Source:http://linkedlifedata.com/resource/pubmed/id/16890283
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2007-1-15
|
| pubmed:abstractText |
The frequency of acute myeloid leukemia (AML) with balanced chromosomal translocations arising after anticancer therapy with DNA-damaging agents such as DNA topoisomerase II inhibitors has increased over the last two decades. However, factors that predispose to these therapy-related disorders are still poorly defined. It has been reported that DNA double-strand break (DSB) repair by the non-homologous end-joining (NHEJ) pathway is impaired in myeloid leukemia cells. This led us to hypothesize that therapy-related AML (t-AML) may result from individual differences in the repair of DSBs generated by the treatment. We show here that DSB repair is accurate, in vivo, in non-tumoral cells derived from patients who developed t-AML with t(9;11) or t(15;17) translocation after treatment for a first cancer with DNA topoisomerase II inhibitors. These results indicate that a major constitutive defect in the NHEJ pathway is unlikely to predispose to t-AML with balanced chromosomal translocations.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0145-2126
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
31
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
353-8
|
| pubmed:dateRevised |
2010-11-18
|
| pubmed:meshHeading |
pubmed-meshheading:16890283-Acute Disease,
pubmed-meshheading:16890283-Adult,
pubmed-meshheading:16890283-Aged,
pubmed-meshheading:16890283-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:16890283-Cell Line, Tumor,
pubmed-meshheading:16890283-Chromosomes, Human, Pair 11,
pubmed-meshheading:16890283-Chromosomes, Human, Pair 15,
pubmed-meshheading:16890283-Chromosomes, Human, Pair 17,
pubmed-meshheading:16890283-Chromosomes, Human, Pair 9,
pubmed-meshheading:16890283-DNA Breaks, Double-Stranded,
pubmed-meshheading:16890283-DNA Repair,
pubmed-meshheading:16890283-DNA Topoisomerases, Type II,
pubmed-meshheading:16890283-Enzyme Inhibitors,
pubmed-meshheading:16890283-Female,
pubmed-meshheading:16890283-Humans,
pubmed-meshheading:16890283-Leukemia, Myeloid,
pubmed-meshheading:16890283-Male,
pubmed-meshheading:16890283-Middle Aged,
pubmed-meshheading:16890283-Neoplasms, Second Primary,
pubmed-meshheading:16890283-Structure-Activity Relationship,
pubmed-meshheading:16890283-Topoisomerase II Inhibitors,
pubmed-meshheading:16890283-Translocation, Genetic
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
Predisposition to therapy-related acute leukemia with balanced chromosomal translocations does not result from a major constitutive defect in DNA double-strand break end joining.
|
| pubmed:affiliation |
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8126, Institut Gustave Roussy, 39 Rue Camille Desmoulins, 94 805 Villejuif Cedex, France.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|