Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 8171402

[Basalioma].

E Diem
View original source ↗Export metadata ↓

Abstract

The basal cell carcinoma (BCC) is one of the most frequent tumours. The entire destruction of the BCC is the aim of the therapy. The different methods of treatment have to respect the biological type, the histologic form of the BCC. Tumours at critical localizations (face, hands and feet) should be controlled microscopically, if the tumour has been excised totally. By the microscopic control fatal destructive recurrence can be avoided. The dermatologic treatment of BCC offers different methods in respect to the biological type and localization of BCC and also in respect to the age of the patient.

Explore related subjects

Basal Cell CarcinomaCombined Modality TherapyDiagnosis, DifferentialElectrosurgeryFacial NeoplasmsHumansSkinSkin NeoplasmsEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E Diem. 1993. [Basalioma].. https://pubmed.ncbi.nlm.nih.gov/8171402/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1999

The sebaceous nevus: a nevus with deletions of the PTCH gene.

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.

Basal Cell Carcinoma↗