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Article: Epigenetic inactivation of INK4/CDK/RB cell cycle pathway in acute leukemias

TitleEpigenetic inactivation of INK4/CDK/RB cell cycle pathway in acute leukemias
Authors
Issue Date2003
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00277/index.htm
Citation
Annals Of Hematology, 2003, v. 82 n. 12, p. 738-742 How to Cite?
AbstractDysregulation of cell cycle is important in oncogenesis. We analyzed the inactivation of the INK4 family CKI/CDK/RB pathway by gene promoter hypermethylation in leukemogenesis. The methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) alleles of the p15, p16, p18, and RB genes was used to study five leukemic cell lines, 50 acute myeloid leukemia (AML) and 25 acute lymphoblastic leukemia (ALL) samples. None of the leukemic cell lines showed p18 and RB methylation. p15 was methylated in Raji, while p16 was methylated in U937 and Raji. In NB4 and Jurkat, both alleles of p15 and p16 appeared to be deleted. At diagnosis, p15 methylation occurred in 29 (58%) AML patients, and 10 (40.0%) ALL patients. p16 methylation occurred in two (4%) AML and two (8%) ALL patients. Only one each of AML and ALL patients had concurrent p15 and p16 methylation. None of the patients had methylation of p18 or RB. In AML, p15 methylation was associated with M2 subtype (p=0.018). Patients with and without p15 methylation had similar complete remission (CR) rates and projected 5-year overall survival (OS) or disease-free survival (DFS). Therefore, methylation inactivation of the INK4/CDK/RB pathway in leukemia involved primarily p15 and occasionally p16, but not p18 or RB. In AML, p15 gene methylation was associated with the M2 subtype, but was not prognostic for CR, OS, or DFS.
Persistent Identifierhttp://hdl.handle.net/10722/76482
ISSN
2015 Impact Factor: 3.022
2015 SCImago Journal Rankings: 1.117
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorWong, ASYen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:21:42Z-
dc.date.available2010-09-06T07:21:42Z-
dc.date.issued2003en_HK
dc.identifier.citationAnnals Of Hematology, 2003, v. 82 n. 12, p. 738-742en_HK
dc.identifier.issn0939-5555en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76482-
dc.description.abstractDysregulation of cell cycle is important in oncogenesis. We analyzed the inactivation of the INK4 family CKI/CDK/RB pathway by gene promoter hypermethylation in leukemogenesis. The methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) alleles of the p15, p16, p18, and RB genes was used to study five leukemic cell lines, 50 acute myeloid leukemia (AML) and 25 acute lymphoblastic leukemia (ALL) samples. None of the leukemic cell lines showed p18 and RB methylation. p15 was methylated in Raji, while p16 was methylated in U937 and Raji. In NB4 and Jurkat, both alleles of p15 and p16 appeared to be deleted. At diagnosis, p15 methylation occurred in 29 (58%) AML patients, and 10 (40.0%) ALL patients. p16 methylation occurred in two (4%) AML and two (8%) ALL patients. Only one each of AML and ALL patients had concurrent p15 and p16 methylation. None of the patients had methylation of p18 or RB. In AML, p15 methylation was associated with M2 subtype (p=0.018). Patients with and without p15 methylation had similar complete remission (CR) rates and projected 5-year overall survival (OS) or disease-free survival (DFS). Therefore, methylation inactivation of the INK4/CDK/RB pathway in leukemia involved primarily p15 and occasionally p16, but not p18 or RB. In AML, p15 gene methylation was associated with the M2 subtype, but was not prognostic for CR, OS, or DFS.en_HK
dc.languageengen_HK
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00277/index.htmen_HK
dc.relation.ispartofAnnals of Hematologyen_HK
dc.subject.meshAcute Diseaseen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshCell Cycle - geneticsen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor Proteins - geneticsen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p15 - geneticsen_HK
dc.subject.meshCyclin-Dependent Kinases - geneticsen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshEpigenesis, Geneticen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Myeloid - diagnosis - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPrecursor Cell Lymphoblastic Leukemia-Lymphoma - diagnosis - geneticsen_HK
dc.subject.meshPrognosisen_HK
dc.subject.meshRetinoblastoma Protein - geneticsen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSignal Transduction - geneticsen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshU937 Cellsen_HK
dc.titleEpigenetic inactivation of INK4/CDK/RB cell cycle pathway in acute leukemiasen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0939-5555&volume=82&issue=12&spage=738&epage=42&date=2003&atitle=Epigenetic+inactivation+of+INK4/CDK/RB+cell+cycle+pathway+in+acute+leukemiasen_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.doi10.1007/s00277-003-0744-8en_HK
dc.identifier.pmid14513284-
dc.identifier.scopuseid_2-s2.0-0348149013en_HK
dc.identifier.hkuros88702en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0348149013&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume82en_HK
dc.identifier.issue12en_HK
dc.identifier.spage738en_HK
dc.identifier.epage742en_HK
dc.identifier.isiWOS:000186952800002-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridWong, ASY=7403144356en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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