According to your logic, I guess you could say that the overall market for all the indications for Ridaforolimus are of "very minor value" then - I think your logic is based on the overall cases of endometrial cancer (35,000 women diagnosed each year with endometrial versus 15,000 patients diagnosed with sarcoma/yearly - and yet, the "analysts" are predicting a few hundred million to near billion in revenues from the sarcoma indication). There aren't a lot of sarcoma cases (compared to many other cancers), in breast cancer, it's likely to be used in combination with MK646 in a small subset of overall BC population, prostate and lung cancers are both up in the air.
Whether its a "minor value driver" or not (in terms of what it produces in revenues), it demonstrates a clear "proof-of-concept" in a randomized trial setting, and has possible implications of a positive read on the SUCCEED trial. Notwithstanding the fact that there are more woman diagnosed with endometrial cancer per year than there are in sarcoma per year, I have a hard time seeing as how Ridaforolimus in endometrial cancer would be a 'very minor driver', especially when the only other alternative treatments are Herceptin (to a minor degree), and old chemotherapy regimes, and hormone therapy (which Ridaforolimus just doubled the PFS when compared to one of the most used current therapies).
Having said that, can someone out there talk about how mTOR-inhibitors actually increase Akt activation through the feedback-loop and actually cause cancer cells to grow? (which is the primary reason for using MK646 with Ridaforolimus and one of the reasons I am negative on the SUCCEED trial).
