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Article: Absence of p300 gene promoter methylation in acute leukemia

TitleAbsence of p300 gene promoter methylation in acute leukemia
Authors
Issue Date2004
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergene
Citation
Cancer Genetics And Cytogenetics, 2004, v. 150 n. 2, p. 164-167 How to Cite?
Abstractp300 is a widely expressed transcriptional coactivator, and is involved in DNA repair, cell growth, differentiation, and apoptosis. Recent data suggest that it may function as a tumor suppressor. We investigated the frequency of aberrant methylation of p300 promoter in seven leukemic cell lines, as well as in the diagnostic samples of 46 patients with acute myelocytic leukemia (11 with M1, 22 with M2, 3 with M4, and 1 with M5), 24 patients with acute promyelocytic leukemia, and 22 patients with acute lymphoblastic leukemia (3 with T-cell, 1 with pre-B, 2 with Burkitt, 2 with early B-precursors, and 14 with common). None of the cell lines and patient samples showed p300 gene methylation. Therefore, hypermethylation of p300 is not an important mechanism in leukemogenesis. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76565
ISSN
2012 Impact Factor: 1.929
2013 SCImago Journal Rankings: 0.872
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorWong, ASYen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:22:35Z-
dc.date.available2010-09-06T07:22:35Z-
dc.date.issued2004en_HK
dc.identifier.citationCancer Genetics And Cytogenetics, 2004, v. 150 n. 2, p. 164-167en_HK
dc.identifier.issn0165-4608en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76565-
dc.description.abstractp300 is a widely expressed transcriptional coactivator, and is involved in DNA repair, cell growth, differentiation, and apoptosis. Recent data suggest that it may function as a tumor suppressor. We investigated the frequency of aberrant methylation of p300 promoter in seven leukemic cell lines, as well as in the diagnostic samples of 46 patients with acute myelocytic leukemia (11 with M1, 22 with M2, 3 with M4, and 1 with M5), 24 patients with acute promyelocytic leukemia, and 22 patients with acute lymphoblastic leukemia (3 with T-cell, 1 with pre-B, 2 with Burkitt, 2 with early B-precursors, and 14 with common). None of the cell lines and patient samples showed p300 gene methylation. Therefore, hypermethylation of p300 is not an important mechanism in leukemogenesis. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/cancergeneen_HK
dc.relation.ispartofCancer Genetics and Cytogeneticsen_HK
dc.rightsCancer Genetics and Cytogenetics. Copyright © Elsevier Inc.en_HK
dc.subject.meshApoptosis - geneticsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshBone Marrow Cells - cytology - pathologyen_HK
dc.subject.meshCell Differentiation - geneticsen_HK
dc.subject.meshCell Division - geneticsen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA Primersen_HK
dc.subject.meshDNA Repair - geneticsen_HK
dc.subject.meshDNA, Neoplasm - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Myeloid, Acute - genetics - pathologyen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshNeoplasm Proteins - geneticsen_HK
dc.subject.meshNuclear Proteins - geneticsen_HK
dc.subject.meshPrecursor Cell Lymphoblastic Leukemia-Lymphoma - genetics - pathologyen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshReference Valuesen_HK
dc.subject.meshSequence Deletionen_HK
dc.subject.meshTrans-Activators - geneticsen_HK
dc.titleAbsence of p300 gene promoter methylation in acute leukemiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0165-4608&volume=150&spage=164&epage=7&date=2004&atitle=Absence+of+p300+gene+promoter+methylation+in+acute+leukemiaen_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cancergencyto.2003.09.006en_HK
dc.identifier.pmid15066326-
dc.identifier.scopuseid_2-s2.0-1842506364en_HK
dc.identifier.hkuros87930en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1842506364&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume150en_HK
dc.identifier.issue2en_HK
dc.identifier.spage164en_HK
dc.identifier.epage167en_HK
dc.identifier.isiWOS:000221025300010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridWong, ASY=7403144356en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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