InvestorsHub Logo
icon url

slcimmuno

03/14/15 6:50 PM

#94439 RE: biodoc #94435

Thx biodoc - I've got lots of homework to do but P53/P21 activation indeed does seem to be a Rubiks Cube of sorts

A while back I posted a link to the folks at IBM trying to model which p53 studies might be the best

http://mobile.nytimes.com/blogs/bits/2014/08/28/questions-for-ibms-watson/

EXCERPT
In the research project, biologists and data scientists used Watson to identify proteins that modify p53, a crucial protein that is sometimes called “the guardian of the genome.” When p53 is mutated, it can set the stage for tumor growth of many kinds of cancer.

It is a most popular subject of research. ****More than 70,000 papers have been published on p53.**** Watson read them all in an automated effort to predict proteins that turn p53’s activity on or off. Using Watson’s analysis, the cancer researchers identified six potential proteins to target for new research. Watson went beyond digging for a known fact; it found previously unrecognized connections.

XXXXXX

If you care to comment, What is your take on the Colorado research I posted earlier... That A17 commented on: the P21/Puma ratio?
icon url

frrol

03/14/15 8:31 PM

#94450 RE: biodoc #94435

Yes sometimes I forget that p21 is not a "perfect" biomarker for us.
icon url

To infinity and beyond!

03/14/15 8:50 PM

#94451 RE: biodoc #94435

Agree with you of course that what really counts is patient survival, and not p21 levels, and that the whole apoptosis thing is very complex.

Did not mean to dredge up Aprea if already discussed well prev, but had not been through that thread. Still trying to understand the whole thing, and I would imagine the science and mechanism of kevetrin-in full- is prob not even understood.

Will K be efficacious in human trials on its own, or only on combo? Interesting that Aprea 246 is in combo trials right up front, from the beginning.