Dwivedi Shailendra, Goel Apul, Mandhani Anil, Khattri Sanjay, Pant Kamlesh Kumar
Department of Pharmacology and Therapeutics, Chhatrapati Sahuji Maharaj Medical University (Erstwhile KGMU), Lucknow, India.
Toxicol Int. 2012 Sep;19(3):310-8. doi: 10.4103/0971-6580.103681.
Prostate cancer is responsible for major deaths globally after lung cancer. However, etiology of prostate cancer is still unknown. Individual risk and incidence of prostate cancer may result from the interaction of genetic susceptibility with exposure to environmental factors such as infectious agents, tobacco, occupational exposure, dietary carcinogens, and/or hormonal imbalances leading to injury of the prostate and to the development of chronic inflammation. About 30% of all human cancers are caused by tobacco smoking and inhaled pollutants. Inflammation is now regarded as an important hallmark of cancer. The present study has been aimed to explore the pro-inflammatory levels in prostate carcinoma patients by examining the serum levels of novel cytokine interleukin-18 (IL-18) expression in tobacco exposed population. A total of 578 (n = 284 biopsy proven prostate cancer patients, n = 294 controls with and without tobacco exposed population) were recruited. Serum IL-18 (Interleukin-18) level was done by ELISA. The IL-18 levels between cancer patients and controls within same mode tobacco exposure as tobacco smoking (overall) showed significant difference (P < 0.0001) and further we compared within stratified group, it significantly differ (P < 0.0001) in bidi and cigarette smoking than control non users. Furthermore, IL-18 levels in tobacco chewers (overall) with gutkha and khaini chewers showed significant difference (P < 0.01) than controls non users. Moreover, the IL-18 levels between cancer patients and controls with in of combined mode chewers smokers and alcohol (CSA), smokers with alcohol showed significant difference (P < 0.01) than controls. The IL-18 levels also differed significantly (P < 0.05) with smokers and chewers in higher stages of III and IV, and showed non significant with in lower stages. Tobacco exposure enhance the inflammation in prostate carcinoma patients in stratified group as it have been represented as a risk factors in various cancers, but this study provide further its role that seems to influence inflammation especially in prostate carcinoma.
前列腺癌是全球继肺癌之后导致主要死亡的原因。然而,前列腺癌的病因仍然不明。个体患前列腺癌的风险和发病率可能源于遗传易感性与接触环境因素(如传染因子、烟草、职业暴露、饮食致癌物和/或激素失衡)之间的相互作用,这些因素会导致前列腺损伤和慢性炎症的发展。约30%的人类癌症是由吸烟和吸入污染物引起的。炎症现在被视为癌症的一个重要标志。本研究旨在通过检测烟草暴露人群中新型细胞因子白细胞介素-18(IL-18)的血清表达水平,探讨前列腺癌患者的促炎水平。共招募了578名受试者(n = 284例经活检证实的前列腺癌患者,n = 294例有或无烟草暴露人群的对照)。采用酶联免疫吸附测定法检测血清IL-18(白细胞介素-18)水平。在相同的烟草暴露模式(如总体吸烟情况)下,癌症患者与对照之间的IL-18水平显示出显著差异(P < 0.0001),进一步在分层组内比较时,与非吸烟对照相比,比迪烟和香烟吸烟者中的差异也非常显著(P < 0.0001)。此外,总体而言,咀嚼烟草(包括古特卡和卡尼)者的IL-18水平与非使用者对照相比有显著差异(P < 0.01)。此外,在咀嚼烟草者与吸烟者及饮酒者的联合模式(CSA)、吸烟者与饮酒者中,癌症患者与对照之间的IL-18水平相比对照有显著差异(P < 0.01)。在III期和IV期较高阶段,吸烟者和咀嚼者的IL-18水平也有显著差异(P < 0.05),而在较低阶段则无显著差异。烟草暴露在分层组中会加重前列腺癌患者的炎症,因为它已被视为各种癌症的危险因素,但本研究进一步揭示了其似乎尤其在前列腺癌中对炎症产生影响的作用。