Thursday, September 5, 2013
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Ribosomal protein S6 kinase (RSK)
phosphorylation to predict response to BRAF,
Studies in patient samples,
cell culture and mice suggest RSK phosphorylation status could predict
response to BRAF, MEK or PI3K inhibitors. In a panel of cancer cell lines,
reduction of RSK phosphorylation after treatment with a MEK or BRAF inhibitor
was a stronger predictor of sensitivity to treatment than previously reported
predictive markers, including PTEN
loss or protein
kinase B (PKB;
phosphorylation. In a patient treated with both a MEK and BRAF inhibitor, RSK
phosphorylation was eliminated prior to a complete response, and subsequent
tumor recurrence was associated with restoration of RSK phosphorylation. In
mouse xenograft models, tumors resistant to a phosphatidylinositol
3-kinase catalytic subunit a-polypeptide
p110a) inhibitor had higher levels of RSK
phosphorylation than sensitive tumors. In these models, adding an mammalian
target of rapamycin (mTOR;
inhibitor decreased RSK phosphorylation and tumor growth compared with adding
vehicle. Ongoing work includes clinical trials combining mTOR inhibitors with
or MEK inhibitors.
Published online Sept. 5, 2013
Patent and licensing status
Corcoran, R.B. et al.
Sci. Transl. Med.; published online July 31, 2013;
Contact: Jeffrey A. Engelman,
Massachusetts General Hospital Cancer Center, Boston, Mass.
Contact: Daniel A. Haber,
same affiliation as above
Elkabets, M. et al. Sci. Transl. Med.; published online July 31, 2013;
Contact: José Baselga, Memorial Sloan-Kettering Cancer
New York, N.Y.
Contact: Maurizio Scaltriti,
same affiliation as above
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