Dr. Oxnard from Dana Farber Cancer Institute provides his insight on which patients with advanced non-small cell lung cancer he pursues molecular testing for, and which molecular markers are the highest priority.

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Here I briefly discuss a challenging case of a patient who has an exon 20 mutation in the EGFR gene, which isn't one of the mutation types associated with a high probability of responding well to an oral EGFR inhibitor.  I cover the approach I favored and also some limited information that has just emerged to help clarify what we might expect for patients with an uncommon to rare variant  of an EGFR mutation (~5% of mutations detected).

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I hope it's interesting and helpful.  As always, I welcome your comments and questions.

There's been a theme with the inhibitors of the epidermal growth factor receptor (EGFR) -- both oral tyrosine kinase inhibitors (TKIs) and IV monoclonal antibodies -- that the patients who demonstrate good results with these agents tend to get a rash, while the patients who don't get a rash do poorly.

Here's the second half of the presentation by Dr. Gerard Silvestri, expert pulmonologist and critical care specialist at the Medical University of South Carolina in Charleston, on pulmonary complications from lung cancer treatment.

A few years ago, I reviewed a blood test called VeriStrat that evaluates the patterns of proteins in the blood and reports a profile of either “Good” (in about 2/3 of patients with advanced NSCLC) or “Poor” (in the remaining 1/3 of patients) for EGFR inhibitor therapy.

In my last post, I described the concept of treating with a targeted therapy like an EGFR tyrosine kinase inhibitor (TKI) or ALK inhibitor at the time of acquired resistance.

Introduction

Thank you to member Craig for asking some excellent questions in response to my Highlights of 2011 webinar.  Thank you also to Dr. West, who emailed me to comment more on the idea of radiation for cells with acquired resistance.

We’ve spoken at length about EGFR and related mutations such as EML4/ALK and ROS1 on GRACE.  For those who are not familiar with these subjects, I will refer you to my webinar for a summary on the most recent data on EGFR, EML4/ALK and ROS1:

Apologies for the long wait since our own Dr. Weiss's upbeat and thoughtful review of the leading stories about lung cancer in 2011.  Dr. Weiss covered a lot of ground in his presentation that was followed by a Q&A session, so we've broken that up into several short pieces that cover a few highlights at a time.

Continued from part 1 Dr. West: You have a huge portion of your patients who have an EGFR mutation and we know that over time patients develop acquired resistance. So how do you approach the patients who have a great response initially, have a known EGFR mutation, and then you see that slipping away at slow progression? Do you continue the EGFR inhibitor? Do you add something to it? Do you change the dose? How do you approach that?

A few weeks ago I had the chance to speak with Dr. Tony Mok, who is a professor in the Department of Clinical Oncology at the Prince of Wales Hospital in Hong Kong and the Chairman of the Hong Kong Cancer Therapy Society.