Several weeks ago, my colleagues Dr. Tom Hensing from North Shore Health System in Chicago, affiliated with the University of Chicago, and Dr. David Jackman from Dana Farber Cancer Institute in Boston, were kind enough to take the time to go over a series of cases in a webinar format. We reviewed the time line of several patients with advanced NSCLC, focusing on two central questions:

1) For various clinical situations, which molecular markers would you be inclined to recommend?

In my last post, I described the novel oral agent PF299804 (PF299), an irreversible "pan-HER" inhibitor not only of the epidermal growth factor receptor but of other members of the human epithelial growth factor receptor (HER) family.

It's only 10 patients, but a brief report in the Journal of Thoracic Oncology that just came out today from a group in Amsterdam has gotten my attention because it suggests that the oral multi-targeted anti-cancer agent Nexavar (sorafenib) may be genuinely effective in patients with advanced NSCLC who have a K-RAS mutation.

Here's the podcast of the Q&A portion of the excellent webinar with Dr. Pennell on Molecular Markers in Management of NSCLC.

[powerpress]

dr-pennell-molecular-markers-qa-audio-podcast

We know that many people interested in the topics we discuss in our webinars may not be able to attend the live programs, but we're committed to offering our content to people as easily as possible. Accordingly, here is the podcast version of Dr. Pennell's very well received presentation on a range of molecular markers currently being used and others emerging in clinical trials as potential tools for the coming years.

Below you'll find the audio versions of the presentation.

Hi again! You can think of this as a companion piece to my last post, examining some recent (but admittedly preliminary) evidence suggesting that Iressa (gefitinib) and Tarceva (erlotinib) may not be equivalent for patients with differing types of EGFR mutations. This is a slightly different topic, but one that has been quite contentious for several years: do KRAS mutations, found in 20% or more of patients with NSCLC, identify a group of patients who are resistant to EGFR inhibitors?