Drs. Mary Pinder, Nate Pennell, and Jack West discuss whether the finding of improving progression-free survival with maintenance sorafenib for SCLC should change the standard of care for treatment of extensive stage disease.

[powerpress]

It has been a long time since we've talked about Nexavar (sorafenib), an oral anti-angiogenic targeted therapy that works as a "multi-kinase inhibitor"  and is FDA approved in some other cancers such as renal cell and liver cancer.  In lung cancer, some small, early research done years ago revealed that it has activity in at least a minority of patients with advanced NSCLC.

Recently, I described the rationale for targeting HER2 mutations in non-small cell lung cancer (NSCLC). Most of our experience with HER2 targeted therapy comes from studies in breast cancer. Now, I'd like to introduce you to BRAF, another novel target in NSCLC that is a central component in cell signalling, growth, and division.

It's only 10 patients, but a brief report in the Journal of Thoracic Oncology that just came out today from a group in Amsterdam has gotten my attention because it suggests that the oral multi-targeted anti-cancer agent Nexavar (sorafenib) may be genuinely effective in patients with advanced NSCLC who have a K-RAS mutation.

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

We’ve been following sorafenib (nexavar), a multi-kinase inhibitor with anti-angiogenic activity (see prior post). This oral agent, which is already approved as an effective treatment for cancers of the liver and kidney.

I'll get back to the storyline of our growing understanding of the differences of individuals based on pharmacogenomics very soon. But I wanted to give people some breaking news that just came out.