Dr. Sarah Goldberg notes that while maintenance therapy after first line treatment of advanced NSCLC is always worthy of a discussion, many patients need and benefit from a break from treatment to recover before pursuing additional therapy.

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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.

Although it's uncommon, hypertrophic osteoarthropahy, or HPOA, is an odd and therefore memorable syndrome that can be a side effect of lung cancer. It features an abnormal proliferation of skin and bone tissue, primarily in the hands and feet. Patients can develop clubbing, which is most commonly associated with NSCLC (up to 1/3 of patients) more than SCLC (only about 5%), and adenocarcinoma in particular. Here's what it looks like:

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.

Erbitux (cetuximab) is a monoclonal antibody to EGFR, and it's actually made from a protein that is part mouse and part human (called a chimeric protein, named for the mythologic creature chimera that was composed of multiple parts from different animals). It's uncommon but not rare for patients to have an allergic reaction to this protein, and in most large national and international studies show rates of hypersensitivity reactions (HSRs) in the 1-3% range.

The improvement in median survival of 1.2 months with the monoclonal antibody to EGFR erbitux (cetuximab) in the FLEX trial that I've previously described was statistically significant, but there's plenty of room to debate whether it's really clinically significant (see prior post). What If we could add some way to refine our predictions of who will benefit from the addition of erbitux?

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.

Those who have followed my writings over time will know that I haven’t been inclined to adopt a reflexive strategy of ordering molecular testing without good evidence that having this information will improve outcomes. Testing tumors for EGFR mutations is advocated by a vocal minority of lung cancer experts in Boston and New York City, but this hasn’t been advocated by the broader lung cancer community yet, or adopted as routine clinical practice.

Though EGFR inhibitors like tarceva can produce some terrific and long-lasting results in many patients, they aren't toxicity-free. The "targeted therapies" we use just have a very different side effect profile from standard chemo, and the EGFR inhibitors are well known to have skin-related side effects as the leading problem, with loose stools/diarrhea as a less nearly ubiquitous second place issue.

One of my earliest posts when I started OncTalk was on the use of oral inhibitors of the epidermal growth factor receptor (EGFR), one of the growth signals that is often over-active in cancer cells, against advanced bronchioloalveolar carcinoma (BAC), a unique subtype of lung cancer that tends to grow within the lungs, sometimes slowly, and not progress elsewhere.