MEDICATION BUST, THE CASE OF CILENGITIDE IN TREATMENT OF GLIOBLASTOMA.

Once again we have seen a failure of a medication that was ill used.  It was used on the simple premise that in Gliomas, the cell over expressed certain integrins.  Therefore an inhibitor of "integrins" would work in this challenging disease.  The Integrins discussed were just as fuzzy.  They seemed to involve cell migration more than angiogenesis, in a disease which does not metastase.  Suggestions of anti-FAK, anti-Src, anti-AKT activities have been made peripherally but the emphasis is that this drug would meet the challenge of some integrins which could be more prognostic than predictive.  These integrins appear to have more diagnostic than predictive.  You need to go after a driver mutation or a significant secondarily amplified mechanism.
In Glioblastoma, the role of NF-1, VGEF, MEK, Interferon Receptor seems to be more of importance.  Integrins involved in metastasis in  Glioma? Really?
When you go after SRC, pick carefully which SRC!
It's like when you go after RAS, pick the right RAS!
When you go after MYC, pick the right MYC !
Globally when you go after differentiation, be selective or go after MEK, the door to differentiation in adult. It is not by mistake that people who where going after K-RAS as a marker went in with an anti-MEK in lung cancer!

If I had to pick a role for Cilengitide, I would use it with Avastin or an anti-MEK
and I would use it in Maintenance setting at least from info I had gathered on it!  And in Glioma, in 2nd line where Avastin is king!

I will here finish by just saying if someone says "anti-Integrin", he has given you no information whatsoever, how many integrins are in a cell.  If you find someone who gives a straight answer, call me please!