File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Cisplatin-induced p53-independent growth arrest and cell death in cancer cells.

TitleCisplatin-induced p53-independent growth arrest and cell death in cancer cells.
Authors
Issue Date1999
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/
Citation
International Journal Of Oncology, 1999, v. 15 n. 6, p. 1097-1102 How to Cite?
AbstractIn a recent study, it was shown that DNA damaging agent cisplatin-induced growth arrest and cell death in cancer cells by a pathway sharing some of the characteristics of replicative senescence. The aim of this study was to determine the role of p53, p21WAF1 and p16INK4A proteins in this alternative route to cancer cell death in additional human cancer cell lines. After exposure to cisplatin, all the cell lines underwent growth arrest and expressed the senescence marker senescence-associated beta-galactosidase, but showed none of the features of apoptosis. However, there was no change in p53 protein expression, and neither p21WAF1 nor p16INK4A was expressed before or up to 4 days after cisplatin exposure. These findings provide further evidence that cells carrying mutations resulting in loss of function in the p53 gene can be killed by cisplatin via a p53-independent route with some similarities to replicative senescence, but not apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/67471
ISSN
2015 Impact Factor: 3.018
2015 SCImago Journal Rankings: 1.270
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorChow, LSen_HK
dc.contributor.authorWong, SCen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorKwong, DLen_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorSham, JSen_HK
dc.contributor.authorNicholls, JMen_HK
dc.date.accessioned2010-09-06T05:55:26Z-
dc.date.available2010-09-06T05:55:26Z-
dc.date.issued1999en_HK
dc.identifier.citationInternational Journal Of Oncology, 1999, v. 15 n. 6, p. 1097-1102en_HK
dc.identifier.issn1019-6439en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67471-
dc.description.abstractIn a recent study, it was shown that DNA damaging agent cisplatin-induced growth arrest and cell death in cancer cells by a pathway sharing some of the characteristics of replicative senescence. The aim of this study was to determine the role of p53, p21WAF1 and p16INK4A proteins in this alternative route to cancer cell death in additional human cancer cell lines. After exposure to cisplatin, all the cell lines underwent growth arrest and expressed the senescence marker senescence-associated beta-galactosidase, but showed none of the features of apoptosis. However, there was no change in p53 protein expression, and neither p21WAF1 nor p16INK4A was expressed before or up to 4 days after cisplatin exposure. These findings provide further evidence that cells carrying mutations resulting in loss of function in the p53 gene can be killed by cisplatin via a p53-independent route with some similarities to replicative senescence, but not apoptosis.en_HK
dc.languageengen_HK
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/en_HK
dc.relation.ispartofInternational journal of oncologyen_HK
dc.subject.meshAntineoplastic Agents - pharmacology-
dc.subject.meshCell Death - drug effects-
dc.subject.meshCell Division - drug effects-
dc.subject.meshCisplatin - pharmacology-
dc.subject.meshTumor Suppressor Protein p53 - drug effects - metabolism - physiology-
dc.titleCisplatin-induced p53-independent growth arrest and cell death in cancer cells.en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1019-6439&volume=15&issue=6&spage=1097&epage=1102&date=1999&atitle=Cisplatin-induced+p53-independent+growth+arrest+and+cell+death+in+cancer+cellsen_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailKwong, DL:dlwkwong@hku.hken_HK
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityKwong, DL=rp00414en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10568814-
dc.identifier.scopuseid_2-s2.0-0033451038en_HK
dc.identifier.hkuros47688en_HK
dc.identifier.volume15en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1097en_HK
dc.identifier.epage1102en_HK
dc.identifier.isiWOS:000083902400007-
dc.publisher.placeGreeceen_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridLiu, Y=26643293600en_HK
dc.identifier.scopusauthoridChow, LS=7202533094en_HK
dc.identifier.scopusauthoridWong, SC=36631358800en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridKwong, DL=15744231600en_HK
dc.identifier.scopusauthoridWang, J=7701342266en_HK
dc.identifier.scopusauthoridSham, JS=7101655565en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats