Inflammation: A protagonist in development of carcinogen induced cervical cancer in mice
Inflammation- induced systemic stress plays an essential role in neoplastic progression. Chronic exposure to chemical carcinogens can induce persistent inflammatory changes which further augment loss in physiological hormesis of an organism thereby favouring carcinogenesis. The present study investigated the role of inflammation and associated systemic stress in the development of cervical carcinoma in a 3-methylcholanthrene (3-MC; a chemical carcinogen) induced in vivo cervical cancer model. When the cervix of 5-6 weeks old virgin female Swiss Albino mice (Mus musculus) was treated with 3-MC (0.6 mg/mL), remarkable alteration in its cervical cytopathology was observed. An increase in duration of 3-MC treatment caused an outburst in the number and variety of infiltrating granulocytes and agranulocytes in mice cervix. Thus, a high leukocyte index was indicative of prevalent cervical inflammatory changes. Elevated activities of SGPT, SGOT, serum alkaline phosphatase enzymes along with the presence of elevated serum creatinine levels suggested liver and renal dysfunctions. These observations were supported by alterations in hepatic histopathology of 3-MC treated mice. Surged activities and expression profiles of inflammatory cytokines (IL-6 and IL-8) in cervix tissue had conclusively established the crucial role played by inflammation- mediated systemic stress in favouring the development of cervical cancer in a carcinogen-induced in vivo model.
Cervical cancer; Chronic inflammation; Cytokines; Dysplasia; Helicobacter pylori; Methylcholanthrene; Systemic stress
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