2013
Vaňhara, Petr; Souček, Karel
Mutual cytokine crosstalk between colon cancer cells and microenvironment initiates development of distant metastases. Journal Article
In: JAK-STAT, vol. 2, no. 2, pp. e23810, 2013, ISSN: 2162-3988 2162-3996, (Place: United States).
Abstract | Links | BibTeX | Tags: dissemination, interleukin 11, Metastasis, metastatic niche, microenvironment, transforming growth factor-β, tumor stroma
@article{vanhara_mutual_2013,
title = {Mutual cytokine crosstalk between colon cancer cells and microenvironment initiates development of distant metastases.},
author = {Petr Vaňhara and Karel Souček},
doi = {10.4161/jkst.23810},
issn = {2162-3988 2162-3996},
year = {2013},
date = {2013-04-01},
journal = {JAK-STAT},
volume = {2},
number = {2},
pages = {e23810},
abstract = {Tumor growth and cancer development are considered clear examples of Darwinian selection, whereby random mutational events in heterogeneous cancer cell populations that best fit the selective microenvironment are preferred.(1) As a result, cancer cells evolve resistance to apoptosis, hide from immune surveillance and acquire the ability to invade other organs. Cancer cells, however, are not necessarily passive subjects of selection; they can actively subvert the host tissue to provide a favorable habitat for their growth. Recent findings by Calon et al. convincingly demonstrate that transforming growth factor-β-induced secretion of interleukin 11 by tumor stromal fibroblasts is a necessary prerequisite for the development of distant metastases in colorectal carcinoma. Thus, understanding the complex molecular feedback loops between cancer cells and the surrounding microenvironment (i.e., the tumor-associated stroma or invaded host tissue) should aid the identification of useful molecular targets for improving clinical management of advanced metastatic cancers.},
note = {Place: United States},
keywords = {dissemination, interleukin 11, Metastasis, metastatic niche, microenvironment, transforming growth factor-β, tumor stroma},
pubstate = {published},
tppubtype = {article}
}
Tumor growth and cancer development are considered clear examples of Darwinian selection, whereby random mutational events in heterogeneous cancer cell populations that best fit the selective microenvironment are preferred.(1) As a result, cancer cells evolve resistance to apoptosis, hide from immune surveillance and acquire the ability to invade other organs. Cancer cells, however, are not necessarily passive subjects of selection; they can actively subvert the host tissue to provide a favorable habitat for their growth. Recent findings by Calon et al. convincingly demonstrate that transforming growth factor-β-induced secretion of interleukin 11 by tumor stromal fibroblasts is a necessary prerequisite for the development of distant metastases in colorectal carcinoma. Thus, understanding the complex molecular feedback loops between cancer cells and the surrounding microenvironment (i.e., the tumor-associated stroma or invaded host tissue) should aid the identification of useful molecular targets for improving clinical management of advanced metastatic cancers.