Oncogenic growth factor signaling mediating tumor escape
from cellular immunity.
Concha-Benavente F1, Ferris RL2.
1.Department of Otolaryngology,
University of Pittsburgh, Pittsburgh, PA, USA; University of Pittsburgh Cancer
Institute, Pittsburgh, PA, USA.
2. Department of Otolaryngology,
University of Pittsburgh, Pittsburgh, PA, USA; University of Pittsburgh Cancer
Institute, Pittsburgh, PA, USA. Electronic address: ferrisrl@upmc.edu.
Unrestrained growth factor
signals can promote carcinogenesis, as well as other hallmarks of cancer such
as immune evasion. Our understanding of the function and complex regulation of
HER family of receptors has led to the development of targeted therapeutic
agents that suppress tumor growth. However, these receptors also mediate escape
from recognition by the host immune system. We discuss how HER family of
oncogenic receptors downregulate tumor antigen presentation and upregulate
suppressive membrane-bound or soluble secreted inhibitory molecules that
ultimately lead to impaired cellular immunity mediated by cytotoxic T
lymphocyte (CTL) recognition. Implementing this knowledge into new therapeutic
strategies to enhance tumor immunogenicity may restore effector cell mediated
immune clearance of tumors and clinical efficacy of tumor-targeted
immunotherapy against HER receptor overexpression.
Curr Opin Immunol. 2017 Feb
13;45:52-59. doi: 10.1016/j.coi.2017.01.004. [Epub ahead of print]
Md.
PhD. Fernando Concha. Ex-miembro del GII
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