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Article: Epigenetic inactivation of the CIP/KIP cell-cycle control pathway in acute leukemias

TitleEpigenetic inactivation of the CIP/KIP cell-cycle control pathway in acute leukemias
Authors
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35105
Citation
American Journal Of Hematology, 2005, v. 80 n. 4, p. 282-287 How to Cite?
AbstractDysregulation of the cell cycle is important in oncogenesis. We analyzed the potential inactivation of the CIP/KIP family of the cyclin E/CDK/RB pathway by gene promoter hypermethylation in leukemias. The methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) alleles of the p21, p27, and p57 genes was used to study five leukemic cell lines, 50 acute myeloid leukemia (AML) samples, and 25 acute lymphoblastic leukemia (ALL) samples. p21 was hemizygously methylated in Raji and Jurkat but remained unmethylated in U937, HL60, and NB4. p27 was hemizygously methylated in Raji but unmethylated in the other cell lines. p57 was completely methylated in Raji and NB4, hemizygously methylated in U937, and unmethylated in HL60 and Jurkat. At diagnosis, p21 methylation was not detected in any case of AML or ALL. p27 methylation occurred in 2 (4%) AML patients and in 1 (4%) ALL patient. p57 methylation occurred in 1 (2%) AML patient and in 1 (4%) ALL patient. Therefore, methylation inactivation of the INK4/CDK/RB pathway in leukemia is infrequent. A review of the literature showed a marked variation in the frequencies of methylation of these genes, which might be attributable to difference in methodologies used to detect gene methylation. © 2005 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/76555
ISSN
2015 Impact Factor: 5.0
2015 SCImago Journal Rankings: 1.761
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorWong, ASYen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T07:22:29Z-
dc.date.available2010-09-06T07:22:29Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Hematology, 2005, v. 80 n. 4, p. 282-287en_HK
dc.identifier.issn0361-8609en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76555-
dc.description.abstractDysregulation of the cell cycle is important in oncogenesis. We analyzed the potential inactivation of the CIP/KIP family of the cyclin E/CDK/RB pathway by gene promoter hypermethylation in leukemias. The methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) alleles of the p21, p27, and p57 genes was used to study five leukemic cell lines, 50 acute myeloid leukemia (AML) samples, and 25 acute lymphoblastic leukemia (ALL) samples. p21 was hemizygously methylated in Raji and Jurkat but remained unmethylated in U937, HL60, and NB4. p27 was hemizygously methylated in Raji but unmethylated in the other cell lines. p57 was completely methylated in Raji and NB4, hemizygously methylated in U937, and unmethylated in HL60 and Jurkat. At diagnosis, p21 methylation was not detected in any case of AML or ALL. p27 methylation occurred in 2 (4%) AML patients and in 1 (4%) ALL patient. p57 methylation occurred in 1 (2%) AML patient and in 1 (4%) ALL patient. Therefore, methylation inactivation of the INK4/CDK/RB pathway in leukemia is infrequent. A review of the literature showed a marked variation in the frequencies of methylation of these genes, which might be attributable to difference in methodologies used to detect gene methylation. © 2005 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35105en_HK
dc.relation.ispartofAmerican Journal of Hematologyen_HK
dc.rightsAmerican Journal of Hematology. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAllelesen_HK
dc.subject.meshCalcium-Binding Proteins - genetics - metabolismen_HK
dc.subject.meshCell Cycleen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor Proteins - genetics - metabolismen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshEpigenesis, Geneticen_HK
dc.subject.meshGene Expression Regulation, Leukemicen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia, Myeloid, Acute - genetics - metabolismen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshPrecursor Cell Lymphoblastic Leukemia-Lymphoma - genetics - metabolismen_HK
dc.subject.meshSignal Transduction - geneticsen_HK
dc.titleEpigenetic inactivation of the CIP/KIP cell-cycle control pathway in acute leukemiasen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0361-8609&volume=80&issue=4&spage=282&epage=7&date=2005&atitle=Epigenetic+inactivation+of+the+CIP/KIP+cell-cycle+control+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.doi10.1002/ajh.20503en_HK
dc.identifier.pmid16315255en_HK
dc.identifier.scopuseid_2-s2.0-28544448867en_HK
dc.identifier.hkuros121987en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28544448867&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume80en_HK
dc.identifier.issue4en_HK
dc.identifier.spage282en_HK
dc.identifier.epage287en_HK
dc.identifier.isiWOS:000233696800005-
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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