Linked Life Data

12203792

Source:http://linkedlifedata.com/resource/pubmed/id/12203792

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-8-30
pubmed:abstractText
Germline mutations in the tumor-suppressor gene PTEN (MMAC1, TEP1) are found in Cowden syndrome, which predisposes to hamartomas, breast cancer, trichilemmomas, and thyroid tumors of follicular epithelium. PTEN has also been found to be somatically deleted, mutated, and/or silenced in various sporadically occurring cancers such as glioblastoma, breast cancer, kidney cancer, malignant melanoma, and endometrial cancer. Loss or reduction of PTEN protein expression as well as inappropriate subcellular compartmentalization is seen in non-medullary thyroid cancers. However, although allelic loss of the PTEN locus in 10q23.3 is frequently seen, this is not coupled with mutations in the PTEN gene. To approach further the frequency and mechanism behind PTEN silencing, we screened a panel of 87 sporadic thyroid tumors for PTEN mRNA expression, including 14 anaplastic carcinomas, 37 follicular carcinomas, 21 atypical adenomas, and 15 ordinary adenomas. Complete loss of PTEN mRNA expression was evident in six of the tumors, including four anaplastic carcinomas, one widely invasive carcinoma, and one ordinary adenoma. The transcriptional silencing of PTEN was significantly associated with the anaplastic subtype, suggesting that PTEN is involved in the carcinogenesis of highly malignant or late-stage thyroid cancers, whereas this particular mechanism appears to be of minor importance in differentiated follicular thyroid tumors. No association was observed between the expression, loss of heterozygosity, and mutation status in the 33 cases in which these parameters were compared. This indicates that PTEN silencing is a result of a wide variety of epigenetic and/or structural silencing mechanisms rather than a consequence of structural biallelic inactivation of the classical type. Furthermore, the high rate of alterations in the 10q23 region might indicate the presence of an as-yet unknown tumor-suppressor gene with an important role in the development of thyroid tumors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1045-2257
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
74-80
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12203792-Adenoma, pubmed-meshheading:12203792-Adult, pubmed-meshheading:12203792-Aged, pubmed-meshheading:12203792-Aged, 80 and over, pubmed-meshheading:12203792-Female, pubmed-meshheading:12203792-Gene Expression Regulation, Neoplastic, pubmed-meshheading:12203792-Gene Silencing, pubmed-meshheading:12203792-Genes, Tumor Suppressor, pubmed-meshheading:12203792-Germ-Line Mutation, pubmed-meshheading:12203792-Humans, pubmed-meshheading:12203792-Loss of Heterozygosity, pubmed-meshheading:12203792-Male, pubmed-meshheading:12203792-Middle Aged, pubmed-meshheading:12203792-Neoplasm Invasiveness, pubmed-meshheading:12203792-PTEN Phosphohydrolase, pubmed-meshheading:12203792-Phosphoric Monoester Hydrolases, pubmed-meshheading:12203792-Thyroid Neoplasms, pubmed-meshheading:12203792-Tumor Suppressor Proteins
pubmed:year
2002
pubmed:articleTitle
Silencing of the PTEN tumor-suppressor gene in anaplastic thyroid cancer.
pubmed:affiliation
Department of Molecular Medicine, Karolinska Hospital, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't