Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
2001-1-11
pubmed:abstractText
Loss of heterozygosity (LOH) at locus 10q23.3 and mutation of the PTEN tumor suppressor gene occur frequently in both endometrial carcinoma and ovarian endometrioid carcinoma. To investigate the potential role of the PTEN gene in the carcinogenesis of ovarian endometrioid carcinoma and its related subtype, clear cell carcinoma, we examined 20 ovarian endometrioid carcinomas, 24 clear cell carcinomas, and 34 solitary endometrial cysts of the ovary for LOH at 10q23.3 and point mutations within the entire coding region of the PTEN gene. LOH was found in 8 of 19 ovarian endometrioid carcinomas (42.1%), 6 of 22 clear cell carcinomas (27.3%), and 13 of 23 solitary endometrial cysts (56.5%). In 5 endometrioid carcinomas synchronous with endometriosis, 3 cases displayed LOH events common to both the carcinoma and the endometriosis, 1 displayed an LOH event in only the carcinoma, and 1 displayed no LOH events in either lesion. In 7 clear cell carcinomas synchronous with endometriosis, 3 displayed LOH events common to both the carcinoma and the endometriosis, 1 displayed an LOH event in only the carcinoma, and 3 displayed no LOH events in either lesion. In no cases were there LOH events in the endometriosis only. Somatic mutations in the PTEN gene were identified in 4 of 20 ovarian endometrioid carcinomas (20.0%), 2 of 24 clear cell carcinomas (8.3%), and 7 of 34 solitary endometrial cysts (20.6%). These results indicate that inactivation of the PTEN tumor suppressor gene is an early event in the development of ovarian endometrioid carcinoma and clear cell carcinoma of the ovary.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7052-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11156411-Adenocarcinoma, Clear Cell, pubmed-meshheading:11156411-Carcinoma, Endometrioid, pubmed-meshheading:11156411-Chromosomes, Human, Pair 10, pubmed-meshheading:11156411-Disease Progression, pubmed-meshheading:11156411-Endometrial Neoplasms, pubmed-meshheading:11156411-Female, pubmed-meshheading:11156411-Humans, pubmed-meshheading:11156411-Lasers, pubmed-meshheading:11156411-Loss of Heterozygosity, pubmed-meshheading:11156411-Microsatellite Repeats, pubmed-meshheading:11156411-Models, Genetic, pubmed-meshheading:11156411-Mutation, pubmed-meshheading:11156411-Ovarian Neoplasms, pubmed-meshheading:11156411-PTEN Phosphohydrolase, pubmed-meshheading:11156411-Phosphoric Monoester Hydrolases, pubmed-meshheading:11156411-Polymorphism, Single-Stranded Conformational, pubmed-meshheading:11156411-Sequence Analysis, DNA, pubmed-meshheading:11156411-Tumor Suppressor Proteins
pubmed:year
2000
pubmed:articleTitle
Loss of heterozygosity on 10q23.3 and mutation of the tumor suppressor gene PTEN in benign endometrial cyst of the ovary: possible sequence progression from benign endometrial cyst to endometrioid carcinoma and clear cell carcinoma of the ovary.
pubmed:affiliation
Department of Obstetrics and Gynecology, Universitv of Tsukuba, Ibaraki, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't