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Cells expressing FLT3/ITD mutations exhibit elevated repair errors generated through alternative NHEJ pathways: implications for genomic instability and therapy
The internal tandem duplication (ITD) mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor found in acute myeloid leukemia patients are associated with poor prognosis. Although DNA double-strand breaks (DSBs) are mainly repaired by the DNA-PK–dependent nonhomologous end-joining (NHEJ) pathway...
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| Главные авторы: | , , , |
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| Формат: | Artigo |
| Язык: | Inglês |
| Опубликовано: |
American Society of Hematology
2010
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| Предметы: | |
| Online-ссылка: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3012544/ https://ncbi.nlm.nih.gov/pubmed/20807885 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1182/blood-2010-03-272591 |
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