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Titolo:
SEBACEOUS CARCINOMA - TUMOR PROGRESSION THROUGH MUTATIONAL INACTIVATION OF P53
Autore:
GONZALEZFERNANDEZ F; KALTREIDER SA; PATNAIK BD; RETIEF JD; BAO YD; NEWMAN S; STOLER MH; LEVINE PA;
Indirizzi:
UNIV VIRGINIA,HLTH SCI CTR,DEPT OPHTHALMOL,COBB HALL,ROOM B032 CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,DEPT NEUROPATHOL CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,GRAD PROGRAM NEUROSCI CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,DEPT MICROBIOL CHARLOTTESVILLE VA 22908 UNIV VIRGINIA,HLTH SCI CTR,DEPT OTOLARYNGOL CHARLOTTESVILLE VA 22908
Titolo Testata:
Ophthalmology
fascicolo: 3, volume: 105, anno: 1998,
pagine: 497 - 506
SICI:
0161-6420(1998)105:3<497:SC-TPT>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLAND CARCINOMA; GENE MUTATION; HUMAN PAPILLOMAVIRUS; SUPPRESSOR GENE; OCULAR ADNEXA; BREAST-CANCER; SKIN-CANCER; CELL-CYCLE; DNA; APOPTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
63
Recensione:
Indirizzi per estratti:
Citazione:
F. Gonzalezfernandez et al., "SEBACEOUS CARCINOMA - TUMOR PROGRESSION THROUGH MUTATIONAL INACTIVATION OF P53", Ophthalmology, 105(3), 1998, pp. 497-506

Abstract

Background: Sebaceous carcinoma may masquerade for years as an inflammatory condition, In many cases, this may be because of the presence of longstanding intraepithelial disease (e.g., dysplasia or carcinoma in situ), which eventually progresses to invasive carcinoma recognized through tumefaction and a worsening clinical presentation, The mechanism for this tumor progression is unknown, In the Far East, human papilloma virus (HPV) has been suggested to play a role in the development of sebaceous carcinoma by inactivating tumor suppressor gene p53, Here, the authors explore the molecular basis of the progression of ocularsebaceous carcinoma. Methods: Cases of sebaceous carcinoma seen at the University of Virginia, Department of Ophthalmology, during the period from 1989 to 1996 were analyzed for HPV infection by in situ hybridization and polymerase chain reaction, The expression of p53, p21(WAF-1), Bcl-2, and epithelial membrane antigen was examined by immunohistochemistry, In one of the cases, frozen tumor was available, allowing exons 5 through 9 of the p53 gene to be sequenced. Results: Seven caseswere identified, all of which were from women. All were negative for HPV, In cases in which disease was restricted to dysplasia (carcinoma in situ), p53 but not p21(WAF-1) was negative, In contrast, cases thatcontained a component of invasive or metastatic carcinoma showed striking hyperexpression of nuclear p53 in all of the malignant cells, In one of these cases, a G:C --> T:A transversion was found in the p53 gene, This mutation, characteristic of bulky carcinogens, substituted phenylalanine for cysteine 277, a residue that participates in hydrogen bonding to the p53 DNA binding consensus sequence. Conclusions: Mutational inactivation of p53 may be involved in the progression of sebaceous carcinoma.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/09/20 alle ore 09:03:18