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Article: Localization of hRad9 in breast cancer

TitleLocalization of hRad9 in breast cancer
Authors
Issue Date2008
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/
Citation
Bmc Cancer, 2008, v. 8 How to Cite?
AbstractBackground: hRad9 is a cell cycle checkpoint gene that is up-regulated in breast cancer. We have previously shown that the mRNA up-regulation correlated with tumor size and local recurrence. Immunohistochemical studies were made to better define the role of hRad9 in breast carcinogenesis. Methods: Localisation of hRad9 protein were performed on paired tumor and normal breast tissues. Immunoblotting with and without dephosphorylation was used to define the protein isolated from breast cancer cells. Results: Increased hRad9 protein was observed in breast cancer cells nucleus compared to non-tumor epithelium. This nuclear protein existed in hyperphosphorylated forms which may be those of the hRad9-hRad1-hHus1 complex. Conclusion: Finding of hyperphosphorylated forms of hRad9 in the nucleus of cancer cells is in keeping with its function in ameliorating DNA instability, whereby it inadvertently assists tumor growth. © 2008 Chan et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/59352
ISSN
2015 Impact Factor: 3.265
2015 SCImago Journal Rankings: 1.627
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, Ven_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorWong, MSen_HK
dc.contributor.authorLau, Ken_HK
dc.contributor.authorSuen, Den_HK
dc.contributor.authorLi, Gen_HK
dc.contributor.authorKwong, Aen_HK
dc.contributor.authorChan, TKen_HK
dc.date.accessioned2010-05-31T03:48:16Z-
dc.date.available2010-05-31T03:48:16Z-
dc.date.issued2008en_HK
dc.identifier.citationBmc Cancer, 2008, v. 8en_HK
dc.identifier.issn1471-2407en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59352-
dc.description.abstractBackground: hRad9 is a cell cycle checkpoint gene that is up-regulated in breast cancer. We have previously shown that the mRNA up-regulation correlated with tumor size and local recurrence. Immunohistochemical studies were made to better define the role of hRad9 in breast carcinogenesis. Methods: Localisation of hRad9 protein were performed on paired tumor and normal breast tissues. Immunoblotting with and without dephosphorylation was used to define the protein isolated from breast cancer cells. Results: Increased hRad9 protein was observed in breast cancer cells nucleus compared to non-tumor epithelium. This nuclear protein existed in hyperphosphorylated forms which may be those of the hRad9-hRad1-hHus1 complex. Conclusion: Finding of hyperphosphorylated forms of hRad9 in the nucleus of cancer cells is in keeping with its function in ameliorating DNA instability, whereby it inadvertently assists tumor growth. © 2008 Chan et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/en_HK
dc.relation.ispartofBMC Canceren_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsB M C Cancer. Copyright © BioMed Central Ltd.en_HK
dc.subject.meshBreast Neoplasms - genetics - pathology-
dc.subject.meshCarcinoma - genetics - pathology-
dc.subject.meshCell Cycle Proteins - biosynthesis - genetics-
dc.subject.meshCell Transformation, Neoplastic - genetics-
dc.subject.meshDNA Repair - genetics-
dc.titleLocalization of hRad9 in breast canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1471-2407&volume=8&issue=196&spage=&epage=&date=2008&atitle=Localization+of+hRad9+in+breast+canceren_HK
dc.identifier.emailChan, V: vnychana@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.emailKwong, A: avakwong@hkucc.hku.hken_HK
dc.identifier.authorityChan, V=rp00320en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.identifier.authorityKwong, A=rp01734en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/1471-2407-8-196en_HK
dc.identifier.pmid18616832-
dc.identifier.pmcidPMC2483722-
dc.identifier.scopuseid_2-s2.0-48449093045en_HK
dc.identifier.hkuros163299en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48449093045&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.issue196-
dc.identifier.isiWOS:000258101300001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, V=7202654865en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridWong, MS=37021126000en_HK
dc.identifier.scopusauthoridLau, K=36722695800en_HK
dc.identifier.scopusauthoridSuen, D=8876971300en_HK
dc.identifier.scopusauthoridLi, G=15034790200en_HK
dc.identifier.scopusauthoridKwong, A=8913654300en_HK
dc.identifier.scopusauthoridChan, TK=7402687762en_HK
dc.identifier.citeulike2996043-

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