Thursday, September 20, 2012
Researchers from the New York University School of Medicine have
shown that induction of NKG2D
ligands on poorly immunogenic tumor cells is a key molecular mechanism that
contributes to the synergy of radiotherapy plus anti-CTLA-4
mAbs.1 The findings could be used to identify patients most likely
to respond to anti-CTLA-4 treatments such as Bristol-Myers Squibb Co.'s
melanoma drug Yervoy
ipilimumab and could help
pinpoint radiation regimens that enhance the treatment to potentially provide a
new standard of care in the disease.
Baas, T. SciBX 5(37); doi:10.1038/scibx.2012.973
Published online Sept. 20, 2012
1. Ruocco, M.G. et al.
J. Clin. Invest.; published online Sept. 4, 2012; doi:10.1172/JCI61931
Contact: Sandra Demaria, New York University School of Medicine, New
2. Demaria, S. et al.
Clin. Cancer Res. 11, 728-734 (2005)
3. Dewan, M.Z. et al.
Clin. Cancer Res.15, 5379-5388 (2009)
4. Postow, M.A. et al.
N. Engl. J. Med. 366, 925-931 (2012)
5. Hiniker, S.M. et al.
N. Engl. J. Med. 366, 2035 (2012)
AND INSTITUTIONS MENTIONED
AstraZeneca plc (LSE:AZN; NYSE:AZN), London, U.K.
Brigham and Women's Hospital, Boston, Mass.
Bristol-Myers Squibb Co. (NYSE:BMY), New York, N.Y.
Dana-Farber Cancer Institute, Boston, Mass.
Harvard Medical School, Cambridge, Mass.
New York University Langone Medical Center, New York, N.Y.
New York University School of Medicine, New York, N.Y.
Pfizer Inc. (NYSE:PFE), New York, N.Y.
Stanford University, Stanford, Calif.
University of Navarra, Pamplona, Spain