PubMed · 9844267
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T Jansen, S Müller, P Kaudewitz, G Plewig. 1998-10-10. [Basalioma].. https://pubmed.ncbi.nlm.nih.gov/9844267/
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A case of vulvar basocellular carcinoma in a 49-year-old woman is presented. The treatment of choice is local excision and the prognosis in general is excellent. The importance of taking biopsies from atypical vulvar lesions is underlined.
Sebaceous nevi (SN) are congenital malformations of the skin with the potential to develop into basal cell carcinoma (BCC). To date, the molecular basis for their carcinogenic potential remains unknown. The genetic defect in BCC is known and involves the human homologue of Drosophila patched (PTCH) on chromosome 9q22.3. The objective of this study was to test whether allelic deletion of the PTCH gene could already be detected in SN. Twenty-one paraffin-embedded SN were investigated in this study. Basaloid cells in conjunction with mature sebaceous glands as well as epidermal layer apart from SN were microdissected and subjected to single-step DNA extraction. We performed the analysis with polymorphic markers at 9q22.3 (D9S15, D9S252, D9S287, and D9S303). Of the 20 informative SN, 8 (40%) exhibited loss of heterozygosity at least at one locus. Here, we provide the first evidence of the involvement of the tumor suppressor gene PTCH in SN. Whether PTCH deletion in SN is associated with progression to BCC and/or other appendageal tumors should be addressed in future studies.
Two main distinct subtypes of epithelial skin cancers can be distinguished, both arising from keratinocytes, most frequently at sun-exposed body sites. Basal cell carcinomas (BCC) grow slowly, nearly never metastases, whereas squamous carcinomas (SCC) are locally more invasive tumors, which have a greater metastatic potential. Skin carcinogenesis is a multiple step process, in which UV light play a major role. Numerous genetic lesions occur, either inactivating tumor suppressor genes (which normally repress cell growth), or activating oncogenes (which promote cellular multiplication). The most important tumor suppressor gene involved in both skin neoplasms is p53, which is inactivated in 40-50% of cases, by specific UV induced mutations. Yet, some differences exist between these two subtypes, which could explain their difference in invasiveness.