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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...

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Detalles Bibliográficos
Autores principales: Rückert, Felix, Sticht, Carsten, Niedergethmann, Marco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2012
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.
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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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