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.
Cervical cancer develops from the preneoplastic cervical intraepithelial neoplasia (CIN). Host factors are critical in regulating tumor growth and cytokines, which modulate immunologic control may be of particular importance. The objective of this study was to assess the production of cytokines by peripheral blood mononuclear cells (PBMCs) in Indian women with cancer cervix and CIN. Sixty patients with cancer cervix (including all FIGO stage I-IV), 35 patients with CIN, and 30 healthy controls were enrolled in this study. The human papillomavirus (HPV) 16 and 18 status was determined in all the study groups. The PBMC culture supernatant was collected for cytokine estimations by enzyme-linked immunosorbent assay (interleukin-2 [IL-2], interferon-gamma [IFN-gamma], interleukin-4 [IL-4], and interleukin-10 [IL-10]). IL-2 levels showed a significant decline in high-grade CIN and cancer patients, whereas IFN-gamma levels were decreased only in patients with advanced cancer cervix. An increase in the levels of IL-4 and IL-10 was found in all cancer cervix and CIN grade III patients, as compared to those with early CIN grades and healthy controls. The cytokine ratios decreased significantly (P < 0.001 for all the ratios), when cervical cancer patients were compared with controls and CIN cases. The type 2 and type 1 cytokine levels were significantly correlated (P < 0.000) with HPV status. We conclude that a pronounced shift from type 1 to type 2 cytokine production is associated with more severe disease. These data reinforce the need for detailed analysis of immune dysregulation in CIN and cancer cervix patients.
Cervical cancer is the most common cancer in Indian women. The aim of this study is to assess the alterations in the circulating lipid peroxide, antioxidant components and activities of defence enzymes in advanced cervical cancer patients, and to monitor the variations in their levels before and after neoadjuvant chemoradiation. Sixty patients with advanced cancer of the cervix (FIGO IIIa-IVb) are included in the study, along with 60 healthy controls. Blood samples are collected before the start of therapy (S1), two weeks after the second course of chemotherapy (S2) and two weeks after completion of tele/brachyradiation (S3). Single blood samples are taken from controls. Lipid peroxides, conjugated dienes, reduced glutathione (GSH), catalase (CAT) and glutathione-S-transferase (GST) are estimated using standard methods. Glutathione peroxidase (GPx) and superoxide dismutase (SOD) are assayed using commercially available kits. The pretreatment levels of plasma lipid peroxide were significantly elevated in cancer patients, while significantly lowered levels of GSH, GPx, GST, SOD and CAT were observed when compared to controls. After chemotherapy, the levels of lipid peroxidation showed a significant decline (P < 0.05), which became highly significant after chemoradiation (P < 0.01). Levels of GSH, GPx, SOD, GST and CAT showed a mild increase after chemotherapy. After chemoradiation, levels reverted to normal or near normal (P < 0.01). Low levels of antioxidants in the circulation of patients with cervical cancer may be due to their increased utilisation to scavenge lipid peroxidation as well as their sequestration by tumour cells. The observed increase in antioxidant concentration after therapy might be due to the death of tumour cells or the arrest of tumour growth by chemotherapeutic agents. The normalisation of these parameters may provide information about the efficacy of neoadjuvant chemoradiation. A larger patient cohort with a longer follow-up period for therapeutic response studies may yield more significant data.
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