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Article: New insights to the MLL recombinome of acute leukemias

TitleNew insights to the MLL recombinome of acute leukemias
Authors
Issue Date2009
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leu
Citation
Leukemia, 2009, v. 23 n. 8, p. 1490-1499 How to Cite?
AbstractChromosomal rearrangements of the human MLL gene are associated with high-risk pediatric, adult and therapy-associated acute leukemias. These patients need to be identified, treated appropriately and minimal residual disease was monitored by quantitative PCR techniques. Genomic DNA was isolated from individual acute leukemia patients to identify and characterize chromosomal rearrangements involving the human MLL gene. A total of 760 MLL-rearranged biopsy samples obtained from 384 pediatric and 376 adult leukemia patients were characterized at the molecular level. The distribution of MLL breakpoints for clinical subtypes (acute lymphoblastic leukemia, acute myeloid leukemia, pediatric and adult) and fused translocation partner genes (TPGs) will be presented, including novel MLL fusion genes. Combined data of our study and recently published data revealed 104 different MLL rearrangements of which 64 TPGs are now characterized on the molecular level. Nine TPGs seem to be predominantly involved in genetic recombinations of MLL: AFF1/AF4, MLLT3/ AF9, MLLT1/ENL, MLLT10/AF10, MLLT4/AF6, ELL, EPS15/AF1P, MLLT6/AF17 and SEPT6, respectively. Moreover, we describe for the first time the genetic network of reciprocal MLL gene fusions deriving from complex rearrangements.
Persistent Identifierhttp://hdl.handle.net/10722/126723
ISSN
2015 Impact Factor: 12.104
2015 SCImago Journal Rankings: 5.142
ISI Accession Number ID
Funding AgencyGrant Number
Deutsche Krebshilfe107819
German Jose Carreras Leukemia foundationR06/22
Polish Ministry of Science and Higher Education2 P054 095 30
Funding Information:

This work was made possible by and conducted within the framework of the International BFM Study Group. This study was supported by grant 107819 from the Deutsche Krebshilfe to RM, TD and TK; supported by grant R06/22 from the German Jose Carreras Leukemia foundation to TB and supported by grant 2 P054 095 30 from the Polish Ministry of Science and Higher Education to TS.

References

 

DC FieldValueLanguage
dc.contributor.authorMeyer, Cen_HK
dc.contributor.authorKowarz, Een_HK
dc.contributor.authorHofmann, Jen_HK
dc.contributor.authorRenneville, Aen_HK
dc.contributor.authorZuna, Jen_HK
dc.contributor.authorTrka, Jen_HK
dc.contributor.authorBen Abdelali, Ren_HK
dc.contributor.authorMacintyre, Een_HK
dc.contributor.authorDe Braekeleer, Een_HK
dc.contributor.authorDe Braekeleer, Men_HK
dc.contributor.authorDelabesse, Een_HK
dc.contributor.authorde Oliveira, MPen_HK
dc.contributor.authorCavé, Hen_HK
dc.contributor.authorClappier, Een_HK
dc.contributor.authorvan Dongen, JJMen_HK
dc.contributor.authorBalgobind, BVen_HK
dc.contributor.authorvan den HeuvelEibrink, MMen_HK
dc.contributor.authorBeverloo, HBen_HK
dc.contributor.authorPanzerGrümayer, Ren_HK
dc.contributor.authorTeiglerSchlegel, Aen_HK
dc.contributor.authorHarbott, Jen_HK
dc.contributor.authorKjeldsen, Een_HK
dc.contributor.authorSchnittger, Sen_HK
dc.contributor.authorKoehl, Uen_HK
dc.contributor.authorGruhn, Ben_HK
dc.contributor.authorHeidenreich, Oen_HK
dc.contributor.authorChan, LCen_HK
dc.contributor.authorYip, SFen_HK
dc.contributor.authorKrzywinski, Men_HK
dc.contributor.authorEckert, Cen_HK
dc.contributor.authorMöricke, Aen_HK
dc.contributor.authorSchrappe, Men_HK
dc.contributor.authorAlonso, CNen_HK
dc.contributor.authorSchäfer, BWen_HK
dc.contributor.authorKrauter, Jen_HK
dc.contributor.authorLee, DAen_HK
dc.contributor.authorzur Stadt, Uen_HK
dc.contributor.authorTe Kronnie, Gen_HK
dc.contributor.authorSutton, Ren_HK
dc.contributor.authorIzraeli, Sen_HK
dc.contributor.authorTrakhtenbrot, Len_HK
dc.contributor.authorLo Nigro, Len_HK
dc.contributor.authorTsaur, Gen_HK
dc.contributor.authorFechina, Len_HK
dc.contributor.authorSzczepanski, Ten_HK
dc.contributor.authorStrehl, Sen_HK
dc.contributor.authorIlencikova, Den_HK
dc.contributor.authorMolkentin, Men_HK
dc.contributor.authorBurmeister, Ten_HK
dc.contributor.authorDingermann, Ten_HK
dc.contributor.authorKlingebiel, Ten_HK
dc.contributor.authorMarschalek, Ren_HK
dc.date.accessioned2010-10-31T12:44:45Z-
dc.date.available2010-10-31T12:44:45Z-
dc.date.issued2009en_HK
dc.identifier.citationLeukemia, 2009, v. 23 n. 8, p. 1490-1499en_HK
dc.identifier.issn0887-6924en_HK
dc.identifier.urihttp://hdl.handle.net/10722/126723-
dc.description.abstractChromosomal rearrangements of the human MLL gene are associated with high-risk pediatric, adult and therapy-associated acute leukemias. These patients need to be identified, treated appropriately and minimal residual disease was monitored by quantitative PCR techniques. Genomic DNA was isolated from individual acute leukemia patients to identify and characterize chromosomal rearrangements involving the human MLL gene. A total of 760 MLL-rearranged biopsy samples obtained from 384 pediatric and 376 adult leukemia patients were characterized at the molecular level. The distribution of MLL breakpoints for clinical subtypes (acute lymphoblastic leukemia, acute myeloid leukemia, pediatric and adult) and fused translocation partner genes (TPGs) will be presented, including novel MLL fusion genes. Combined data of our study and recently published data revealed 104 different MLL rearrangements of which 64 TPGs are now characterized on the molecular level. Nine TPGs seem to be predominantly involved in genetic recombinations of MLL: AFF1/AF4, MLLT3/ AF9, MLLT1/ENL, MLLT10/AF10, MLLT4/AF6, ELL, EPS15/AF1P, MLLT6/AF17 and SEPT6, respectively. Moreover, we describe for the first time the genetic network of reciprocal MLL gene fusions deriving from complex rearrangements.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leuen_HK
dc.relation.ispartofLeukemiaen_HK
dc.subject.meshAcute Diseaseen_HK
dc.subject.meshAdulten_HK
dc.subject.meshBiopsyen_HK
dc.subject.meshBone Marrow - chemistry - pathologyen_HK
dc.subject.meshChilden_HK
dc.subject.meshChromosome Breakageen_HK
dc.subject.meshChromosomes, Human, Pair 11 - genetics - ultrastructureen_HK
dc.subject.meshComputational Biologyen_HK
dc.subject.meshDNA, Neoplasm - blood - geneticsen_HK
dc.subject.meshGene Duplicationen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLeukemia - geneticsen_HK
dc.subject.meshMyeloid-Lymphoid Leukemia Protein - geneticsen_HK
dc.subject.meshNeoplasm Proteins - geneticsen_HK
dc.subject.meshOncogene Proteins, Fusion - geneticsen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshRecombination, Geneticen_HK
dc.subject.meshTranslocation, Geneticen_HK
dc.titleNew insights to the MLL recombinome of acute leukemiasen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0887-6924&volume=23&issue=8&spage=1490&epage=1499&date=2009&atitle=New+insights+to+the+MLL+recombinome+of+acute+leukemiasen_HK
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/leu.2009.33en_HK
dc.identifier.pmid19262598-
dc.identifier.scopuseid_2-s2.0-68749120703en_HK
dc.identifier.hkuros181199en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-68749120703&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1490en_HK
dc.identifier.epage1499en_HK
dc.identifier.isiWOS:000268862000017-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.citeulike4141695-

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