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Article: Absence of microsatellite instability in primary myelodysplastic syndrome.

TitleAbsence of microsatellite instability in primary myelodysplastic syndrome.
Authors
Issue Date2000
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htm
Citation
International Journal Of Molecular Medicine, 2000, v. 5 n. 2, p. 159-163 How to Cite?
AbstractUsing polymerase chain reaction (PCR), we examined a panel of 10 microsatellite markers (BAT26, BAT40, D2S123, D4S171, D8S87, D10S197, D12S89, Tp53, D18S58, PLCpr) covering nine chromosomal arms for microsatellite instability (MSI) in 29 patients with primary MDS. Bone marrow DNA was compared with corresponding constitutional DNA derived from buccal epithelial cells. Apart from BAT26 and BAT40 that were mononucleotide (poly A) repeats, the others were dinucleotide (CA) repeats. The patients comprised 10 cases of refractory anemia (RA), three cases of refractory anemia with ringed sideroblasts (RARS), nine cases of refractory anemia with excess of blasts (RAEB), four cases of refractory anemia with excess of blasts in transformation (RAEBt), and three cases of chronic myelomonocytic leukemia (CMML). Serial samples were available in seven patients, in which four showed transformation into higher disease grade or acute myeloid leukemia (AML). Genetic alterations at one locus (three at D2S123, one at D4S171) were evident in four cases, and loss of heterozygosity at Tp53 was detected in one case. Accordingly, none of the 29 patients with primary MDS nor the seven with disease progression in this study exhibited MSI. This shows that MSI may not be important in the pathogenesis or progression of MDS in contrast to other genetic mechanisms, notably recurrent chromosomal abnormalities that dysregulate the expression or function of genes controlling cell growth, differentiation and apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/148203
ISSN
2015 Impact Factor: 2.348
2015 SCImago Journal Rankings: 0.868
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMa, SKen_US
dc.contributor.authorKong, CTen_US
dc.contributor.authorWan, TSen_US
dc.contributor.authorAu, WYen_US
dc.contributor.authorChan, JCen_US
dc.contributor.authorYip, SFen_US
dc.contributor.authorChan, LCen_US
dc.date.accessioned2012-05-29T06:11:28Z-
dc.date.available2012-05-29T06:11:28Z-
dc.date.issued2000en_US
dc.identifier.citationInternational Journal Of Molecular Medicine, 2000, v. 5 n. 2, p. 159-163en_US
dc.identifier.issn1107-3756en_US
dc.identifier.urihttp://hdl.handle.net/10722/148203-
dc.description.abstractUsing polymerase chain reaction (PCR), we examined a panel of 10 microsatellite markers (BAT26, BAT40, D2S123, D4S171, D8S87, D10S197, D12S89, Tp53, D18S58, PLCpr) covering nine chromosomal arms for microsatellite instability (MSI) in 29 patients with primary MDS. Bone marrow DNA was compared with corresponding constitutional DNA derived from buccal epithelial cells. Apart from BAT26 and BAT40 that were mononucleotide (poly A) repeats, the others were dinucleotide (CA) repeats. The patients comprised 10 cases of refractory anemia (RA), three cases of refractory anemia with ringed sideroblasts (RARS), nine cases of refractory anemia with excess of blasts (RAEB), four cases of refractory anemia with excess of blasts in transformation (RAEBt), and three cases of chronic myelomonocytic leukemia (CMML). Serial samples were available in seven patients, in which four showed transformation into higher disease grade or acute myeloid leukemia (AML). Genetic alterations at one locus (three at D2S123, one at D4S171) were evident in four cases, and loss of heterozygosity at Tp53 was detected in one case. Accordingly, none of the 29 patients with primary MDS nor the seven with disease progression in this study exhibited MSI. This shows that MSI may not be important in the pathogenesis or progression of MDS in contrast to other genetic mechanisms, notably recurrent chromosomal abnormalities that dysregulate the expression or function of genes controlling cell growth, differentiation and apoptosis.en_US
dc.languageengen_US
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htmen_US
dc.relation.ispartofInternational journal of molecular medicineen_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshBone Marrowen_US
dc.subject.meshDna, Neoplasm - Analysisen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMicrosatellite Repeatsen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMyelodysplastic Syndromes - Geneticsen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.titleAbsence of microsatellite instability in primary myelodysplastic syndrome.en_US
dc.typeArticleen_US
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_US
dc.identifier.authorityChan, LC=rp00373en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid10639595-
dc.identifier.scopuseid_2-s2.0-0034132002en_US
dc.identifier.hkuros50821-
dc.identifier.volume5en_US
dc.identifier.issue2en_US
dc.identifier.spage159en_US
dc.identifier.epage163en_US
dc.identifier.isiWOS:000084827500008-
dc.publisher.placeGreeceen_US

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