Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1997-5-22
pubmed:abstractText
The molecular defects responsible for tumorigenesis in adult de novo acute myeloid leukemia (AML) with a normal karyotype or an additional copy of one chromosome (i.e., trisomy) remain largely unknown. We recently discovered that approximately 90% of adult patients with de novo AML and trisomy 11 (+11) as a sole abnormality and 11% of adult patients with de novo AML and normal cytogenetics carry a molecular rearrangement of the ALL1 (MLL, HRX, or HTRX) gene. The rearranged ALL1 gene has been shown to result from the direct tandem duplication of a portion of ALL1 itself. To better understand the underlying mechanisms of leukemogenesis, we asked whether in cytogenetically normal cases one or both chromosomes carry the mutated allele and whether in trisomic cases the mutation is present in one, two, or three chromosomes. Herein we show that in cytogenetically normal cases of AML and in cases with +11 as a sole cytogenetic abnormality, only one chromosome contains the mutated ALL1 allele. Thus a single mutated ALL1 allele with the partial tandem duplication is sufficient for ALL1-associated leukemogenesis, irrespective of the number of normal genes present. The frequently occurring specific association of +11 and ALL1 gene mutation in the leukemic clone remains unexplained.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1303259, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1311214, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1423624, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1423625, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1614537, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1720549, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1835902, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-1988146, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-3494520, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-3862359, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-6633649, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-6952920, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-7477409, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-7542910, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-8016145, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-8044771, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-8275471, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-8640834, http://linkedlifedata.com/resource/pubmed/commentcorrection/9108076-9045303
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3899-902
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
The partial tandem duplication of ALL1 in acute myeloid leukemia with normal cytogenetics or trisomy 11 is restricted to one chromosome.
pubmed:affiliation
Department of Hematologic Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. caligiuri@dm3100.med.buffalo.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't