title: Inflammation: its role and interplay in the development of cancer, with special focus on gynecological malignancies.
abstract: The relationship between inflammation and cancer is intriguing. Mechanisms contributing to the pathobiology of carcinogenesis are multiple and complex. Many aspects still elude researchers and are subjects of intense speculation and debate, for example, the triggering factor for malignant transformation in inflammation. A comprehensive literature search was conducted from the Web sites of the National Library of Medicine and Pubmed Central, the US National Library of Medicine's digital archive of life sciences literature. The data were accessed from books and journals that published recent articles in this field. Several recent studies have identified nuclear factor-kappa B as a key modulator in driving inflammation to cancers. An inflammatory microenvironment inhabiting various inflammatory cells and a network of signaling molecules is essential for the malignant progression of transformed cells. This is attributed to the mutagenic predisposition of persistent infection-fighting agents at sites of chronic inflammation. The appreciation of the role of inflammation in carcinogenesis provides a mechanistic framework to understand clinical benefits of newer therapeutic strategies An in-depth knowledge about various pathogenic mechanisms involved in cancer will help clinicians in better management of the disease.
authors.affiliation: Department of Biochemistry, Maulana Azad Medical College, New Delhi, India.
authors.forename: B
authors.initials: B
authors.lastname: Goswami
authors.forename: M
authors.initials: M
authors.lastname: Rajappa
authors.forename: M
authors.initials: M
authors.lastname: Sharma
authors.forename: A
authors.initials: A
authors.lastname: Sharma
mesh_terms: D002471:Cell Transformation, Neoplastic / Q000276:immunology; D018450:Disease Progression; D005260:Female; D005833:Genital Neoplasms, Female / Q000209:etiology* / Q000276:immunology / Q000628:therapy; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000502:physiology; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology* / Q000276:immunology / Q000628:therapy; D015398:Signal Transduction / Q000276:immunology
chemical_list: D018836:Inflammation Mediators