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Article: Correlation of AIB1 overexpression with advanced clinical stage of human colorectal carcinoma

TitleCorrelation of AIB1 overexpression with advanced clinical stage of human colorectal carcinoma
Authors
KeywordsAIB1
Amplification
Chromosome instability
Colorectal carcinoma
Immunohistochemistry
p53
Tissue microarray
Issue Date2005
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath
Citation
Human Pathology, 2005, v. 36 n. 7, p. 777-783 How to Cite?
AbstractAIB1, a member of the steroid receptor coactivator 1 family, has been cloned on 20q12 and is a candidate oncogene in human breast cancer. It is commonly amplified and overexpressed in several types of human cancers. In this study, we examined the expression of AIB1, as related to clinicopathologic features, in 85 human colorectal cancers (CRCs). The status of the number of AIB1 copies, p53 expression, and DNA ploidy was also analyzed. The overexpression of AIB1 was detected in 35% of CRCs. Amplification of AIB1 was observed in 10% of CRCs. In addition, the overexpression of AIB1 was observed more frequently in CRCs in later clinical stages (T3 N1 M0/T3 N0 2M1), compared with that in T3 N0 M0 stage (P < .05). These results suggest that overexpression of AIB1 might provide a selective advantage for the developmental growth and/or progression of subsets of CRCs. In addition, a significant correlation (P < .05) of overexpression of AIB1 with p53 overexpression as well as with aneuploid DNA content was observed in these CRCs. The overexpression of p53 was also correlated significantly with CRC DNA ploidy (P < .05). Furthermore, there was a substantial population of CRCs showing overexpression of both AIB1 and p53 protein and all had aneuploid DNA content; most of these were in the later clinical stage. These findings suggest a possible convergence of AIB1 with a pathway involving p53, which might induce chromosomal instability and affect the clinical phenotype of a subset of CRCs.
Persistent Identifierhttp://hdl.handle.net/10722/71996
ISSN
2023 Impact Factor: 2.7
2023 SCImago Journal Rankings: 0.936
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXie, Den_HK
dc.contributor.authorSham, JSTen_HK
dc.contributor.authorZeng, WFen_HK
dc.contributor.authorLin, HLen_HK
dc.contributor.authorBi, Jen_HK
dc.contributor.authorChe, LHen_HK
dc.contributor.authorHu, Len_HK
dc.contributor.authorZeng, YXen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-09-06T06:37:18Z-
dc.date.available2010-09-06T06:37:18Z-
dc.date.issued2005en_HK
dc.identifier.citationHuman Pathology, 2005, v. 36 n. 7, p. 777-783en_HK
dc.identifier.issn0046-8177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71996-
dc.description.abstractAIB1, a member of the steroid receptor coactivator 1 family, has been cloned on 20q12 and is a candidate oncogene in human breast cancer. It is commonly amplified and overexpressed in several types of human cancers. In this study, we examined the expression of AIB1, as related to clinicopathologic features, in 85 human colorectal cancers (CRCs). The status of the number of AIB1 copies, p53 expression, and DNA ploidy was also analyzed. The overexpression of AIB1 was detected in 35% of CRCs. Amplification of AIB1 was observed in 10% of CRCs. In addition, the overexpression of AIB1 was observed more frequently in CRCs in later clinical stages (T3 N1 M0/T3 N0 2M1), compared with that in T3 N0 M0 stage (P < .05). These results suggest that overexpression of AIB1 might provide a selective advantage for the developmental growth and/or progression of subsets of CRCs. In addition, a significant correlation (P < .05) of overexpression of AIB1 with p53 overexpression as well as with aneuploid DNA content was observed in these CRCs. The overexpression of p53 was also correlated significantly with CRC DNA ploidy (P < .05). Furthermore, there was a substantial population of CRCs showing overexpression of both AIB1 and p53 protein and all had aneuploid DNA content; most of these were in the later clinical stage. These findings suggest a possible convergence of AIB1 with a pathway involving p53, which might induce chromosomal instability and affect the clinical phenotype of a subset of CRCs.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpathen_HK
dc.relation.ispartofHuman Pathologyen_HK
dc.subjectAIB1-
dc.subjectAmplification-
dc.subjectChromosome instability-
dc.subjectColorectal carcinoma-
dc.subjectImmunohistochemistry-
dc.subjectp53-
dc.subjectTissue microarray-
dc.subject.meshAcetyltransferases - metabolismen_HK
dc.subject.meshAdenocarcinoma - genetics - metabolism - secondaryen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshAneuploidyen_HK
dc.subject.meshCell Nucleus - metabolism - pathologyen_HK
dc.subject.meshColorectal Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshDNA, Neoplasm - analysisen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGene Amplificationen_HK
dc.subject.meshHistone Acetyltransferasesen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoenzyme Techniquesen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshLymph Nodes - metabolism - pathologyen_HK
dc.subject.meshLymphatic Metastasis - pathologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNuclear Receptor Coactivator 3en_HK
dc.subject.meshOncogene Proteins - metabolismen_HK
dc.subject.meshProtein Array Analysisen_HK
dc.subject.meshTrans-Activators - metabolismen_HK
dc.subject.meshTumor Suppressor Protein p53 - metabolismen_HK
dc.titleCorrelation of AIB1 overexpression with advanced clinical stage of human colorectal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0046-8177&volume=36&issue=7&spage=777&epage=783&date=2005&atitle=Correlation+of+AIB1+overexpression+with+advanced+clinical+stage+of+human+colorectal+carcinomaen_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.humpath.2005.05.007en_HK
dc.identifier.pmid16084947-
dc.identifier.scopuseid_2-s2.0-23444449306en_HK
dc.identifier.hkuros100386en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23444449306&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume36en_HK
dc.identifier.issue7en_HK
dc.identifier.spage777en_HK
dc.identifier.epage783en_HK
dc.identifier.isiWOS:000231305800012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridSham, JST=7101655565en_HK
dc.identifier.scopusauthoridZeng, WF=8338623800en_HK
dc.identifier.scopusauthoridLin, HL=8950219500en_HK
dc.identifier.scopusauthoridBi, J=7103093361en_HK
dc.identifier.scopusauthoridChe, LH=7003959690en_HK
dc.identifier.scopusauthoridHu, L=34770075600en_HK
dc.identifier.scopusauthoridZeng, YX=7402981579en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.issnl0046-8177-

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