Papillomavirus, p53 Alteration, and Primary Carcinoma of the Vulva
| Autor: | Franco Rilke, M. Giarola, A. Longoni, Lucia D'Amato, De Palo G, Della Torre G, S. Pilotti, R. Donghi, M.A. Pierotti, Giuseppe Sampietro |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Adult
Pathology medicine.medical_specialty Vulvar Squamous Cell Carcinoma Molecular Sequence Data In situ hybridization Gene mutation Biology Pathology and Forensic Medicine law.invention law Proto-Oncogene Proteins Carcinoma medicine Humans Point Mutation Papillomaviridae Molecular Biology Polymorphism Single-Stranded Conformational Polymerase chain reaction Aged Neoplasm Staging Southern blot Base Sequence Vulvar Neoplasms Carcinoma in situ Papillomavirus Infections Cell Biology Middle Aged Genes p53 Uterine Cervical Dysplasia medicine.disease Immunohistochemistry Neoplasm Proteins Tumor Virus Infections Lymphatic Metastasis DNA Viral Carcinoma Squamous Cell Female Vulvar Carcinoma Tumor Suppressor Protein p53 |
| Zdroj: | Scopus-Elsevier Europe PubMed Central |
| ISSN: | 1052-9551 |
| Popis: | Twenty-nine samples from 28 cases of vulvar squamous cell carcinoma, of which 13 fulfilled the criteria of the bowenoid subtype (mean age 45 years, range 31-68) and 16 of the usual subtype of invasive squamous cell carcinoma (ISCC) (mean age 67.5 years, range 34-83) were investigated for human papillomavirus (HPV) DNA, TP53 alterations, and mdm2 and bcl-2 gene product deregulation. Microscopically all the bowenoid subtype cases (group I) showed a high-grade intraepithelial (VIN 3, carcinoma in situ) lesion associated with early invasive carcinoma in six cases and overt invasive carcinoma in one. By contrast, no evidence of early carcinoma was present in the ISCCs (group II). By in situ hybridization and/or Southern blot hybridization or polymerase chain reaction (PCR), HPV DNA was detected in all cases of group I and in four of 16 cases (25%) of group II, two only by Southern blot after PCR. By single-strand conformation polymorphism and immunocytochemistry only wild-type TP53 and absence of detectable p53 product, respectively, were found in all cases of group I, i.e., in high-risk HPV-positive carcinomas, whereas mutations and/or p53 overexpression accounted for 75% in group II, i.e., in mainly HPV-negative carcinomas. The TP53 gene mutations observed in invasive carcinomas were significantly related to node-positive cases (p = 0.04). Taken together and in agreement with in vitro data, these results support the view that an alteration of TP53, gained either by interaction with viral oncoproteins or by somatic mutations, is a crucial event in the pathogenesis of vulvar carcinomas, but that TP53 mutations are mainly associated with disease progression. Finally, a preliminary immunocytochemical analysis seems to speak against the possible involvement of both MDM2 and BCL-2 gene products in the development of vulvar carcinoma. |
| Databáze: | OpenAIRE |
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