Volume 2, 2019
Disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “Epistemology of the origin of cancer”
|Number of page(s)||21|
|Section||Life Sciences - Medicine|
|Published online||25 April 2019|
Precancerous niche (PCN), a product of fibrosis with remodeling by incessant chronic inflammation
Theodor-Billroth-Academy®, Germany, USA
2 INCORE, International Consortium of Research Excellence of the Theodor-Billroth-Academy®, Germany, USA
3 Department of Surgery, Carl-Thiem-Klinikum, Cottbus, Germany
4 Risk-Based Decisions Inc., Sacramento, CA, USA
* Corresponding author: email@example.com
Accepted: 19 December 2018
Fibroblasts are actively involved in the creation of the stroma and the extracellular matrix which are important for cell adhesion, cell–cell communication, and tissue metabolism. The role of fibrosis in carcinogenesis can be examined by analogy to tissues of various cancers. The orchestration of letters in the interplay of manifold components with signaling and crosstalk is incompletely understood but available evidence suggests a hitherto underappreciated role for fibrosis in carcinogenesis. Complex signaling and crosstalk by pathogenic stimuli evoke persistent subclinical inflammation, which in turn, results in a cascade of different cell types, ubiquitous proteins and their corresponding enzymes, cytokine releases, and multiple signaling pathways promoting the onset of fibrosis. There is considerable evidence that the body's attempt to resolve such a modified extracellular environment leads to further disruption of homeostasis and the genesis of the precancerous niche as part of the six-step process that describes carcinogenesis. The precancerous niche is formed and can be understood to develop as a result of (1) pathogenic stimulus, (2) chronic inflammation, and (3) fibrosis with alterations of the extracellular matrix, stromal rigidity, and mechano-transduction. This is why carcinogenesis is not just a process of aberrant cell growth with damaged genetic material but the role of the PCN in its entirety reveals how carcinogenesis can occur without invoking the need for somatic mutations.
Key words: Cancer / Carcinogenesis / Cell transition / Chronic inflammation / Epidemiology / Epigenetics / Fibrosis / Genomics / microRNA / Mutation / Pathogenesis / Precancerous niche / Proteomics / Somatic mutation theory
© B.L.D.M. Brücher and I.S. Jamall, Published by EDP Sciences 2019
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Current usage metrics show cumulative count of Article Views (full-text article views including HTML views, PDF and ePub downloads, according to the available data) and Abstracts Views on Vision4Press platform.
Data correspond to usage on the plateform after 2015. The current usage metrics is available 48-96 hours after online publication and is updated daily on week days.
Initial download of the metrics may take a while.