The negative trials don't get a lot of discussion, but the ZEPHYR trial, a phase III study that directly compared Zactima (vandetanib), an oral inhibitor of EGFR and angiogenesis, vs. placebo, was one that merits some follow-up after my reporting that it failed to show a survival benefit, which was essentially the only thing we learned about the trial prior to ASCO this year.

This morning, Joe provided a link to a story about the Safety of Avastin in Lung cancer (SAiL) study, which is just being published in Lancet Oncology.

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

In this week’s Journal of Clinical Oncology the final results of the phase III trial investigating chemotherapy with or without thalidomide in previously untreated NSCLC patients were published. Most people remember thalidomide for the horrifying birth defects (absence of arms and legs, etc) that resulted in the 1960s when pregnant women were given thalidomide for morning sickness.

At the time that OncTalk (the predecessor to GRACE) was just getting off the ground in the fall of 2006 (wow, three years have gone quickly!), Avastin (bevacizumab) was just getting FDA approval in the first line treatment of advanced NSCLC.

Although there has always been lattitude for individualizing treatment, I think developments in the last few years have added so many options that pretty much any standards we had from a few years ago have eroded.

A press release today informs us that the ATLAS trial of maintenance avastin (bevacizumab) combined with tarceva (erlotinib) vs. avastin with placebo was positive for a significant improvement in progression-free survival (PFS). We had already learned that the very similar SATURN, of maintenance tarceva vs.

Video presentation describing the concept behind angiogenesis and the evidence on the anti-angiogenic agent avastin (bevacizumab) in NSCLC.

[powerpress]

Or access via web link here.

As I described in a post last year, one of the common features of angiogensis inhibitors is that lesion often cavitate, shrinking not only from the outside in, but hollowing out and dying from the inside out.

In my last post I outlined the typical clinical scenario for pneumonic bronchioloalveolar carcinoma (BAC), which is typically the mucinous subtype of this unusual disease. In fact, we are still actively learning a great deal about BAC, enough for the lung cancer experts to begin to develop a more sophisticated view that the mucinous and non-mucinous subtypes have different behaviors and respond differently to treatments.