A recessive gene on chromosome 17 encodes a protein, known as p53, which normally acts to regulate the cell cycle, its mutation and over-expression being amongst the commonest genetic abnormalities in human malignant neoplasms. As detected by immunolabelling using the anti-p53 protein antibodies PAb1801, DO7 and CM1, over-expression was demonstrable in 13 of 59 tissue biopsy specimens from a series of patients with newly-diagnosed primary bronchial carcinoma from whom accurate data on smoking history had been obtained prior to bronchoscopy. There was a statistically significant relationship between over-expression and total exposure to cigarette smoke (p53-positive, median 46 pack-years; p53-negative, median 32 pack-years; P<0.001) and between over-expression and intensity of exposure (p53-positive, median 20 cigarettes/day; p-53 negative, median 14 cigarettes/day; P<0.001), but no difference between the two groups in terms of total duration of this exposure (p53-positive, median 47 y; p53-negative, median 46 y). These data confirm findings of previous studies suggesting a possible link between cigarette smoke and those derangements of the structure or function of the p53-encoding gene which lead to its over-expression by malignant bronchial tumours. They support, in addition, a specific mutagenic role for the chemical carcinogens it contains. Over-expression of p53 did not appear to influence survival.

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