Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer
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, CD1...
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Gastroenterology Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2016/6261721 |
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| _version_ | 1832558514855215104 |
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| author | Pietro Parcesepe Guido Giordano Carmelo Laudanna Antonio Febbraro Massimo Pancione |
| author_facet | Pietro Parcesepe Guido Giordano Carmelo Laudanna Antonio Febbraro Massimo Pancione |
| author_sort | Pietro Parcesepe |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-3da4618bb88444729481350b3e479c87 |
| institution | Kabale University |
| issn | 1687-6121 1687-630X |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Gastroenterology Research and Practice |
| spelling | doaj-art-3da4618bb88444729481350b3e479c872025-02-03T01:32:12ZengWileyGastroenterology Research and Practice1687-61211687-630X2016-01-01201610.1155/2016/62617216261721Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal CancerPietro Parcesepe0Guido Giordano1Carmelo Laudanna2Antonio Febbraro3Massimo Pancione4Department of Pathology and Diagnostics, University of Verona, 31134 Verona, ItalyMedical Oncology Unit, Fatebenefratelli Hospital, 82100 Benevento, ItalyDepartment of Experimental and Clinical Medicine “Gaetano Salvatore”, University “Magna Grecia”, 88100 Catanzaro, ItalyMedical Oncology Unit, Fatebenefratelli Hospital, 82100 Benevento, ItalyDepartment of Sciences and Technologies, University of Sannio, 82100 Benevento, ItalyData 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.http://dx.doi.org/10.1155/2016/6261721 |
| spellingShingle | Pietro Parcesepe Guido Giordano Carmelo Laudanna Antonio Febbraro Massimo Pancione Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer Gastroenterology Research and Practice |
| title | Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer |
| title_full | Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer |
| title_fullStr | Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer |
| title_full_unstemmed | Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer |
| title_short | Cancer-Associated Immune Resistance and Evasion of Immune Surveillance in Colorectal Cancer |
| title_sort | cancer associated immune resistance and evasion of immune surveillance in colorectal cancer |
| url | http://dx.doi.org/10.1155/2016/6261721 |
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