Chronic inflammation: key player and biomarker-set to predict and prevent cancer development and progression based on individualized patient profiles – ScienceOpen
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      Chronic inflammation: key player and biomarker-set to predict and prevent cancer development and progression based on individualized patient profiles

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          Abstract

          A strong relationship exists between tumor and inflammation, which is the hot point in cancer research. Inflammation can promote the occurrence and development of cancer by promoting blood vessel growth, cancer cell proliferation, and tumor invasiveness, negatively regulating immune response, and changing the efficacy of certain anti-tumor drugs. It has been demonstrated that there are a large number of inflammatory factors and inflammatory cells in the tumor microenvironment, and tumor-promoting immunity and anti-tumor immunity exist simultaneously in the tumor microenvironment. The typical relationship between chronic inflammation and tumor has been presented by the relationships between Helicobacter pylori, chronic gastritis, and gastric cancer; between smoking, development of chronic pneumonia, and lung cancer; and between hepatitis virus (mainly hepatitis virus B and C), development of chronic hepatitis, and liver cancer. The prevention of chronic inflammation is a factor that can prevent cancer, so it effectively inhibits or blocks the occurrence, development, and progression of the chronic inflammation process playing important roles in the prevention of cancer. Monitoring of the causes and inflammatory factors in chronic inflammation processes is a useful way to predict cancer and assess the efficiency of cancer prevention. Chronic inflammation-based biomarkers are useful tools to predict and prevent cancer.

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          Inflammation and cancer: how hot is the link?

          Although inflammation has long been known as a localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss of function, there has been a new realization about its role in a wide variety of diseases, including cancer. While acute inflammation is a part of the defense response, chronic inflammation can lead to cancer, diabetes, cardiovascular, pulmonary, and neurological diseases. Several pro-inflammatory gene products have been identified that mediate a critical role in suppression of apoptosis, proliferation, angiogenesis, invasion, and metastasis. Among these gene products are TNF and members of its superfamily, IL-1alpha, IL-1beta, IL-6, IL-8, IL-18, chemokines, MMP-9, VEGF, COX-2, and 5-LOX. The expression of all these genes are mainly regulated by the transcription factor NF-kappaB, which is constitutively active in most tumors and is induced by carcinogens (such as cigarette smoke), tumor promoters, carcinogenic viral proteins (HIV-tat, HIV-nef, HIV-vpr, KHSV, EBV-LMP1, HTLV1-tax, HPV, HCV, and HBV), chemotherapeutic agents, and gamma-irradiation. These observations imply that anti-inflammatory agents that suppress NF-kappaB or NF-kappaB-regulated products should have a potential in both the prevention and treatment of cancer. The current review describes in detail the critical link between inflammation and cancer.
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            Oncogenic mechanisms of the Helicobacter pylori CagA protein.

            Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA) gene is associated with gastric carcinoma. Recent studies have shed light on the mechanism through which the cagA gene product, CagA, elicits pathophysiological actions. CagA is delivered into gastric epithelial cells by the bacterial type IV secretion system, where it deregulates the SHP2 oncoprotein. Intriguingly, CagA is noted for its variation, particularly at the SHP2-binding site, which could affect the potential of different strains of H. pylori to promote gastric carcinogenesis.
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              Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases: A Mechanistic Review

              Many studies have been undertaken to reveal how tobacco smoke skews immune responses contributing to the development of chronic obstructive pulmonary disease (COPD) and other lung diseases. Recently, environmental tobacco smoke (ETS) has been linked with asthma and allergic diseases in children. This review presents the most actual knowledge on exact molecular mechanisms responsible for the skewed inflammatory profile that aggravates inflammation, promotes infections, induces tissue damage, and may promote the development of allergy in individuals exposed to ETS. We demonstrate how the imbalance between oxidants and antioxidants resulting from exposure to tobacco smoke leads to oxidative stress, increased mucosal inflammation, and increased expression of inflammatory cytokines (such as interleukin (IL)-8, IL-6 and tumor necrosis factor α ([TNF]-α). Direct cellular effects of ETS on epithelial cells results in increased permeability, mucus overproduction, impaired mucociliary clearance, increased release of proinflammatory cytokines and chemokines, enhanced recruitment of macrophages and neutrophils and disturbed lymphocyte balance towards Th2. The plethora of presented phenomena fully justifies a restrictive policy aiming at limiting the domestic and public exposure to ETS.
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                Author and article information

                Contributors
                +86-731-84327905 , yjzhan2011@gmail.com
                Journal
                EPMA J
                EPMA J
                The EPMA Journal
                Springer International Publishing (Cham )
                1878-5077
                1878-5085
                20 November 2019
                20 November 2019
                December 2019
                : 10
                : 4
                : 365-381
                Affiliations
                [1 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, Key Laboratory of Cancer Proteomics of Chinese Ministry of Health, Xiangya Hospital, , Central South University, ; 87 Xiangya Road, Changsha, 410008 Hunan People’s Republic of China
                [2 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, Hunan Engineering Laboratory for Structural Biology and Drug Design, Xiangya Hospital, , Central South University, ; 87 Xiangya Road, Changsha, 410008 Hunan People’s Republic of China
                [3 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, State Local Joint Engineering Laboratory for Anticancer Drugs, Xiangya Hospital, , Central South University, ; 87 Xiangya Road, Changsha, 410008 Hunan People’s Republic of China
                [4 ]GRID grid.10388.32, ISNI 0000 0001 2240 3300, Radiological Clinic, UKB, , Excellence Rheinische Friedrich-Wilhelms-University of Bonn, ; Sigmund-Freud-Str 25, 53105 Bonn, Germany
                [5 ]GRID grid.10388.32, ISNI 0000 0001 2240 3300, Breast Cancer Research Centre, UKB, , Excellence Rheinische Friedrich-Wilhelms-University of Bonn, ; Bonn, Germany
                [6 ]GRID grid.10388.32, ISNI 0000 0001 2240 3300, Centre for Integrated Oncology, Cologne-Bonn, , Excellence Rheinische Friedrich-Wilhelms-University of Bonn, ; Bonn, Germany
                [7 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, Department of Oncology, Xiangya Hospital, , Central South University, ; Changsha, 410008 Hunan People’s Republic of China
                [8 ]GRID grid.216417.7, ISNI 0000 0001 0379 7164, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, , Central South University, ; Changsha, 410008 Hunan People’s Republic of China
                Author information
                http://orcid.org/0000-0002-4984-3549
                Article
                194
                10.1007/s13167-019-00194-x
                6882964
                31832112
                6c7238f2-e943-4f74-9cfb-6b7a3da69040
                © The Author(s) 2019

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 28 October 2019
                : 6 November 2019
                Funding
                Funded by: the Hunan Provincial Hundred Talent Plan
                Award ID: to XZ
                Award Recipient :
                Funded by: the Xiangya Hospital Funds for Talent Introduction
                Award ID: to XZ
                Award Recipient :
                Funded by: the China “863” Plan Project
                Award ID: 2014AA020610-1
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81572278 and 81272798
                Award Recipient :
                Categories
                Review
                Custom metadata
                © European Association for Predictive, Preventive and Personalised Medicine (EPMA) 2019

                Molecular medicine
                chronic inflammation,cancer,inflammatory factors,biomarkers,predictive preventive personalized medicine,patient stratification,individualized patient profile,risk factors,modifiable and preventable,genetics,epigenetics,multiomics,machine learning,big data analysis,global statistics,collateral pathologies,phenotyping

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