Source:http://linkedlifedata.com/resource/pubmed/id/16015647
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2005-9-6
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pubmed:abstractText |
Deletion of the long arm of chromosome 9, del(9q), is a recurring chromosomal aberration in acute myeloid leukemia (AML) that is frequently associated with t(8;21). The critical gene products affected by del(9q) are unknown but likely cooperate with the AML1/ETO fusion gene created by t(8;21) in leukemogenesis. In 43 AML samples with del(9q), we used high-density microsatellite markers to define the commonly deleted region (CDR) to less than 2.4 Mb. We found no homozygous loss at any locus tested. The CDR contains 7 known genes, FRMD3, UBQLN1, GKAP42, KIF27, HNRPK, SLC28A3, and NTRK2, and 4 novel genes, RASEF, C9orf103, C9orf64, and C9orf76. In addition, TLE1 and TLE4 are adjacent to the CDR. We performed a comprehensive mutational analysis of the coding regions of all these genes. No sequence variations absent in normal controls were seen in more than a single del(9q) AML sample. Expression of 7 of the 10 genes examined was significantly down-regulated in del(19q)AML as compared with the CD34-purified progenitors from normal individuals, a pattern distinct from that seen in AML samples with a normal karyotype. The results of our studies are consistent with a model of tumor suppression mediated by haploinsufficiency of critical genes in del(9q) AML.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1045-2257
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pubmed:author |
pubmed-author:BernsteinIrwin DID,
pubmed-author:BlombergAdam AAA,
pubmed-author:BoultwoodJacquelineJ,
pubmed-author:DalySarah BSB,
pubmed-author:DayyaniFarshidF,
pubmed-author:DewaldGordon WGW,
pubmed-author:HaalandChristinaC,
pubmed-author:HeeremaNyla ANA,
pubmed-author:PaiettaElisabethE,
pubmed-author:PeniketAndrew JAJ,
pubmed-author:SlovakMarilyn LML,
pubmed-author:SweetserDavid ADA,
pubmed-author:WainscoatJames SJS,
pubmed-author:WillmanCheryl LCL,
pubmed-author:ZaidiSyed TanweerST,
pubmed-author:ZhangYuntianY,
pubmed-author:ZhengZhaoZ
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pubmed:copyrightInfo |
(c) 2005 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:volume |
44
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
279-91
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16015647-Acute Disease,
pubmed-meshheading:16015647-Chromosome Deletion,
pubmed-meshheading:16015647-Chromosomes, Human, Pair 5,
pubmed-meshheading:16015647-Chromosomes, Human, Pair 8,
pubmed-meshheading:16015647-Chromosomes, Human, Pair 9,
pubmed-meshheading:16015647-Cohort Studies,
pubmed-meshheading:16015647-DNA Primers,
pubmed-meshheading:16015647-Genes, Tumor Suppressor,
pubmed-meshheading:16015647-Humans,
pubmed-meshheading:16015647-Leukemia, Myeloid,
pubmed-meshheading:16015647-Microsatellite Repeats,
pubmed-meshheading:16015647-Mutation,
pubmed-meshheading:16015647-Translocation, Genetic
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pubmed:year |
2005
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pubmed:articleTitle |
Delineation of the minimal commonly deleted segment and identification of candidate tumor-suppressor genes in del(9q) acute myeloid leukemia.
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pubmed:affiliation |
Department of Pediatrics, Massachusetts General Hospital, 55 Fruit Street--Jackson 904, Boston, MA 02114, USA. dsweetser@partners.org
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't,
Multicenter Study,
Research Support, N.I.H., Extramural
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