Lung Cancer

After the last several posts have discussed our friend and lung cancer expert Dr. Ross Camidge, we'll turn to the related topic of ROS mutations, which have been the subject of research by Dr. Ross Camidge (though apparently not named for him) and also researchers at Massachusetts General Hospital. This is a gene for a DNA repair protein, and the tyrosine kinase binding portion (the part that gets turned on to set off a cascade of downstream intracellular events) for ROS1 is very similar to that for ALK.

Continuing with Dr. Ross Camidge as our focus (see yesterday's post for a brief update from him on the afatinib/cetuximab trial), today let's turn to the recent webinar program he and Dr. Ben Solomon did with us on the subject of ALK Inhibition: From Biology to FDA-Approved Therapy for Advanced NSCLC". After Dr.

Our friend, Dr. Ross Camidge from the University of Colorado in Denver, provided a bit of personal commentary in the context of his participation in the trial of the combination of afatinib and cetuximab for patients with acquired resistance to EGFR tyrosine kinase inhibitor (TKI) therapy, as described by Dr. Pennell in a post a few months ago.

One of the things we learn when studying the clinical research in lung cancer is that "global studies" often include patients with locally advanced (stage III) NSCLC along with those who have advanced (stage IV) NSCLC. Part of the confusion has been the ungainly status of stage IIIB NSCLC with a malignant pleural effusion -- historically termed "wet IIIB disease" -- in the IIIB camp but not having the curability of patients with "dry IIIB disease" --unresectable locally advanced NSCLC without a malignant pleural effusion.

I met DC in April. He was 62 years old and was principal of a Montessori school. He had smoked a half pack a day for three years in college (which makes him a former/light smoker in my book) and was in fairly good health until the December before when he developed a cough. His cough didn't get better and thanks to all the talk about lung cancer screening, he requested a chest x-ray. The x-ray revealed a mass, which led to CT scanning.

Several weeks ago, we were fortunate enough to be joined by not one but two international stars in lung cancer research that is being translated directly from lab bench to bedside of the patient. I don't think there's a more clear and inspiring example of good science leading to effective therapy, albeit for a limited patient population, than the story of the anaplastic lymphoma kinase (ALK) inhibitor crizotinib (recently FDA approved and commercially launched as XALKORI) for patients with an EML4-ALK rearrangement (approximately 4% of the broader NSCLC population). Drs.

Continuing Dr. West's theme discussing new therapies for patients with acquired resistance, I'd like to answer a few questions about HSP 90 inhibitors that have caught my attention on GRACE over the past few weeks, and in particular, highlight my "pet" targeted agent, AUY922. HSP 90 inhibitors are drugs that many of you already know about-they are being studied in patients with ALK(+)lung cancer and as a 2^nd line therapy option for all patients with lung cancer with Taxotere.

It was almost exactly a year ago that I described the basic results of the global LUX Lung-1 trial that enrolled 585 patients with advanced NSCLC who had gone at least 12 weeks without progression on Tarceva (erlotinib) or Iressa (gefitinib) in a 2:1 fashion to either the oral targeted therapy afatinib (an irreversible inhibitor of the human epidermal receptor (HER) family, of which EGFR

Thank you fortmyr for bringing our attention to the recent publication of exciting data on talactoferrin. We've talked about talactoferrin before on GRACE. This is an exciting new drug that both Dr. West and I feel has a lot of promise.

We've discussed the potential importance of micrometastatic disease or circulating tumor cells, but another way to assess them is to check for the presence of occult (and microscopic) metastases (OMs) in bone marrow or lymph nodes.