Abstract
Objective. Inflammation is an important hallmark of all cancers and net inflammatory response is determined by a delicate balance between pro- and anti-inflammatory cytokines, which may be affected by tobacco exposure, so the present study was designed to explore the effect of various modes of tobacco exposure on interleukin-12 (IL-12) and interleukin-10 (IL-10) inflammatory cytokine levels and survival in prostate carcinoma (PCa) patients. Methods. 285 cancer patients and equal controls with 94 BPH (benign prostatic hyperplasia) were recruited; baseline levels of serum IL-12 and IL-10 were measured and analyzed in various tobacco exposed groups by appropriate statistical tool. Five-year survivals of patients were analyzed by Log-rank (Mantel-Cox) test (graph pad version 5). Results. The expression of serum proinflammatory (IL-12) and anti-inflammatory (IL-10) cytokines was correlated with tobacco exposed group as smokers, chewers, and alcohol users have shown significantly higher levels (P < 0.001) with significantly lower median survivals (27.1 months, standard error = 2.86, and 95% CI: 21.4–32.62); than nonusers. Stages III and IV of tobacco addicted patients have also shown significantly increased levels of IL-12 and IL-10. Conclusions. IL-12 and IL-10 seem to be affected by various modes of tobacco exposure and inflammation also affects median survival of cancer patients.
Highlights
Prostate cancer (PCa) is the second most commonly diagnosed cancer in men (13.6% of the total) with the fifth most common cancer overall and sixth leading cause of cancer death in men [1]
Present study was conducted in densely populated North Indian region to explore the association of inflammation with various modes of tobacco exposure in prostate carcinoma patients and their survivals by measuring the serum IL-12 and IL-10 cytokine levels
Present study provides support that tobacco chewing and smoking may be important contributors for inflammation as pr-inflammatory IL-12 levels were increased in prostate cancer (PCa) patients but surprisingly we noticed that IL-10 cytokines, that is, anti-inflammatory levels, were increased
Summary
Prostate cancer (PCa) is the second most commonly diagnosed cancer in men (13.6% of the total) with the fifth most common cancer overall and sixth leading cause of cancer death in men [1]. Important hallmarks included so far are sustaining proliferative signalling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis [3]. Recent studies have begun to decipher molecular pathways linking inflammation and cancer. It has been recognized that inflammation contributes to proliferation, malignancy, angiogenesis, metastasis, adaptive immunity modulation, and unresponsiveness to hormones and chemotherapeutic agents [5]. Chronic inflammation has BioMed Research International been concerned as an important environmental influence that can cause cancer. Recent study showed that the cause of chronic inflammation in cancer patients was chronic infection in 20%, tobacco exposure and inhaled pollutant in 30%, and dietary factors in 35% [12]. Inflammation has been linked in various steps including tumorigenesis, cellular transformation, survival, proliferation, invasion, angiogenesis, and metastasis [13]
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