Linked Life Data

9737787

Source:http://linkedlifedata.com/resource/pubmed/id/9737787

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-9-25
pubmed:abstractText
There is evidence that ovarian cancer may be derived from the progressive transformation of benign and/or borderline tumours. Mutations involving different oncogenes and tumour suppressor genes accumulate during the process of malignant transformation, and the alterations of genes involved in the pathogenesis of familial ovarian cancer are probably early events in ovarian tumorigenesis. BRCA-1 and BRCA-2 act as classical tumour suppressor genes in hereditary tumours, but their role in sporadic tumours remains controversial; however, a high frequency of allele losses in BRCA-1 (17q) and BRCA-2 (13q) loci has been observed in both familial and sporadic tumours. The possible role of mismatch repair genes and microsatellite instability is also controversial, but a role for them has been proposed in borderline tumours. Mutations in K-ras are specific for mucinous tumours and may be related to mucinous differentiation. Finally, a role in tumour progression has been proposed for both c-erb B-2 and p53, but their practical value in prognosis remains questionable.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0945-6317
pubmed:author
pubmed:issnType
Print
pubmed:volume
433
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
103-11
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Molecular pathology of ovarian carcinomas.
pubmed:affiliation
Department of Pathology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Spain.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't