In the last several years we have seen an explosion in the knowledge and understanding of the molecular basis of cancer behavior. The identification of EGFR mutations, and their utilization in predicting response and survival in patients with untreated advanced lung cancer, provides lung cancer oncologists with the optimism that we may truly be able to offer effective “personalized therapy” for patients with lung cancer in the near future.

I would consider the recently published IPASS trial that compared Iressa (gefitinib) to standard chemo of carbo/taxol (paclitaxel) to be an extremely influential trial in lung cancer that has essentially ushered in a new era of molecularly-defined guidance of our treatment for many patients with advanced NSCLC, and we can expect that this is how we’ll be approaching a much broader population of lung cancer patients.

As more and more oncologists become aware of the importance of testing for at least the EGFR mutation in tumor, and soon, perhaps, in blood, it seems likely that more patients will have their first systemic treatment for advanced non-small cell lung cancer (NSCLC) be an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), usually Tarceva (erlotinib), until Iressa (gefitinib) is re-approved (perhaps).

In the same issue of the New England Journal of Medicine that contained the IPASS trial results, Dr. Rosell and colleagues reported results of their effort to institute large-scale EGFR mutation testing in lung cancer patients in Spain, who then received erlotinib (Tarceva).

This week’s New England Journal of Medicine includes not one but two seminal publications on EGFR mutation status, response to EGFR tyrosine kinase inhibitors (TKIs) and sequencing of therapy in advanced NSCLC.

Shortly after ASCO 2009, Dr. Pennell provided the highlights of the early report of the SATURN trial, conducted primarily in Europe, that randomized patients to maintenance tarceva (erlotinib) or placebo after four cycles of first line chemotherapy. The early report described a modest but statistically significant improvement in progression-free survival (PFS), but overall survival (OS) wasn't reported at ASCO.

The ASCO meeting I'm at right now is so busy that there really isn't time to write a new post (though I'm still "tweeting from the meeting"). Though the talk show hows just air re-runs of old shows when they're on vacation, I'm trying to continue to add new content to the website during this time (and it's about as far from a vacation as anyone has in Orlando).

The ASCO meeting I'm at right now is so insanely busy during the days and nights that it's next to impossible to carve out the time to write posts during the meeting. While the talk show hosts just show re-runs while they're on vacation, we're at least going to put up some new content, even if it's from work previously done (and this is far from a vacation).

We know that cancer cells mutate over time -- in fact, that's how they became cancer cells. In fact, oncologists see the heterogeneity of cancer cells in our daily practice every day. Although there are certainly many reasons why patients have some of their cancer cells respond and others not (blood supply, local microenvironmental factors, etc.), one of the important factors is genetic heterogeneity within the cancer cell population -- some cells die and others don't.

It has become a common topic of conversation on this site (and in the lung cancer community at large) to discuss mutations in the epidermal growth factor receptor (EGFR). However, since we frequently throw out the terms “deletion 19 mutation”, “L858R”, and “T790M”, I thought would be worthwhile to explain a little bit about the different EGFR mutations and what we know about their clinical significance.