Boann,
Yes - and the variability is a huge problem for us. Because trial after trial will "not meet their end points" for the majority of the trial participants, but SOME of the participants will do well, and endpoints WILL be met for certain individuals.
Carolyn got neurturin in the CERE-120 phase II trial, and it DID work for her. It just didn't work for the majority of the participants.
Spheremine is another such example. It worked for Peg.
So what to do? What to do? I see promising treatments not meeting endpoints. And for some of us is a real loss because it appears that these treatments would have helped at lease SOME of us.
But how do we prove that? How are we tested to know who will be helped by what treatments?
This is a huge problem.
Quote:
Originally Posted by boann
this may be old news to folks - i tune in so rarely i am a little out of touch, i am sure - but it appears that there are different types of mutations that cause different types of breast cancer - one mutation, HER2, which results in a particularly aggressive cancer, is responsible for 25% of breast cancer cases, and a drug, herceptin, has been developed to treat HER2 cancer specifically. in clinical trials, women treated with herceptin for one year had - depending on what other therapies they also had - a 33-52% lower rate of recurrence.
so, it is possible that what we call a single disease can arise from multiple sources, and it is possible to identify and treat some - and, in theory, eventually all - of those sources.
i believe this is where interest in pd subtypes comes from, in addition to the search for genetic clues.
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