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Gastroenterology Research and Practice
Volume 2016, Article ID 6261721, 8 pages
http://dx.doi.org/10.1155/2016/6261721
Review Article

Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer

1Department of Pathology and Diagnostics, University of Verona, 31134 Verona, Italy
2Medical Oncology Unit, Fatebenefratelli Hospital, 82100 Benevento, Italy
3Department of Experimental and Clinical Medicine “Gaetano Salvatore”, University “Magna Grecia”, 88100 Catanzaro, Italy
4Department of Sciences and Technologies, University of Sannio, 82100 Benevento, Italy

Received 30 October 2015; Revised 11 January 2016; Accepted 20 January 2016

Academic Editor: Hassan Ashktorab

Copyright © 2016 Pietro Parcesepe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Data from molecular profiles of tumors and tumor associated cells provide a model in which cancer cells can acquire the capability of avoiding immune surveillance by expressing an immune-like phenotype. Recent works reveal that expression of immune antigens (PDL1, CD47, CD73, CD14, CD68, MAC387, CD163, DAP12, and CD15) by tumor cells “immune resistance,” combined with prometastatic function of nonmalignant infiltrating cells, may represent a strategy to overcome the rate-limiting steps of metastatic cascade through (a) enhanced interactions with protumorigenic myeloid cells and escape from T-dependent immune response mediated by CD8+ and natural killer (NK) cells; (b) production of immune mediators that establish a local and systemic tumor-supportive environment (premetastatic niche); (c) ability to survive either in the peripheral blood as circulating tumor cells (CTCs) or at the metastatic site forming a cooperative prometastatic loop with foreign “myeloid” cells, macrophages, and neutrophils, respectively. The development of cancer-specific “immune resistance” can be orchestrated either by cooperation with tumor microenvironment or by successive rounds of genetic/epigenetic changes. Recognition of the applicability of this model may provide effective therapeutic avenues for complete elimination of immune-resistant metastatic cells and for enhanced antitumor immunity as part of a combinatorial strategy.