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

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

Hematological oncology - 1 Feb 2023

Lagunas-Rangel Francisco Alejandro

Abstract excerpt

Acute myeloid leukemia is a group of hematological diseases that have a high mortality rate. During the development of this pathology, hematopoietic cells acquire chromosomal rearrangements and multiple genetic mutations, including FLT3-ITD. FLT3-ITD is a marker associated with a poor clinical prognosis and involves the activation of pathways such as PI3K/AKT, MAPK/ERK, and JAK/STAT that favor the survival and...

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 Clonal Evolution

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Disease Progression

Share to DNA Damage

Share to fms-Like Tyrosine Kinase 3

Share to Leukemia, Myeloid, Acute

Share to Mutation

Share to Phosphatidylinositol 3-Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 36131612
DOI: 10.1002/hon.3076
PMCID: PMC10087755

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

DNA damage accumulation and repair defects in FLT3-ITD acute myeloid leukemia: Implications for clonal evolution and disease progression.PMID 36131612Read ↗

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 ↗

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

Advances in the pathogenesis of FLT3 -mutated acute myeloid leukemia and targeted treatments.Semantic proximity Read ↗

FLT3 Mutations in Acute Myeloid Leukemia: Unraveling the Molecular Mechanisms and Implications for Targeted TherapiesSemantic proximity Read ↗

Downstream molecular pathways of FLT3 in the pathogenesis of acute myeloid leukemia: biology and therapeutic implications.Semantic proximity Read ↗

FLT3-ITD and its current role in acute myeloid leukaemia.Semantic proximity Read ↗

Targeting FLT3 mutations in AML: review of current knowledge and evidenceSemantic proximity Read ↗

Tyrosine kinase inhibitors targeting FLT3 in the treatment of acute myeloid leukemiaSemantic proximity Read ↗

“FLipping” the Story: FLT3-Mutated Acute Myeloid Leukemia and the Evolving Role of FLT3 InhibitorsSemantic proximity Read ↗

FLT3 mutations in acute myeloid leukemia: Therapeutic paradigm beyond inhibitor developmentSemantic proximity Read ↗

Biology, clinical relevance, and molecularly targeted therapy in acute leukemia with FLT3 mutation.Semantic proximity Read ↗

Structural and functional alterations of FLT3 in acute myeloid leukemia.Semantic proximity Read ↗

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