Volume 2, 2019
Disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “Epistemology of the origin of cancer”
|Number of page(s)||22|
|Section||Life Sciences - Medicine|
|Published online||25 April 2019|
Chronic inflammation evoked by pathogenic stimulus during carcinogenesis
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: firstname.lastname@example.org
Accepted: 21 November 2018
A pathogenic (biological or chemical) stimulus is the earliest information received by a cell that can result in the disruption of homeostasis with consequent development of disease. Chronic inflammation involves many cell types with numerous cytokines and signaling pathways, the release of different components by the cells, and the crosstalk provoked by such stimuli involving subclinical chronic inflammation and is mechanistically manifold. Exosomes secrete chemicals that trigger the epithelium to produce exosome-like nanoparticles promoting chronic inflammation. Small molecules, together with various cytokines, selectively target signaling pathways inducing crosstalk that suppress apoptosis. 16S rRNA gene sequencing has become routine to provide information on the composition and abundance of bacteria found in human tissues and in reservoirs. The deregulation of autophagy with chronic stimulation of inflammation is an early phenomenon in carcinogenesis. The disruption of cell–cell integrity enables transcellular CagA migration and triggers deregulation of autophagy with the net result being chronic inflammation. The complex and insidious nature of chronic inflammation can be seen both inside and outside the cell and even with intracellular nuclear fragments such as chromatin, which itself can elicit a chronic inflammatory response within the cytoplasm and affect autophagy. The ultimate result of unresolved chronic inflammation is fibrosis, a step before tissue remodeling results in the formation of a precancerous niche (PCN). Various pathogenic stimuli associated with different neoplasms result in persistent inflammation. This ongoing disruption of homeostasis in the micromilieu of cells, tissues, and organs is an essential preamble to carcinogenesis and occurs early in that process.
Key words: Adenoma / Adhesion / Akt / ALOX / Apoptosis / Aquaporin / Autophagy / Bacterium / BIM / Blastoma / Cancer / Carcinoma / Carcinogenesis / CCC / Cdc42 / Cdk2 / Cholangiocellular carcinoma / Crohn's disease / Chronic inflammation / Colitis / Colorectal cancer / COX / Cyclin / Cyclooxygenase / CYP / Cytochrome P450 / Cytokine / CXCR4 / E2F4/5 / E-cadherin / Eicosanoide / EBV / Epstein–Barr virus / ERK / ETE / Fibroblast / Fibrosis / Fluke / FOXO3a / Gastric cancer / Gastritis / Glycocalyx / HBV / HCV / Helicobacter pylori / Hepatitis B virus / Hepatitis C virus / HETE / Homeostasis / HCC / HIV / HPV / HSV / Human herpes virus / Human papilloma virus / IBD / ICAM / IDO / IL / IL-β1, Interleukin / Inflammation / Leukemia / Lipoxygenase / LTA4 / LTB4 / LTC4 / LTD4 / LTE4 / Liver cancer / LOX / LOXL3 / Lymphoma / Lysyl oxidase / MAPK / MDA / Metalloproteinase / MMP / Mutation / NF-κB / AP1 / API2 / PCN / PGD2 / PGG2 / PGH2 / PGFF2a / Phagocytes / PI3K / Polyp / Precancerous niche / Prostate cancer / PUMA / Rac1 / RNS / ROS / Sarcoma / SPhK / S1P / S1PR3 / Simvastatin / SK2 / SOX / Tissue / TGF / TNF / TOR / TXA2 / VCAM / Virus / VZV
© 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.