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Article: METHYLATION of PIS and P16 GENES in ADULT ACUTE LEUKEMIA

TitleMETHYLATION of PIS and P16 GENES in ADULT ACUTE LEUKEMIA
Authors
Issue Date2001
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
Citation
Blood, 2001, v. 96 n. 11 PART II, p. 172b How to Cite?
AbstractWe investigated the frequency and prognostic significance of plS and p!6 gene methylation in adult acute leukemia. The methylation specific polymerase chain reaction (MS-PCR) was used to analyze plS and pl6 gene methylation in 49 cases of acute lymphoblastic leukemia (ALL) and 29 cases of acute myelogenous leukemia (AML). At presentation, 93 % of cases in AML (8/8 Ml, 10/11 M2, 2/2 M4, 5/6 M5 and 2/2 M6) showedp/5 methylation, but none showedp!6 methylation. In ALL, 57% (5/8 T-ALL, 14/ 26 common-ALL, 4/5 pre-B ALL, 1/3 early B precursor ALL and 4/7 mixed lineage ALL) showed pi5 methylation. Only 6% showed pI6 methylation, all of whom had concomitant pi5 methylation. One patient acquired p!6 methylation during relapse. For 23 ALL cases karyotyped,/>/5 methylation was found in 6/9 cases with normal karyotype, 3/7 cases with the Philadelphia chromosome, 3/3 cases with 9p-, 2/2 cases with complex karyotypes and 1/1 case with hyperdiploidy. Three more cases with unsuccessful karyotyping but BCR' ABL fusion showed plS methylation as well. Five ALL patients were tested serially for minimal residual disease (MRD) with MS-PCR that has a sensitivity of ICH to 10J. All showed continuous positive MS-PCR that heralded hématologie relapse. The prognostic significance of pi 5 methylation was tested in ALL patients, showing no impact on complete; remission rate, 5-year overall survival and 5-year disease free survival.
Persistent Identifierhttp://hdl.handle.net/10722/163021
ISSN
2015 Impact Factor: 11.841
2015 SCImago Journal Rankings: 6.395

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_US
dc.contributor.authorTam, CYYen_US
dc.contributor.authorLiang, Ren_US
dc.contributor.authorKwong, YLen_US
dc.date.accessioned2012-09-05T05:26:38Z-
dc.date.available2012-09-05T05:26:38Z-
dc.date.issued2001en_US
dc.identifier.citationBlood, 2001, v. 96 n. 11 PART II, p. 172ben_US
dc.identifier.issn0006-4971en_US
dc.identifier.urihttp://hdl.handle.net/10722/163021-
dc.description.abstractWe investigated the frequency and prognostic significance of plS and p!6 gene methylation in adult acute leukemia. The methylation specific polymerase chain reaction (MS-PCR) was used to analyze plS and pl6 gene methylation in 49 cases of acute lymphoblastic leukemia (ALL) and 29 cases of acute myelogenous leukemia (AML). At presentation, 93 % of cases in AML (8/8 Ml, 10/11 M2, 2/2 M4, 5/6 M5 and 2/2 M6) showedp/5 methylation, but none showedp!6 methylation. In ALL, 57% (5/8 T-ALL, 14/ 26 common-ALL, 4/5 pre-B ALL, 1/3 early B precursor ALL and 4/7 mixed lineage ALL) showed pi5 methylation. Only 6% showed pI6 methylation, all of whom had concomitant pi5 methylation. One patient acquired p!6 methylation during relapse. For 23 ALL cases karyotyped,/>/5 methylation was found in 6/9 cases with normal karyotype, 3/7 cases with the Philadelphia chromosome, 3/3 cases with 9p-, 2/2 cases with complex karyotypes and 1/1 case with hyperdiploidy. Three more cases with unsuccessful karyotyping but BCR' ABL fusion showed plS methylation as well. Five ALL patients were tested serially for minimal residual disease (MRD) with MS-PCR that has a sensitivity of ICH to 10J. All showed continuous positive MS-PCR that heralded hématologie relapse. The prognostic significance of pi 5 methylation was tested in ALL patients, showing no impact on complete; remission rate, 5-year overall survival and 5-year disease free survival.en_US
dc.languageengen_US
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/en_US
dc.relation.ispartofBlooden_US
dc.titleMETHYLATION of PIS and P16 GENES in ADULT ACUTE LEUKEMIAen_US
dc.typeArticleen_US
dc.identifier.emailChim, CS:jcschim@hku.hken_US
dc.identifier.emailLiang, R:rliang@hku.hken_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.authorityChim, CS=rp00408en_US
dc.identifier.authorityLiang, R=rp00345en_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-33748574897en_US
dc.identifier.volume96en_US
dc.identifier.issue11 PART IIen_US
dc.identifier.spage172ben_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChim, CS=7004597253en_US
dc.identifier.scopusauthoridTam, CYY=10045311200en_US
dc.identifier.scopusauthoridLiang, R=26643224900en_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US

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