Blog
About

45
views
0
recommends
+1 Recommend
1 collections
    1
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Chronic inflammation evoked by pathogenic stimulus during carcinogenesis

      , 1 , 2 , 3 , * , 1 , 2 , 4

      4open

      EDP Sciences

      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

      Read this article at

      ScienceOpenPublisher
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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.

          Related collections

          Most cited references 293

          • Record: found
          • Abstract: found
          • Article: not found

          Human papillomavirus is a necessary cause of invasive cervical cancer worldwide.

          A recent report that 93 per cent of invasive cervical cancers worldwide contain human papillomavirus (HPV) may be an underestimate, due to sample inadequacy or integration events affecting the HPV L1 gene, which is the target of the polymerase chain reaction (PCR)-based test which was used. The formerly HPV-negative cases from this study have therefore been reanalyzed for HPV serum antibodies and HPV DNA. Serology for HPV 16 VLPs, E6, and E7 antibodies was performed on 49 of the 66 cases which were HPV-negative and a sample of 48 of the 866 cases which were HPV-positive in the original study. Moreover, 55 of the 66 formerly HPV-negative biopsies were also reanalyzed by a sandwich procedure in which the outer sections in a series of sections are used for histological review, while the inner sections are assayed by three different HPV PCR assays targeting different open reading frames (ORFs). No significant difference was found in serology for HPV 16 proteins between the cases that were originally HPV PCR-negative and -positive. Type-specific E7 PCR for 14 high-risk HPV types detected HPV DNA in 38 (69 per cent) of the 55 originally HPV-negative and amplifiable specimens. The HPV types detected were 16, 18, 31, 33, 39, 45, 52, and 58. Two (4 per cent) additional cases were only HPV DNA-positive by E1 and/or L1 consensus PCR. Histological analysis of the 55 specimens revealed that 21 were qualitatively inadequate. Only two of the 34 adequate samples were HPV-negative on all PCR tests, as against 13 of the 21 that were inadequate ( p< 0.001). Combining the data from this and the previous study and excluding inadequate specimens, the worldwide HPV prevalence in cervical carcinomas is 99.7 per cent. The presence of HPV in virtually all cervical cancers implies the highest worldwide attributable fraction so far reported for a specific cause of any major human cancer. The extreme rarity of HPV-negative cancers reinforces the rationale for HPV testing in addition to, or even instead of, cervical cytology in routine cervical screening. Copyright 1999 John Wiley & Sons, Ltd.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Mechanisms of fibrosis: therapeutic translation for fibrotic disease.

            Fibrosis is a pathological feature of most chronic inflammatory diseases. Fibrosis, or scarring, is defined by the accumulation of excess extracellular matrix components. If highly progressive, the fibrotic process eventually leads to organ malfunction and death. Fibrosis affects nearly every tissue in the body. Here we discuss how key components of the innate and adaptive immune response contribute to the pathogenesis of fibrosis. We also describe how cell-intrinsic changes in important structural cells can perpetuate the fibrotic response by regulating the differentiation, recruitment, proliferation and activation of extracellular matrix-producing myofibroblasts. Finally, we highlight some of the key mechanisms and pathways of fibrosis that are being targeted as potential therapies for a variety of important human diseases.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The biology and function of fibroblasts in cancer.

               Raghu Kalluri (2016)
              Among all cells, fibroblasts could be considered the cockroaches of the human body. They survive severe stress that is usually lethal to all other cells, and they are the only normal cell type that can be live-cultured from post-mortem and decaying tissue. Their resilient adaptation may reside in their intrinsic survival programmes and cellular plasticity. Cancer is associated with fibroblasts at all stages of disease progression, including metastasis, and they are a considerable component of the general host response to tissue damage caused by cancer cells. Cancer-associated fibroblasts (CAFs) become synthetic machines that produce many different tumour components. CAFs have a role in creating extracellular matrix (ECM) structure and metabolic and immune reprogramming of the tumour microenvironment with an impact on adaptive resistance to chemotherapy. The pleiotropic actions of CAFs on tumour cells are probably reflective of them being a heterogeneous and plastic population with context-dependent influence on cancer.
                Bookmark

                Author and article information

                Journal
                fopen
                https://www.4open-sciences.org
                4open
                4open
                EDP Sciences
                2557-0250
                25 April 2019
                25 April 2019
                2019
                : 2
                : ( publisher-idID: fopen/2019/01 )
                Affiliations
                [1 ] 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,
                Author notes
                [* ]Corresponding author: b-bruecher@ 123456gmx.de
                Article
                fopen180014
                10.1051/fopen/2018006
                © 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.

                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 305, Pages: 22
                Product
                Self URI (journal page): https://www.4open-sciences.org/
                Categories
                Life Sciences - Medicine
                Disruption of homeostasis-induced signaling and crosstalk in the carcinogenesis paradigm “Epistemology of the origin of cancer”
                Review Article
                Custom metadata
                4open 2019, 2, 8
                2019
                2019
                2019

                Comments

                Comment on this article