Alimta and Lung Cancer Histology: Targeting Conventional Chemo Effectively
I think one of the most important lead stories from ASCO 2008 got buried. Nobody's really talking about it yet, but they should.
I think one of the most important lead stories from ASCO 2008 got buried. Nobody's really talking about it yet, but they should.
A couple of weeks ago I described in a prior post the design and general results of a trial coded as JMEN by the sponsor company, Eli Lilly. This study randomized patients to either maintenance/early second line alimta (pemetrexed) or a placebo after four cycles of initial platinum-based doublet chemo with a drug other than alimta.
Within the lung cancer community, the biggest story from the ASCO meeting was the long-awaited plenary session presentation (abstract here) of the FLEX trial of chemo with or without the EGFR monoclonal antibody Erbitux (cetuximab) that we knew was statistically significantly positive for an overall survival benefit as far back as September of last year (see
Last year, a provocative trial was presented at ASCO that compared early vs. later taxotere as second line therapy. I described that study here, and it showed a very significant improvement in progression-free survival (PFS) and a near significant improvement in overall survival (OS) for the recipients of taxotere immediately after four cycles of first line chemo for advanced NSCLC.
So I’ve been invited to be on the faculty of a lung cancer conference in Kauai next month (yes, a good gig, but this is the first year that the flights are so expensive that I can’t bring my family to this normally very family-friendly event), and my topic is to argue in a debate about whether molecular testing for EGFR should be routinely used in clinical practice.
In a recent issue of the Journal of Clinical Oncology, Dr. Vince Miller and colleagues published the results of an important trial of the EGFR inhibitor tarceva (erlotinib) in the unusual NSCLC subtype bronchioloalveolar carcinoma, or BAC (abstract here). This work was predicated on the observation, also by Dr.
One of the issues we struggle the most with, as oncologists, patients, and families, is how to choose a therapy that won’t make someone feel worse. There are so many things to factor into these decisions: what is the baseline function of the person, what comorbidities (other chronic illnesses) might interact or interfere, what side effects are acceptable or worth the risk, to what degree is the cancer interfering with their functioning and can this be reversed with chemo, and of course what does any individual patient want and expect from chemo?
There's a website called Adjuvant! Online, developed by oncologist Peter Ravdin, that is best known for its use after surgery for breast cancer in assessing the value of post-operative chemo. Because I don't really treat breast cancer, I haven't spent time on the website, but I do know that it's a valued resource among practicing oncologists who care for patients with breast cancer.
I had previously written about a spectrum from pure bronchioloalveolar carcinoma (BAC) to invasive adenocarcinoma in one of my first posts here, but the real credit for this concept goes back to Dr.
As I've mentioned in some prior posts, there is increasing recognition that lung cancer in never-smokers may be a different disease. Some of this has been defined by working backward from treatment results, where we've seen that never-smokers are consistently among the greatest beneficiaries of EGFR inhibitor therapies like Iressa or Tarceva. But there are some general principles and recurring themes with regard to the genetics of lung cancer in never-smokers.
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