Risk of malignant melanoma in relation to drug intake, alcohol, smoking and hormonal factors

Abstract

Risk of malignant melanoma in relation to drug intake, alcohol, smoking and hormonal factors J Westerdahl', H Olsson2, A Masback3, C Ingvar' and N Jonsson3 Departments of 'Surgery, 2Oncology, 3Pathology, University Hospital, S-22J85 Lund, Sweden.Summary In a population-based, matched case-control study from southern Sweden of 400 patients with a first diagnosis of malignant melanoma and 640 healthy control subjects aged 15-75 years, the association between commonly prescribed drugs, alcohol, smoking and malignant melanoma was evaluated. In addition, the relation between reproductive and hormonal factors and melanoma in women was studied. It was found that certain specific types of prescribed drugs, i.e. beta-blockers, hydralazines and benzodiazepines, may increase the risk of melanoma development. However, these associations were diminished, at least for benzodiazepines, after controlling for host factors. As these findings are unconfirmed, and may be due to chance or confounding, further studies are warranted. The risk of malignant melanoma was not influenced by alcohol consumption or smoking habits. Our results do not suggest an association between oral contraceptives and melanoma. Furthermore, reproductive factors were not independent risk factors for melanoma. However, increasing number of live births seemed to be protective (P for trend = 0.01). There is a need for further research to be able to draw firm conclusions on the relation between number of live births and melanoma. The results based on histopathological re-examinations and those based on tumour registry data were essentially the same.

Oral contraceptive use and risk of melanoma in premenopausal women

“…However, subsequent research has not generally supported this finding (Helmrich et al, 1984;Holman et al, 1984;Gallagher et al, 1985;Osterlind et al, 1988b;Zanetti et al, 1990;Hannaford et al, 1991;Palmer et al, 1992;Holly et al, 1995;Westerdahl et al, 1996). Failure to find an association between melanoma and oral contraceptive use may be due to the broad categorization of 'ever users'.…”

A pooled analysis of 10 case–control studies of melanoma and oral contraceptive use

“…However, even in these large cohorts, the numbers of exposed and unexposed cases were relatively small (six exposed cases in NHS and eight in NHS II). Two other recent and relatively large case -control studies reported from Connecticut and Sweden (Westerdahl et al, 1996;Smith et al, 1998) observed no relation between ever use or duration of oral contraceptive use and risk of melanoma. But, neither of these studies specifically examined current vs past use of oral contraceptives.…”

“…However, these findings were based on a relatively small number of cases, and another cohort study found no excess risk (Adam et al, 1981). Subsequent case -control and cohort studies (Bain et al, 1982;Holly et al, 1983Holly et al, , 1995Holman et al, 1984;Helmrich et al, 1984;Beral et al, 1984;Gallagher et al, 1985;Green and Bain, 1985;Østerlind et al, 1988;Zanetti et al, 1990;Hannaford et al, 1991;Le et al, 1992;Palmer et al, 1992;Westerdahl et al, 1996;Gefeller et al, 1998;Smith et al, 1998;Feskanich et al, 1999) provided little evidence of an overall excess risk among ever users compared to never users, but a possible increase among long-term users (summarised in (Prentice and Thomas, 1987)). More recently, data from the Nurse's Health Studies indicated a risk of melanoma related to duration of oral contraceptive use, but only among current users (Feskanich et al, 1999).…”

The specific activation of gadd45 following UVB radiation requires the POU family gene product N-oct3 in human melanoma cells

“…Experimental studies performed on animals have revealed that UVA can participate in the induction of melanomas (Setlow et al, 1989;Wolf et al, 1994). Furthermore, epidemiological data have shown that exposition to UVA constitutes a risk factor for melanoma (Wang et al, 2001;Westerdahl et al, 2000). UVB also trigger an oxidative reaction, but they predominantly produce DNA lesions (cyclobutane pyrimidine dimers and pyrimidine (6 ± 4) pyrimidone photoproducts) which are recognized by the nucleotide excision repair system.…”