Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-7-19
pubmed:abstractText
Cisplatin-induced apoptosis in epithelial ovarian cancer cells is in part a consequence of suppressed Xiap expression and upregulation of the Fas/FasL system. Changes in the expression of these 'cell death' and 'cell survival' genes lead to activation of caspase-3, and cleavage of MDM2 and FAK. Failure of cancer cells to maintain a balance in the expression of these genes in favor of apoptotic cell death may be an important factor of chemoresistance. Xiap may be a novel target for gene therapy of human ovarian epithelial cancer and, dependent on P53 status, expression of Xiap antisense alone or in combination with wild-type P53 sense may offer a new approach for the treatment of the chemoresistant cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1422-4933
pubmed:author
pubmed:copyrightInfo
Copyright 2000 S. Karger AG, Basel
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
122-30
pubmed:dateRevised
2008-5-14
pubmed:meshHeading
pubmed:articleTitle
Apoptosis and chemoresistance in human ovarian cancer: is Xiap a determinant?
pubmed:affiliation
Department of Obstetrics and Gynaecology and Department of Cellular and Molecular Medicine, University of Ottawa, Loeb Health Research Institute, The Ottawa Hospital (Civic Campus), Canada.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't