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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
1993-6-11
|
| pubmed:abstractText |
A nonrandom translocation between chromosomes 3 and 21, t(3;21)(q26.2;q22) has been detected in patients with a myelodysplastic syndrome or acute myeloid leukemia after treatment (t-MDS/t-AML) for a primary malignant disease and in chronic myelogenous leukemia in blast crisis (CML-BC). In these patients, the breakpoint on chromosome 21 is at band 21q22. This band is also involved in the t(8;21)(q22;q22) detected in 40% of the patients with acute myeloid leukemia subtype M2 (AML-M2) de novo who have an abnormal karyotype. In the t(8;21), the AML1 gene is the site of the breakpoint on chromosome 21. The AML1 gene is transcribed from telomere to centromere, and in the t(8;21) the 5' part of AML1 is fused to the ETO gene on chromosome 8 to produce the chimeric AML1/ETO on the der(8) chromosome. We found that AML1 is also rearranged in two t-AML patients and in one CML-BC patient with the t(3;21), but the breakpoints are approximately 40 to 60 kb downstream to those of AML-M2 patients. This region contains at least one additional exon of AML1, as determined by using an AML1 cDNA as a probe in Southern blot analysis. The t(3;21) breakpoints for the remaining patients could not be determined because, by fluorescence in situ hybridization analysis, the breaks are outside of the region covered by the available probes.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
0006-4971
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
81
|
| pubmed:geneSymbol |
AML1
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
2728-34
|
| pubmed:dateRevised |
2007-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:8490181-Adult,
pubmed-meshheading:8490181-Aged,
pubmed-meshheading:8490181-Base Sequence,
pubmed-meshheading:8490181-Blast Crisis,
pubmed-meshheading:8490181-Blotting, Southern,
pubmed-meshheading:8490181-Chromosome Banding,
pubmed-meshheading:8490181-Chromosome Mapping,
pubmed-meshheading:8490181-Chromosome Walking,
pubmed-meshheading:8490181-Chromosomes, Human, Pair 21,
pubmed-meshheading:8490181-Chromosomes, Human, Pair 3,
pubmed-meshheading:8490181-DNA, Neoplasm,
pubmed-meshheading:8490181-Female,
pubmed-meshheading:8490181-Humans,
pubmed-meshheading:8490181-Karyotyping,
pubmed-meshheading:8490181-Leukemia,
pubmed-meshheading:8490181-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:8490181-Male,
pubmed-meshheading:8490181-Middle Aged,
pubmed-meshheading:8490181-Molecular Sequence Data,
pubmed-meshheading:8490181-Myelodysplastic Syndromes,
pubmed-meshheading:8490181-Oligodeoxyribonucleotides,
pubmed-meshheading:8490181-Polymerase Chain Reaction,
pubmed-meshheading:8490181-Restriction Mapping,
pubmed-meshheading:8490181-Translocation, Genetic
|
| pubmed:year |
1993
|
| pubmed:articleTitle |
Involvement of the AML1 gene in the t(3;21) in therapy-related leukemia and in chronic myeloid leukemia in blast crisis.
|
| pubmed:affiliation |
Department of Medicine, University of Chicago, IL.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|