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Molecular mechanism of the “feedback loop” model of carcinogenesis
It is commonly accepted that cancer is a genetic disease. The current prevailing theory of carcinogenesis is the somatic mutation theory of carcinogenesis and metastasis (SMT). This theory postulates that mutations in epithelial cells lead to uncontrolled proliferation of tumor cells in a cell-auton...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Landes Bioscience
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502218/ https://www.ncbi.nlm.nih.gov/pubmed/23739683 http://dx.doi.org/10.4161/cib.21177 |
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author | Rückert, Felix Sticht, Carsten Niedergethmann, Marco |
author_facet | Rückert, Felix Sticht, Carsten Niedergethmann, Marco |
author_sort | Rückert, Felix |
collection | PubMed |
description | It is commonly accepted that cancer is a genetic disease. The current prevailing theory of carcinogenesis is the somatic mutation theory of carcinogenesis and metastasis (SMT). This theory postulates that mutations in epithelial cells lead to uncontrolled proliferation of tumor cells in a cell-autonomous fashion. This cell-autonomy is increasingly criticized. Current data suggest that the tumor microenvironment is also strongly involved in carcinogenesis. Recently, we published a hypothesis that considers the important contribution of the tumor microenvironment in carcinogenesis and complements the classical clonal evolution model. Essentially, this “feedback loop model” (FBM) postulates that the physiological communication between cancer cells and stromal cells in inflammatory or proliferative conditions is altered by anomalous signal processing within the parenchymal cells. The inability of parenchymal cells to correctly finalize the intercellular communication might result in a perpetuation of the activated state of cells and the tumor micromilieu. The FBM is unique among the tissue-based models because in this model tumor and stromal cells interact together in a reciprocal manner to form the cancer phenotype. Contrary to the SMT, the FBM postulates that mutated genes act in a cell-heteronomous fashion, not in a cell-autonomously fashion. |
format | Online Article Text |
id | pubmed-3502218 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-35022182012-11-23 Molecular mechanism of the “feedback loop” model of carcinogenesis Rückert, Felix Sticht, Carsten Niedergethmann, Marco Commun Integr Biol Article Addendum It is commonly accepted that cancer is a genetic disease. The current prevailing theory of carcinogenesis is the somatic mutation theory of carcinogenesis and metastasis (SMT). This theory postulates that mutations in epithelial cells lead to uncontrolled proliferation of tumor cells in a cell-autonomous fashion. This cell-autonomy is increasingly criticized. Current data suggest that the tumor microenvironment is also strongly involved in carcinogenesis. Recently, we published a hypothesis that considers the important contribution of the tumor microenvironment in carcinogenesis and complements the classical clonal evolution model. Essentially, this “feedback loop model” (FBM) postulates that the physiological communication between cancer cells and stromal cells in inflammatory or proliferative conditions is altered by anomalous signal processing within the parenchymal cells. The inability of parenchymal cells to correctly finalize the intercellular communication might result in a perpetuation of the activated state of cells and the tumor micromilieu. The FBM is unique among the tissue-based models because in this model tumor and stromal cells interact together in a reciprocal manner to form the cancer phenotype. Contrary to the SMT, the FBM postulates that mutated genes act in a cell-heteronomous fashion, not in a cell-autonomously fashion. Landes Bioscience 2012-09-01 /pmc/articles/PMC3502218/ /pubmed/23739683 http://dx.doi.org/10.4161/cib.21177 Text en Copyright © 2012 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Article Addendum Rückert, Felix Sticht, Carsten Niedergethmann, Marco Molecular mechanism of the “feedback loop” model of carcinogenesis |
title | Molecular mechanism of the “feedback loop” model of carcinogenesis |
title_full | Molecular mechanism of the “feedback loop” model of carcinogenesis |
title_fullStr | Molecular mechanism of the “feedback loop” model of carcinogenesis |
title_full_unstemmed | Molecular mechanism of the “feedback loop” model of carcinogenesis |
title_short | Molecular mechanism of the “feedback loop” model of carcinogenesis |
title_sort | molecular mechanism of the “feedback loop” model of carcinogenesis |
topic | Article Addendum |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3502218/ https://www.ncbi.nlm.nih.gov/pubmed/23739683 http://dx.doi.org/10.4161/cib.21177 |
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