Replies to post #142763 on Biotech Values

[iwfal]

Notably, in KRAS mutant and RAS/RAF wild-type tumours, RAF inhibitors activate the RAF-MEK-ERK pathway in a RAS-dependent manner, thus enhancing tumour growth in some xenograft models.

Ok - understood that (from previous conversations - with genesi or you I believe), although I only vaguely remembered it so thanks for the reminder. What I don't understand is how Zelboraf, which is supposed to be specific to a mutated BRAF, and inert in wild type, causes any effect in in a RASm tumor with, presumably, wt BRAF?

PS I think the paper you cited provides a good example of how it is that kinase actors, in retarding the growth of one subtype of cancer, can actually accelerate another subtype. I.e. It provides an example of the type of MOA by which you can get MetMab type results.

PPS I also note that I see no reason, in the above example, to believe that these kinds of effects (slow-one-subtype, speed-another-subtype) should be limited to just direct kinase inhibitors. Anything that acts on a kinase pathway (e.g. HSP90 inhibitors) could, in theory, do the same thing since it appears to be inherent in the complex control loop interaction of the kinases.

[vinmantoo]

Peter,

Thanks for the informative abstract and video.

I was recently sent an email about a web site sponsored by HHMI/ASCB. It was started by Ron Vale at UCSF and is FREE. The web site has a lot of good links for scientists, students or anyone else interested in learning. I was asked to forward it to colleagues, so thought some people here might find it useful and informative.


http://ibioseminars.org/newsletters/september_2011.html


If you scroll down, there is an IBioseminar.org link which has ~ 60 seminars by many experts in their field.


Vinny