Mutation of the onco-suppressor gene encoding the protein known as p53 may cause synthesis of a mutant p53 protein which can bind to and inactivate its wild-type equivalent. This protein is detectable in many malignant neoplasms, including bronchial carcinoma, and has been associated with cigarette smoking. Of 59 tissue biopsy specimens of primary bronchial malignancies immunolabeled for p53 by the avidin-biotin technique using the antibodies PAb 1801, CM1, and D07, 13 (22%) expressed the protein. Of these 13 patients, 10 (77%) smoked more than 20 cigarettes a day and their mean total exposure was 53 pack-years. Corresponding figures for those with p53-negative tumors were 21 (46%) smoking more than 20 cigarettes a day with a mean total exposure of 36 pack-years. There was, however, no difference between the groups in total duration of exposure (46 vs. 47 years). Although p53 was expressed more commonly in adenocarcinoma (30% of 10) and squamous carcinoma (28% of 29) than in small cell tumors (10% of 20), this could be accounted for by the smoking history. This study supports a relationship between mutations of the p53-encoding gene associated with overexpression of its protein product and intensity of exposure to cigarette smoke.
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Gosney et al. (1993) studied this question.
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