Cigarette Smoking and Colorectal Cancer: From Epidemiology to Bench

Wei, Po Li; Lin, Shyr Yi; Chang, Yu Jia

doi:10.1016/j.jecm.2011.10.002

Cited by 13 publications

(12 citation statements)

References 60 publications

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“…Previous studies have proved that the intensity and duration of smoking are associated positively with colorectal epithelial damage either the growth of colorectal adenomas, hyperplastic polyps, and carcinoma (Mutch et al, 2009;Wei et al, 2011). Based on population studies, the time required for cigarette smoke to induce colorectal carcinoma ranged from 30 to 40 years (Giovannucci, et al, 1994).…”

Section: Resultsmentioning

confidence: 99%

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Cigarette Smoke Induces Colorectal Carcinogenesis in Wistar Rats by Decreasing The Expression of APC, MSH2 and MLH1

et al. 2017

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Colorectal carcinogenesis induced by cigarette smoke requires at least 30-40 years. This long time duration causes an animal research conducted becomes relevant. This research was carried out to observe colorectal carcinogenesis due to cigarette smoke exposure in Wistar Rat. The observations focused on changes in epithelial morphology and expression of APC, MSH2 and MLH1. Twenty male Wistar rats inbreed strain were randomly allocated into control group and experimental group exposure to cigarettes smoke for 14 weeks and 28 weeks sequentially. Colorectal epithelial morphology was assessed on the histopathology examination, whereas the expression of APC, MSH2 and MLH1 was assessed on aspect of immunohistochemistry. The comparative analysis between the two groups was performed using nonparametric Mann-Whitney U test. Histology of colorectal epithelium showed pattern of colitis associated cancer that was significant both in 14 weeks and 28 weeks of treatment. This research indicated negative expression of APC, MSH2 and MLH1 in the colorectal cancer that were significant at 28 weeks of exposure. This research implies that chronic exposure to cigarette smoke can induce colitis associated colorectal cancer through decreased expression of APC, MSH2 and MLH1.

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Section: Resultsmentioning

confidence: 99%

“…The main carcinogens in cigarette smoke are polycyclic aromatic hydrocarbons (PAHs), aromatic amines, nitrosamines, and heterocyclic amines (HCAs) (Kasahara et al, 2008). Nicotine and its metabolite, 4-(methylnitrosamino) -1-(3-pyridyl) -1-butanone (NNK) are believed to be the two main causes of smoking-related cancer (Wei, et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Cigarette Smoke Induces Colorectal Carcinogenesis in Wistar Rats by Decreasing The Expression of APC, MSH2 and MLH1

et al. 2017

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“…In addition, it is also suggested that other natural dietary compounds that act through modulating cigarette smoking-induced signaling pathways such as a9-nAChR in breast cancer, 68,69 can provide a further potential application for cancer chemopreventive action in cigarette smoke-related cancers. 70,71 …”

Section: Novel Therapeutic Approaches For Bladder Cancer Using Pterosmentioning

confidence: 99%

Molecular Mechanisms of Nicotine-induced Bladder Cancer

Chen

2011

Journal of Experimental & Clinical Medicine

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“…1e3 In addition, epidemiologic studies have implicated cigarette smoking in colon cancer. 4 Up-regulated nuclear factor-kB (NF-kB), increased oxidative stress and genotoxic stress occur in the gastrointestinal tract of smokers. 5 Oral nicotine administration has been reported to enhance tumor growth in a human colon cancer xenograft in nude mice.…”

Section: Introductionmentioning

confidence: 99%