Pregled bibliografske jedinice broj: 83319
Patched in development malformations and cancer. Alterations of Patched in ovarian fibromas and non inflammatory cysts
Patched in development malformations and cancer. Alterations of Patched in ovarian fibromas and non inflammatory cysts // Abstracts of the 17th meeting of the European Association for Cancer Research : u: Revista de Oncología 44 (2202) (1) / Jimenez, Miguel Martin (ur.).
Madrid: FESEO ; INCAN, 2002. str. 46-46 (poster, nije recenziran, sažetak, znanstveni)
CROSBI ID: 83319 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Patched in development malformations and cancer. Alterations of Patched in ovarian fibromas and non inflammatory cysts
Autori
Levanat, Sonja ; Crnić, Ivana ; Orešković, Slavko ; Musani, Vesna ; Komar, Arijana ; Babić, Darko
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Abstracts of the 17th meeting of the European Association for Cancer Research : u: Revista de Oncología 44 (2202) (1)
/ Jimenez, Miguel Martin - Madrid : FESEO ; INCAN, 2002, 46-46
Skup
Meeting of the European Association for Cancer Research (17 ; 2002)
Mjesto i datum
Granada, Španjolska, 08.06.2002. - 11.06.2002
Vrsta sudjelovanja
Poster
Vrsta recenzije
Nije recenziran
Ključne riječi
signaling; Patched; development; cancer
Sažetak
Constitutional hemizygous inactivation of PTCH, the Shh/Ptch signaling pathway gene, which moderates Shh signalling, manifests itself as Nevoid Basal Cell Carcinoma Syndrome (NBCCS), a condition variably characterized by developmental disorders and malformations, and by predisposition to certain malignancies. The PTCH gene, a human homologue of the Drosophila segment polarity gene patched, maps to chromosome 9q22.3 and loss of heterozygosity (LOH) at this site in both sporadic and hereditary basal cell carcinomas, meduloblastomas and ovarian fibromas suggests that it functions as a tumor suppressor. We used DNA from fresh tissues and blood leukocytes, which were typed for several short tandem repeat polymorphism's at 9q21-q31, and SSCP of PTCH exons, analyzing variability in PTCH exons. PCR reactions were performed and products were fractionated on 5 - 8 % polyacrylamide gels. We found LOH in sporadic basocellular carcinomas in more than 70 % of cases and in 30 % of ovarian fibromas. So far we detected in more than 60 % of cases that the cyst lining of jaws loses the normal copy of the PTCH while retaining the mutant copy. Our studies of LOH in sporadic ovarian fibromas and noninflammatory cysts, and aberrant SSCP pattern for PTCH exons, contribute to the ptch role in their genesis. More generally, PTCH alterations may prove to be a necessary, and perhaps the initiating event, in formation and growth of various noninflammatory cysts, especially with our observations of incomplete heterozygosity which we interpreted as LOH in this region for ovarian dermoid cysts. This would be consistent with our view that local PTCH inactivation can, under predisposing circumstances, lead to persistent though not by itself truly aggressive cell proliferation.
Izvorni jezik
Engleski
Znanstvena područja
Kliničke medicinske znanosti
POVEZANOST RADA
Ustanove:
Institut "Ruđer Bošković", Zagreb
Profili:
Arijana Zorić
(autor)
Vesna Musani
(autor)
Ivana Crnić
(autor)
Sonja Levanat
(autor)
Slavko Orešković
(autor)