Skip Navigation LinksHome > August 2012 - Volume 71 - Issue 2 > Cancer Immunoediting in Malignant Glioma
doi: 10.1227/NEU.0b013e31824f840d
Review: Editor's Choice

Cancer Immunoediting in Malignant Glioma

Dunn, Gavin P. MD, PhD; Fecci, Peter E. MD, PhD; Curry, William T. MD

Editor's Choice
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Significant work from many laboratories over the last decade in the study of cancer immunology has resulted in the development of the cancer immunoediting hypothesis. This contemporary framework of the naturally arising immune system–tumor interaction is thought to comprise 3 phases: elimination, wherein immunity subserves an extrinsic tumor suppressor function and destroys nascent tumor cells; equilibrium, wherein tumor cells are constrained in a period of latency under immune control; and escape, wherein tumor cells outpace immunity and progress clinically. In this review, we address in detail the relevance of the cancer immunoediting concept to neurosurgeons and neuro-oncologists treating and studying malignant glioma by exploring the de novo immune response to these tumors, how these tumors may persist in vivo, the mechanisms by which these cells may escape/attenuate immunity, and ultimately how this concept may influence our immunotherapeutic approaches.

ABBREVIATIONS: APC, antigen-presenting cell

CTL, cytotoxic T lymphocyte

DC, dendritic cell

eGFR, endothelial growth factor receptor

IL, interleukin

IFN, interferon-γ

MHC, major histocompatibility complex

MICA/B, MHC class I chain-related A/B

NK, natural killer

PD-L1, programmed death receptor ligand 1

RAG2, recombinase activating gene 2

STAT3, signal transducer and activator of transcription 3

TGF-β, transforming growth factor-β

TIL, tumor-infiltrating lymphocyte

Treg, regulatory T cell

ULBP, UL16-binding protein

Copyright © by the Congress of Neurological Surgeons


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