*Researchers who conducted the study who conducted the use of Selumetinib in low grade serous Ovarian cancer were still puzzled because its activity did not follow presence of KRAS or BRAF. They have been wondering if it used another pathway. But remember MEK is the revolving door to de-differentiation and to the reversal of mesengialization and as such increase tor susceptibility not only to chemotherapy drugs, but also to the secondary angiogenic potentiation of MEK. That is, with anti-MEK, there is a down regulation of MAPK (as suggested) and therefore the C-JUN and TGF and cyclins, but also down regulation of the VEGF!
They say " Our results suggest that selumetinib is an active agent, but
not necessarily because of BRAF or KRAS mutational activation per se,”
the authors concluded.
In an interview, Gershenson said that one reason for the
lack of correlation could be biomarker instability. Among the 52
patients, specimens were available for only 40, mutational analysis was
done in 34, and in 28 of those the tissue was from the primary therapy
and not from the recurrent tumor. “The question arises, are these
biomarkers stable over time or do they change, so that what you find in
the primary tumor may not be what you find in the recurrent tumor,” he
said." They suggesting here that the lack of correlation could be due to a changing nature of Biomarker. But the existence of other factors and pathways could not be be excluded!
Gene-Expression Profiling May Help Select Best Drugs for Pancreatic Cancer
Caroline Helwick
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In this study patient with pancreatic cancer had reportedly circulating cell and their genes could predict response to therapy but unfortunately they did not spell out which genes were reviewed. We will investigate further this article...
