Comment on “Epidermal Growth Factor Receptor Is Essential for Toll-Like Receptor 3 Signaling”

Sci. Signal., 11 December 2012
Vol. 5, Issue 254, p. lc5
DOI: 10.1126/scisignal.2003734

Comment on “Epidermal Growth Factor Receptor Is Essential for Toll-Like Receptor 3 Signaling”

  1. Barbara Burtness1,2,
  2. Shanthi Marur3,
  3. Julie E. Bauman4,
  4. Erica A. Golemis2,*,
  5. Ranee Mehra1,2, and
  6. Steven J. Cohen1,2
  1. 1Department of Medical Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
  2. 2Program in Developmental Therapeutics, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
  3. 3Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
  4. 4Department of Hematology and Oncology, University of New Mexico Cancer Center, Albuquerque, NM 87102, USA.
  1. *Corresponding author. E-mail: erica.golemis{at}fccc.edu

Abstract

Epidermal growth factor receptor (EGFR) and mammalian target of rapamycin (mTOR) play important roles in tumor growth, which has stimulated efforts toward the design of targeted cancer therapeutics that inhibit their function. A growing body of literature indicates that EGFR and mTOR are also essential to support a functional innate immune response. Hence, although combination therapies that block both EGFR and mTOR may have improved activity against tumors, they may also place patients at risk of fulminant infections. We discuss data supporting this hypothesis.

Citation:

B. Burtness, S. Marur, J. E. Bauman, E. A. Golemis, R. Mehra, and S. J. Cohen, Comment on “Epidermal Growth Factor Receptor Is Essential for Toll-Like Receptor 3 Signaling”. Sci. Signal. 5, lc5 (2012).

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