Strategic synergy
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.
CTLA-4 (CD152)-mediated inhibition of T cell activation can prevent the development of antitumor T cell responses. Although there is a clear rationale for blocking CTLA-4, monotherapy with such agents is more successful in treating intrinsically immunogenic tumors than poorly immunogenic ones...