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A study on a BRAF(V600E) melanoma cell line treated with RAF, MEK, ERK or combined RAF-MEK inhibitors revealed a cAMP-dependent melanocytic signaling network not previously associated with drug resistance, including G-protein-coupled receptors (GPCRs), adenyl cyclase, protein kinase A (PKA) and cAMP response element binding protein (CREB).
" histone-deacetylase inhibitors suppressed MITF expression and cAMP-mediated resistance (Nature, December 2013" QUIAGEN
This observation from journal nature reported to us by QIAGEN
tells us
1. a second look at a old story does not hurt
BRAF INHIBITION IS A NEW THING HAPPENING TO A OLD STORY
AND LOOK WE HAVE BEEN SITTING ON OUR HANDS IN MELANOMA UNTIL IT SUNK ON US TO TARGET THERAPY! NOW LET'S ENJOY THE SUCCESS OF VEMURAFENIB IN OUR FIGHT FOR THE CURE!
2.THIS IDEA THAT MITF AND c-AMP MAY HAVE THE POWER IN THEM TO CAUSE DRUG RESISTANCE IS EXTREMELY IMPORTANT, IT MAY BE THE JUSTIFICATION OF 2 IMPORTANT PHENOMENA
2.1 THAT EGFR/VEGF INHIBITION IS TEMPORARY, THAT ULTIMATELY AVASTING WILL FAIL BECAUSE OF THESE ACTORS (OR ARE THEY BYSTANDERS?)
2.2 THAT MTOR INHIBITION CAN STOP THIS RESISTANCE ONCE IT IS DOCUMENTED BY AMPLIFICATION OF THESE 2 GENES. SO YOU GIVE AVASTIN, AND WATCH THESE 2 GENES, AND IF THEY CREEP UP, YOU KNOW AVASTIN RESISTANCE IS IN PLACE, AND HOP! YOU GIVE MTOR INHIBITOR! WHAT'S THIS FOR A CONCEPT TO BE PROVEN!
LET'S GO TO WORK!
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