Yesterday was our GSC-wide lab meeting, a quarterly event that crams 400+ people into an undersized auditorium. The guest speaker was Ramaswamy Govindan (MD), a medical oncologist from the Siteman Cancer Center. He gave a great 20-minute talk about lung cancer. He could easily have spoken to us for two hours on this topic, but alas, time is short. One topic he discussed that’s very germane to our work is the EGFR cancer pathway, which may account for 10% or more of lung cancers. Interestingly Asians, women, and NON-smokers are far more likely to have EGFR mutations (there was a fourth risk factor that I didn’t have time to write down).
From what I understand, EGFR encodes an epidermal growth factor receptor and as I understand it is expressed in normal tissues only during development. There is a drug called gefitinib that inhibits EGF receptors – a simple tablet that’s taken orally. Dr. Govindan showed some superior-view images of the chest cavity of a lung cancer patient before and after gefitinib therapy. The difference was amazing. Before treatment one lung was completely cancerous, and 2 years later (after treatment) the cancer was totally gone. It was a compelling example of what the future of cancer therapy might look like.
Speaking of which, the speaker went on to talk a bit about pharmacogenetics – the study of how genetics affect differential response to treatment among individuals. Evidently, classifying lung cancer patients by EGFR mutation status is extremely effective in predicting the outcome of chemotherapy. Patients with EGFR mutations respond well, while other patients see little or no benefit. Worse, some patients might have a toxic response to the drug. The ability to identify responders, non-responders, and toxic-responders by genotyping or gene expression profiling is perhaps one of the most important goals of cancer genetics.