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Although epidemiological studies of the relationship between cigarette smoking and colorectal cancer risk have been equivocal, a positive association is consistently found for colorectal adenoma development. We performed an epidemiological study to determine whether p53 protein overexpression, in tumours obtained at the time of resection, is associated with cigarette exposure in colorectal cancer. A total of 163 colorectal cancer cases and 326 healthy controls responded to a standardised questionnaire on colorectal cancer risk factors including detailed information on their history of cigarette smoking. All patients' tumours were analysed immunohistochemically for p53 overexpression using an avidin-biotin immunoperoxidase procedure and polyclonal anti-p53 antibody CM1. Comparison of colorectal cases with controls revealed an elevated risk for ex-smokers (OR = 1.34, 95% CI 0.85-2.12) and current smokers (OR = 1.13, 95% CI 0.63-2.02) when compared with non-smokers. No dose-response relationship was found for total pack-years of smoking (trend test: P = 0.19). However, a trend for total pack-years of smoking was found when p53-positive cases were compared with p53-negative cases suggesting aetiological, heterogeneity (trend test: P = 0.06). Estimating the individual relative risk of developing a p53-positive tumour relative to controls showed no associations for smoking status or total pack-years of smoking. However, when p53-negative cases were compared with controls, an elevated risk was found for ex-smokers (OR = 1.84, 95% CI 1.00-3.37) and current years of smoking (trend test: P = 0.03). Colorectal tumours developing through p53-positive dependent pathways were not associated with smoking exposure. A significant increase in risk was observed for the p53-negative independent pathway with smoking. p53 overexpression appears to be associated with smoking exposure in colorectal cancer.

This electronmicroscope study of the histogenesis of mucoepidermoid carcinoma is based on 15 cases from the major and minor salivary glands. Six major cell types were identified: undifferentiated (cuboid) stem cells, intermediate (columnar) ceils, serous/mucoid secretory cells, mucus-producing goblet ceils. squamous/epidermoid cells and myoepithelium It is proposed that undifferentiated stein ceils serve as pluripotential reserves which give rise to the various cell types seen in mucoepidermoid carcinoma. Reserve cells in the acinar-intercalated duct components of the salivary glands appeared to give rise to the serous/mucoid and myoepithelial cell populations of mucoepidermoid carcinoma. Reserve cells in the proximal ducts system (intra/extralobular striated ducts and excretory ducts) differentiated into myoepithelium. intermediate (columnar) cells, squamous/epidermoid and mucus-producing goblet cell lines, It is proposed that neoplastic reserve cells give rise to different tumor types in the salivary glands. These types result from varying admixtures and arrangements of tumor cells at different stages of their structural and functional cytodifferentiation from reserve cells. It is further proposed that neoplastic reserve cells differentiate along similar cell lines as the embryonic "stem cells" in the development of normal salivary glands. [ABSTRACT FROM AUTHOR]