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.

I'm just now returning from the International Association for the Study of Lung Cancer's "12th Annual Targeted Therapies in Lung Cancer Conference", which consisted of about 170 very brief talks about several classes of agents, as I described in my last post.  Some of these are likely to emerge as viable, truly beneficial therapies for patients; many others will fall by the wayside.

It's not uncommon for a question here to be about the a pathologist's terminology on a report that equivocates about whether a lesion is bronchioloalveolar carcinoma (BAC) or another form of adenocarcinoma, perhaps "well-differentiated adenocarcinoma", especially if it has a radiographic appearance of a hazy infiltrate or many small ground glass opacities.

Thyroid transcription factor-1 (TTF-1) is a protein seen on the surface of thyroid cells, but also on about 70-75% lung adenocarcinomas and only a small minority (~10%) of squamous cell NSCLC tumors. In fact, the presence of TTF-1 on a NSCLC tumor provides a good hint for the pathologist that this is an adenocarcinoma. It's an immunohistochemical (IHC) test that is done on the vast majority of lung cancers, and there's some new information that suggests it may also be useful for predicting which patients are especially unlikely to have an EGFR mutation or ALK rearrangement.

Here's the second talk from our recent webinar, partnering with LUNGevity Foundation to cover the ASCO Highlights in Lung Cancer, and this talk followed after

The question of "who should be tested?" for an epidermal growth factor receptor (EGFR) mutation and potentially other molecular markers is among the most timely questions in lung cancer management today. The field has changed dramatically since the initial description of the mutation, associated with a high probability of an impressive and often prolonged response to EGFR tyrosine kinase inhibitor (TKI) therapy, back in 2004.

The following is laden with personal opinion as much as actual evidence. Feel free to take it or leave it.

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.