JNCI | Editorials 617
Advance Access publication on April 4, 2011.
© The Author 2011. Published by Oxford University Press. All rights reserved.
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In this issue of the Journal, De Bacco et al. (1) report that expres-
sion of the scatter factor/hepatocyte growth factor (SF/HGF) re-
ceptor, c-MET, is increased in response to ionizing radiation (IR)
through the ataxia-telangiectasia mutated (ATM)–NF-kB signaling
pathway. The authors show that c-MET contributes to radioresis-
tance and promotes cancer invasion by autocrine and paracrine
prosurvival signaling to increase cell motility and inhibit apoptosis.
The efficacy of a novel pharmacological inhibitor of c-MET as a
candidate radiosensitizer was evaluated in tumor xenografts in their
Radiotherapy remains the most effective nonsurgical treatment
for most solid tumors (2). According to the National Cancer
Institute, approximately half of all cancer patients receive radiation
as a part of treatment. Radiotherapy or radiochemotherapy aims to
How Scatter Factor Receptor c-MET Contributes to Tumor
Radioresistance: Ready, Set, Scatter!
Olga A. Guryanova, Shideng Bao
Correspondence to: Shideng Bao, PhD, Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, 9500
Euclid Ave, NE30, Cleveland, OH 44195 (e-mail: firstname.lastname@example.org).
by guest on January 4, 2016