Steve Baylin, my two co-chairs, for their support. I also want to thank my colleagues at the Washington University School of Medicine, specifically those at the Genome Institute, Dr. Richard Wilson, Dr. Elaine Mardis, and Dr. Li Ding, for their collaboration.
0:56
I want to begin with a story. This is a patient of mine with advanced non-small cell lung cancer, who came to see me after receiving multiple lines of chemotherapy. When we saw her, she had advanced disease and she had a lot of symptoms related to her cancer, she was unable to work full-time. We biopsied her tumor, as you can see here she has a fairly large and impressive tumor on the right side. The biopsy showed a 12 base-pair insertion in exon 20 of the ERBB2 gene. This is a known oncogenic alteration seen in a small number of patients with non-small cell lung cancer. When we treated her as a part of the phase 1 study with neratinib and temsirolimus, she had an impressive response, as you can see here, from before to after treatment, she had a very nice decrease in the tumor size and had significant benefit clinically as well as radiographically. She in fact went back to work full-time, and worked for nearly a year before the cancer progressed, she's now currently on salvage chemotherapy but she had a very good one year with the combination of neratinib and temsirolimus, because of the recognition that her tumor had this activating mutation in the ERBB2 gene.