Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Cells expressing FLT3/ITD mutations exhibit elevated repair errors generated through alternative NHEJ pathways: implications for genomic instability and therapy

1 Sept 2010

Abstract excerpt

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 in normal mammalian cells, an alternative and less well-defined NHEJ pathway, characterized by microhomology at the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acute Myeloid Leukemia Research
Share to Cancer Genomics and Diagnostics
Share to DNA Repair Mechanisms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 20807885
DOI: 10.1182/blood-2010-03-272591

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cells expressing FLT3/ITD mutations exhibit elevated repair errors generated through alternative NHEJ pathways: implications for genomic instability and therapyPMID 20807885Read ↗

Genomic instability is a principle pathologic feature of FLT3 ITD kinase activity in acute myeloid leukemia leading to clonal evolution and disease progression.Semantic proximity Read ↗

Defective nonhomologous end joining blocks B-cell development in FLT3/ITD mice.Semantic proximity Read ↗

c-MYC Generates Repair Errors via Increased Transcription of Alternative-NHEJ Factors, LIG3 and PARP1, in Tyrosine Kinase–Activated LeukemiasSemantic proximity Read ↗

Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AMLSemantic proximity Read ↗

DNA damage accumulation and repair defects in FLT3-ITD acute myeloid leukemia: Implications for clonal evolution and disease progression.Semantic proximity Read ↗

Human DNA ligases I and III, but not ligase IV, are required for microhomology-mediated end joining of DNA double-strand breaksSemantic proximity Read ↗

Ku regulates the non-homologous end joining pathway choice of DNA double-strand break repair in human somatic cells.Semantic proximity Read ↗

DNA-PKcs suppresses illegitimate chromosome rearrangementsSemantic proximity Read ↗

DNA-PKcs Suppresses Illegitimate Chromosome RearrangementsSemantic proximity Read ↗

Tyrosine kinase inhibitor-induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors.Semantic proximity Read ↗

MuLV-related endogenous retroviral elements and Flt3 participate in aberrant end-joining events that promote B-cell leukemogenesis.Semantic proximity Read ↗

Imprecision and DNA Break Repair Biased towards Incompatible End Joining in LeukemiaSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.