Evidence map›Paper›PMID 36131612›Full record

ReviewHematological oncology2023

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

Francisco Alejandro Lagunas-Rangel

Abstract readReview
In one paragraph

Review in Hematological oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Francisco Alejandro Lagunas-RangelDepartment of Surgical Sciences, Uppsala University, Uppsala, Sweden.ORCID https://orcid.org/0000-0001-7730-6452

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 proliferation of leukemic cells. In addition, FLT3-ITD leads to overproduction of reactive oxygen species and defective DNA damage repair, both implicated in the appearance of new mutations and leukemic clones. Thus, the purpose of this review is to illustrate the molecular mechanisms through which FLT3-ITD generates genetic instability and how it facilitates clonal evolution with the generation of more resistant and aggressive cells. Likewise, this article discusses the feasibility of combined therapies with FLT3 inhibitors and inhibitors of DNA repair pathways.

Indexed as

Leukemia, Myeloid, AcutePhosphatidylinositol 3-KinasesClonal EvolutionDisease ProgressionDNA Damagefms-Like Tyrosine Kinase 3HumansMutationFLT3 protein, humanfms-Like Tyrosine Kinase 3Phosphatidylinositol 3-KinasesAMLFLT3 inhibitorhomologous recombinationNHEJpoor clinical prognosisROS

Identifiers

PMID36131612
PMCPMC10087755

What Socratic holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.