Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis

Massimo Pancione, Guido Giordano, Andrea Remo, Antonio Febbraro, Lina Sabatino, Erminia Manfrin, Michele Ceccarelli, Vittorio Colantuoni

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination. Many factors, produced or de novo synthesized by immune, stromal, or malignant cells, acting in a paracrine and autocrine fashion, remodel TME and the adaptive immune response culminating in metastasis. Taking into account the recent accomplishments in the field of immune oncology and using metastatic colorectal cancer (mCRC) as a model, we propose that the evasion of the immune surveillance and metastatic spread can be achieved through a number of mechanisms that include (a) intrinsic plasticity and adaptability of immune and malignant cells to paracrine and autocrine stimuli or genotoxic stresses; (b) alteration of positional schemes of myeloid-lineage cells, produced by factors controlling the balance between tumour-suppressing and tumour-promoting activities; (c) acquisition by cancer cells of aberrant immune-phenotypic traits (NT5E/CD73, CD68, and CD163) that enhance the interactions among TME components through the production of immune-suppressive mediators. These properties may represent the driving force of metastatic progression and thus clinically exploitable for cancer prevention and therapy. In this review we summarize results and suggest new hypotheses that favour the growing impact of tumor-infiltrating immune cells on tumour progression, metastasis, and therapy resistance.

Original languageEnglish
Pages (from-to)686879
Number of pages1
JournalJournal of Immunology Research
Volume2014
DOIs
Publication statusPublished - 2014
Externally publishedYes

Fingerprint

Liver Neoplasms
Colorectal Neoplasms
Neoplasm Metastasis
Tumor Microenvironment
Neoplasms
Immune Evasion
Adaptive Immunity
Myeloid Cells
Epigenomics
DNA Damage
Cell Survival
Therapeutics

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Pancione, M., Giordano, G., Remo, A., Febbraro, A., Sabatino, L., Manfrin, E., ... Colantuoni, V. (2014). Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis. Journal of Immunology Research, 2014, 686879. https://doi.org/10.1155/2014/686879

Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis. / Pancione, Massimo; Giordano, Guido; Remo, Andrea; Febbraro, Antonio; Sabatino, Lina; Manfrin, Erminia; Ceccarelli, Michele; Colantuoni, Vittorio.

In: Journal of Immunology Research, Vol. 2014, 2014, p. 686879.

Research output: Contribution to journalArticle

Pancione, M, Giordano, G, Remo, A, Febbraro, A, Sabatino, L, Manfrin, E, Ceccarelli, M & Colantuoni, V 2014, 'Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis', Journal of Immunology Research, vol. 2014, pp. 686879. https://doi.org/10.1155/2014/686879
Pancione, Massimo ; Giordano, Guido ; Remo, Andrea ; Febbraro, Antonio ; Sabatino, Lina ; Manfrin, Erminia ; Ceccarelli, Michele ; Colantuoni, Vittorio. / Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis. In: Journal of Immunology Research. 2014 ; Vol. 2014. pp. 686879.
@article{0ebb3303c0bc4660bfc7e70d222b33b5,
title = "Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis",
abstract = "Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination. Many factors, produced or de novo synthesized by immune, stromal, or malignant cells, acting in a paracrine and autocrine fashion, remodel TME and the adaptive immune response culminating in metastasis. Taking into account the recent accomplishments in the field of immune oncology and using metastatic colorectal cancer (mCRC) as a model, we propose that the evasion of the immune surveillance and metastatic spread can be achieved through a number of mechanisms that include (a) intrinsic plasticity and adaptability of immune and malignant cells to paracrine and autocrine stimuli or genotoxic stresses; (b) alteration of positional schemes of myeloid-lineage cells, produced by factors controlling the balance between tumour-suppressing and tumour-promoting activities; (c) acquisition by cancer cells of aberrant immune-phenotypic traits (NT5E/CD73, CD68, and CD163) that enhance the interactions among TME components through the production of immune-suppressive mediators. These properties may represent the driving force of metastatic progression and thus clinically exploitable for cancer prevention and therapy. In this review we summarize results and suggest new hypotheses that favour the growing impact of tumor-infiltrating immune cells on tumour progression, metastasis, and therapy resistance.",
author = "Massimo Pancione and Guido Giordano and Andrea Remo and Antonio Febbraro and Lina Sabatino and Erminia Manfrin and Michele Ceccarelli and Vittorio Colantuoni",
year = "2014",
doi = "10.1155/2014/686879",
language = "English",
volume = "2014",
pages = "686879",
journal = "Journal of Immunology Research",
issn = "2314-8861",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Immune escape mechanisms in colorectal cancer pathogenesis and liver metastasis

AU - Pancione, Massimo

AU - Giordano, Guido

AU - Remo, Andrea

AU - Febbraro, Antonio

AU - Sabatino, Lina

AU - Manfrin, Erminia

AU - Ceccarelli, Michele

AU - Colantuoni, Vittorio

PY - 2014

Y1 - 2014

N2 - Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination. Many factors, produced or de novo synthesized by immune, stromal, or malignant cells, acting in a paracrine and autocrine fashion, remodel TME and the adaptive immune response culminating in metastasis. Taking into account the recent accomplishments in the field of immune oncology and using metastatic colorectal cancer (mCRC) as a model, we propose that the evasion of the immune surveillance and metastatic spread can be achieved through a number of mechanisms that include (a) intrinsic plasticity and adaptability of immune and malignant cells to paracrine and autocrine stimuli or genotoxic stresses; (b) alteration of positional schemes of myeloid-lineage cells, produced by factors controlling the balance between tumour-suppressing and tumour-promoting activities; (c) acquisition by cancer cells of aberrant immune-phenotypic traits (NT5E/CD73, CD68, and CD163) that enhance the interactions among TME components through the production of immune-suppressive mediators. These properties may represent the driving force of metastatic progression and thus clinically exploitable for cancer prevention and therapy. In this review we summarize results and suggest new hypotheses that favour the growing impact of tumor-infiltrating immune cells on tumour progression, metastasis, and therapy resistance.

AB - Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination. Many factors, produced or de novo synthesized by immune, stromal, or malignant cells, acting in a paracrine and autocrine fashion, remodel TME and the adaptive immune response culminating in metastasis. Taking into account the recent accomplishments in the field of immune oncology and using metastatic colorectal cancer (mCRC) as a model, we propose that the evasion of the immune surveillance and metastatic spread can be achieved through a number of mechanisms that include (a) intrinsic plasticity and adaptability of immune and malignant cells to paracrine and autocrine stimuli or genotoxic stresses; (b) alteration of positional schemes of myeloid-lineage cells, produced by factors controlling the balance between tumour-suppressing and tumour-promoting activities; (c) acquisition by cancer cells of aberrant immune-phenotypic traits (NT5E/CD73, CD68, and CD163) that enhance the interactions among TME components through the production of immune-suppressive mediators. These properties may represent the driving force of metastatic progression and thus clinically exploitable for cancer prevention and therapy. In this review we summarize results and suggest new hypotheses that favour the growing impact of tumor-infiltrating immune cells on tumour progression, metastasis, and therapy resistance.

UR - http://www.scopus.com/inward/record.url?scp=84916625554&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84916625554&partnerID=8YFLogxK

U2 - 10.1155/2014/686879

DO - 10.1155/2014/686879

M3 - Article

VL - 2014

SP - 686879

JO - Journal of Immunology Research

JF - Journal of Immunology Research

SN - 2314-8861

ER -