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Article: Functional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia
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TitleFunctional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia
 
AuthorsSun, Q1
So, CC1
Yip, SF2
Wan, TSK2
Ma, SK1
Chan, LC1
 
Issue Date2008
 
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukres
 
CitationLeukemia Research, 2008, v. 32 n. 9, p. 1374-1381 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.leukres.2008.02.011
 
AbstractThe functional behavior of hematopoietic stem cell (HSC) and progenitors in chronic myelomonocytic leukemia (CMML) and on disease progression is little known. We performed cell proliferation, apoptosis, hematopoietic colony forming/replating and differentiation potential studies in the purified subpopulations of Lin-CD34+CD38- and Lin-CD34+CD38+ cells from 16 CMML with 6 cases after acute myeloid leukemia transformation (AML-t). We observed an expansion of the hematopoietic progenitor pool (Lin-CD34+ cells) in AML-t comprising mainly Lin-CD34+CD38+ cells. The Lin-CD34+CD38+ cells in AML-t displayed high proliferative activity, resistance to apoptosis, enhanced myeloid colony formation/replating ability and a complete dendritic cell (DC) differentiation block. Our findings suggest Lin-CD34+CD38+ cells instead of Lin-CD34+CD38- cells could be the target(s) of secondary genetic lesions underpinning progression from CMML to AML, which have implications for the further study of the biology of leukemic transformation and the design of new strategies for the effective treatment of CMML. © 2008 Elsevier Ltd. All rights reserved.
 
ISSN0145-2126
2013 Impact Factor: 2.692
2013 SCImago Journal Rankings: 1.080
 
DOIhttp://dx.doi.org/10.1016/j.leukres.2008.02.011
 
ISI Accession Number IDWOS:000256650800007
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorSun, Q
 
dc.contributor.authorSo, CC
 
dc.contributor.authorYip, SF
 
dc.contributor.authorWan, TSK
 
dc.contributor.authorMa, SK
 
dc.contributor.authorChan, LC
 
dc.date.accessioned2010-05-31T04:13:58Z
 
dc.date.available2010-05-31T04:13:58Z
 
dc.date.issued2008
 
dc.description.abstractThe functional behavior of hematopoietic stem cell (HSC) and progenitors in chronic myelomonocytic leukemia (CMML) and on disease progression is little known. We performed cell proliferation, apoptosis, hematopoietic colony forming/replating and differentiation potential studies in the purified subpopulations of Lin-CD34+CD38- and Lin-CD34+CD38+ cells from 16 CMML with 6 cases after acute myeloid leukemia transformation (AML-t). We observed an expansion of the hematopoietic progenitor pool (Lin-CD34+ cells) in AML-t comprising mainly Lin-CD34+CD38+ cells. The Lin-CD34+CD38+ cells in AML-t displayed high proliferative activity, resistance to apoptosis, enhanced myeloid colony formation/replating ability and a complete dendritic cell (DC) differentiation block. Our findings suggest Lin-CD34+CD38+ cells instead of Lin-CD34+CD38- cells could be the target(s) of secondary genetic lesions underpinning progression from CMML to AML, which have implications for the further study of the biology of leukemic transformation and the design of new strategies for the effective treatment of CMML. © 2008 Elsevier Ltd. All rights reserved.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationLeukemia Research, 2008, v. 32 n. 9, p. 1374-1381 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.leukres.2008.02.011
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.leukres.2008.02.011
 
dc.identifier.epage1381
 
dc.identifier.hkuros150513
 
dc.identifier.isiWOS:000256650800007
 
dc.identifier.issn0145-2126
2013 Impact Factor: 2.692
2013 SCImago Journal Rankings: 1.080
 
dc.identifier.issue9
 
dc.identifier.openurl
 
dc.identifier.pmid18372040
 
dc.identifier.scopuseid_2-s2.0-43149110811
 
dc.identifier.spage1374
 
dc.identifier.urihttp://hdl.handle.net/10722/60574
 
dc.identifier.volume32
 
dc.languageeng
 
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukres
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofLeukemia Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAdult
 
dc.subject.meshAged
 
dc.subject.meshAged, 80 and over
 
dc.subject.meshAntigens, CD34 - metabolism
 
dc.subject.meshAntigens, CD38 - metabolism
 
dc.subject.meshApoptosis - physiology
 
dc.subject.meshCell Cycle - physiology
 
dc.subject.meshCell Proliferation
 
dc.subject.meshCell Transformation, Neoplastic
 
dc.subject.meshColony-Forming Units Assay
 
dc.subject.meshDendritic Cells - metabolism
 
dc.subject.meshDisease Progression
 
dc.subject.meshFlow Cytometry
 
dc.subject.meshGranulocyte Colony-Stimulating Factor - administration & dosage
 
dc.subject.meshHematopoietic Stem Cells
 
dc.subject.meshHumans
 
dc.subject.meshLeukemia, Myeloid, Acute - metabolism - pathology
 
dc.subject.meshLeukemia, Myelomonocytic, Chronic - metabolism - pathology
 
dc.subject.meshMembrane Glycoproteins - metabolism
 
dc.subject.meshMiddle Aged
 
dc.subject.meshTumor Necrosis Factor-alpha - pharmacology
 
dc.titleFunctional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia
 
dc.typeArticle
 
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<description.abstract>The functional behavior of hematopoietic stem cell (HSC) and progenitors in chronic myelomonocytic leukemia (CMML) and on disease progression is little known. We performed cell proliferation, apoptosis, hematopoietic colony forming/replating and differentiation potential studies in the purified subpopulations of Lin-CD34+CD38- and Lin-CD34+CD38+ cells from 16 CMML with 6 cases after acute myeloid leukemia transformation (AML-t). We observed an expansion of the hematopoietic progenitor pool (Lin-CD34+ cells) in AML-t comprising mainly Lin-CD34+CD38+ cells. The Lin-CD34+CD38+ cells in AML-t displayed high proliferative activity, resistance to apoptosis, enhanced myeloid colony formation/replating ability and a complete dendritic cell (DC) differentiation block. Our findings suggest Lin-CD34+CD38+ cells instead of Lin-CD34+CD38- cells could be the target(s) of secondary genetic lesions underpinning progression from CMML to AML, which have implications for the further study of the biology of leukemic transformation and the design of new strategies for the effective treatment of CMML. &#169; 2008 Elsevier Ltd. All rights reserved.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Queen Mary Hospital Hong Kong