title: Prolonged inflammatory microenvironment is crucial for pro-neoplastic growth and genome instability: a detailed review.
abstract: BACKGROUND
  Chronic inflammation can affect the normal cell homeostasis and metabolism by rendering the cells susceptible to genomic instability that may lead to uncontrolled cellular growth and proliferation ensuing tumorigenesis. The causal agents for inflammation may be pathogenic infections like microbial agents ranging from viruses to bacteria. These infections lead to DNA damage or disruption of normal cell metabolism and alter the genome integrity.
  
  
  RESULTS
  In this review, we have highlighted the role of recurrent infections in tumor microenvironment can lead to recruitment of pro-inflammatory cells, cytokines and growth factors to the site of inflammation. This makes the environment rich in cytokines, chemokines, DNA-damaging agents (ROS, RNS) and growth factors which activate DNA damage response pathway and help in sustained proliferation of the tumor cells. In any inflammatory response, the production of cytokines and related signaling molecules is self-regulating and limiting. But in case of neoplastic risk, deregulation of these factors may lead to abnormalities and related pathogenesis.
  
  
  CONCLUSIONS
  The scope of the present review is to explore the probable mechanistic link and factors responsible for chronic inflammation. The relation between chronic inflammation and DNA damage response was further elucidated to understand the mechanism by which it makes the cells susceptible to carcinogenesis.
authors.affiliation: Molecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India.
authors.forename: Kumari
authors.initials: K
authors.lastname: Anuja
authors.affiliation: Molecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India.
authors.forename: Souvick
authors.initials: S
authors.lastname: Roy
authors.affiliation: Molecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India.
authors.forename: Chinmoy
authors.initials: C
authors.lastname: Ghosh
authors.affiliation: Department of Molecular Biology and Bioinformatics, Tripura University (A Central University), Suryamaninagar, Agartala, Tripura, 799022, India.
authors.forename: Priya
authors.initials: P
authors.lastname: Gupta
authors.affiliation: Department of Molecular Biology and Bioinformatics, Tripura University (A Central University), Suryamaninagar, Agartala, Tripura, 799022, India. surajit77@tripurauniv.in.
authors.forename: Surajit
authors.initials: S
authors.lastname: Bhattacharjee
authors.affiliation: Molecular Stress and Stem Cell Biology Group, School of Biotechnology, KIIT University, Bhubaneshwar, Odisha, 751024, India. bnbanerjee@kiitbiotech.ac.in.
authors.forename: Birendranath
authors.initials: B
authors.lastname: Banerjee
mesh_terms: D000818:Animals; D004249:DNA Damage; D042822:Genomic Instability; D006801:Humans; D007239:Infections / Q000276:immunology; D007249:Inflammation / Q000276:immunology*; D009369:Neoplasms / Q000276:immunology*; D018384:Oxidative Stress; D059016:Tumor Microenvironment / Q000276:immunology*
keywords: Carcinogenesis; Chronic inflammation; DNA damage response; Genomic instability; Immune response; Oxidative stress