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Article: Methylation of p15 and p16 genes in acute promyelocytic leukemia: Potential diagnostic and prognostic significance

TitleMethylation of p15 and p16 genes in acute promyelocytic leukemia: Potential diagnostic and prognostic significance
Authors
Issue Date2001
PublisherAmerican Society of Clinical Oncology. The Journal's web site is located at http://www.jco.org/
Citation
Journal Of Clinical Oncology, 2001, v. 19 n. 7, p. 2033-2040 How to Cite?
AbstractPurpose: To investigate the frequency of p15 and p16 gene promoter methylation in acute promyelocytic leukemia (APL), and to define its value in the detection of minimal residual disease (MRD) and treatment prognostication. Patients and Methods: Bone marrow DNA obtained from 26 patients with APL at diagnosis and during follow-up was studied with the methylation-specific polymerase chain reaction (MS-PCR). Serial marrow DNA was studied by MS-PCR for MRD, and disease-free and overall survival were correlated with p15 methylation status at diagnosis. Results: MS-PCR for p16 and p15 gene methylation has a maximum sensitivity of 10-4 and 10-5. At diagnosis, 19 patients (73.1%) exhibited p15 methylation, whereas only three patients (11.5%) exhibited p16 methylation, all of whom had concomitant p15 methylation. During follow-up, p16 methylation was acquired in two patients, one during the third hematologic relapse, and the other during transformation into therapy-related myelodysplastic syndrome. Six patients were evaluated serially with MS-PCR for p15 methylation at diagnosis and at follow-up examinations. Persistent p15 methylation preceded subsequent hematologic relapses in two patients, and conversion to negative MS-PCR for p15 methylation correlated with prolonged survival in another four patients. The 5-year disease-free survival of patients with p15 methylation was significantly inferior to that of patients without p15 methylation (15% v 62.5%; P = .02), and this remained significant in multivariate analysis. Conclusion: In APL, p15 but not p16 gene methylation is frequent. It is possible that p16 methylation is acquired during clonal evolution, p15 methylation is a potential marker of MRD and might be of prognostic significance. © 2001 by American Society of Clinical Oncology.
Persistent Identifierhttp://hdl.handle.net/10722/162523
ISSN
2023 Impact Factor: 42.1
2023 SCImago Journal Rankings: 10.639
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, JCSen_US
dc.contributor.authorLiang, Ren_US
dc.contributor.authorTam, CYYen_US
dc.contributor.authorKwong, YLen_US
dc.date.accessioned2012-09-05T05:20:45Z-
dc.date.available2012-09-05T05:20:45Z-
dc.date.issued2001en_US
dc.identifier.citationJournal Of Clinical Oncology, 2001, v. 19 n. 7, p. 2033-2040en_US
dc.identifier.issn0732-183Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/162523-
dc.description.abstractPurpose: To investigate the frequency of p15 and p16 gene promoter methylation in acute promyelocytic leukemia (APL), and to define its value in the detection of minimal residual disease (MRD) and treatment prognostication. Patients and Methods: Bone marrow DNA obtained from 26 patients with APL at diagnosis and during follow-up was studied with the methylation-specific polymerase chain reaction (MS-PCR). Serial marrow DNA was studied by MS-PCR for MRD, and disease-free and overall survival were correlated with p15 methylation status at diagnosis. Results: MS-PCR for p16 and p15 gene methylation has a maximum sensitivity of 10-4 and 10-5. At diagnosis, 19 patients (73.1%) exhibited p15 methylation, whereas only three patients (11.5%) exhibited p16 methylation, all of whom had concomitant p15 methylation. During follow-up, p16 methylation was acquired in two patients, one during the third hematologic relapse, and the other during transformation into therapy-related myelodysplastic syndrome. Six patients were evaluated serially with MS-PCR for p15 methylation at diagnosis and at follow-up examinations. Persistent p15 methylation preceded subsequent hematologic relapses in two patients, and conversion to negative MS-PCR for p15 methylation correlated with prolonged survival in another four patients. The 5-year disease-free survival of patients with p15 methylation was significantly inferior to that of patients without p15 methylation (15% v 62.5%; P = .02), and this remained significant in multivariate analysis. Conclusion: In APL, p15 but not p16 gene methylation is frequent. It is possible that p16 methylation is acquired during clonal evolution, p15 methylation is a potential marker of MRD and might be of prognostic significance. © 2001 by American Society of Clinical Oncology.en_US
dc.languageengen_US
dc.publisherAmerican Society of Clinical Oncology. The Journal's web site is located at http://www.jco.org/en_US
dc.relation.ispartofJournal of Clinical Oncologyen_US
dc.subject.meshActuarial Analysisen_US
dc.subject.meshAdulten_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDna Primersen_US
dc.subject.meshDisease-Free Survivalen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenes, Tumor Suppressoren_US
dc.subject.meshGenes, P16en_US
dc.subject.meshHumansen_US
dc.subject.meshLeukemia, Promyelocytic, Acute - Diagnosis - Geneticsen_US
dc.subject.meshLogistic Modelsen_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasm, Residualen_US
dc.subject.meshPolymerase Chain Reaction - Methodsen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshProportional Hazards Modelsen_US
dc.subject.meshSensitivity And Specificityen_US
dc.subject.meshSurvival Rateen_US
dc.subject.meshTumor Markers, Biological - Geneticsen_US
dc.titleMethylation of p15 and p16 genes in acute promyelocytic leukemia: Potential diagnostic and prognostic significanceen_US
dc.typeArticleen_US
dc.identifier.emailChim, JCS:jcschim@hku.hken_US
dc.identifier.emailLiang, R:rliang@hku.hken_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.authorityChim, JCS=rp00408en_US
dc.identifier.authorityLiang, R=rp00345en_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1200/JCO.2001.19.7.2033-
dc.identifier.pmid11283136-
dc.identifier.scopuseid_2-s2.0-0035300727en_US
dc.identifier.hkuros60214-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035300727&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume19en_US
dc.identifier.issue7en_US
dc.identifier.spage2033en_US
dc.identifier.epage2040en_US
dc.identifier.isiWOS:000167920300019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChim, JCS=7004597253en_US
dc.identifier.scopusauthoridLiang, R=26643224900en_US
dc.identifier.scopusauthoridTam, CYY=10045311200en_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US
dc.identifier.issnl0732-183X-

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