Evidence map›Paper›PMID 32690020›Full record

ReviewJournal of biomedical science2020

Genomic landscape in acute myeloid leukemia and its implications in risk classification and targeted therapies.

Hsin-An Hou, Hwei-Fang Tien

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
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

48 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  8. Identification of novelTherapeutic advances in hematology · 2026
    Article
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  13. Shared genetic association between inflammatory bowel disease and acute myeloid leukemia: insights from mendelian randomization and transcriptomic analyses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  14. Article
  15. Review
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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

2 authors at 1 institution in 1 country.

Hsin-An HouDivision of Hematology, Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan.
Hwei-Fang TienDivision of Hematology, Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan. hftien@ntu.edu.tw.
National Taiwan University Hospital · TW

Funding

Ministry of Health and Welfare 107-TDU-B-211-114009Ministry of Science and Technology, Taiwan (TW) 104-2314-B-002-128-MY4Ministry of Science and Technology (TW) 106-2314-B-002-226-MY3
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy in terms of clinical features, underlying pathogenesis and treatment outcomes. Recent advances in genomic techniques have unraveled the molecular complexity of AML leukemogenesis, which in turn have led to refinement of risk stratification and personalized therapeutic strategies for patients with AML. Incorporation of prognostic and druggable genetic biomarkers into clinical practice to guide patient-specific treatment is going to be the mainstay in AML therapeutics. Since 2017 there has been an explosion of novel treatment options to tailor personalized therapy for AML patients. In the past 3 years, the U.S. Food and Drug Administration approved a total of eight drugs for the treatment of AML; most specifically target certain gene mutations, biological pathways, or surface antigen. These novel agents are especially beneficial for older patients or those with comorbidities, in whom the treatment choice is limited and the clinical outcome is very poor. How to balance efficacy and toxicity to further improve patient outcome is clinically relevant. In this review article, we give an overview of the most relevant genetic markers in AML with special focus on the therapeutic implications of these aberrations.

Indexed as

Genome, HumanGenetic MarkersGenetic TherapyGenomicsHumansLeukemia, Myeloid, AcutePrognosisRisk FactorsGenetic MarkersAcute myeloid leukemiaGenetic markersRisk stratificationTherapeutics

Identifiers

PMID32690020
PMCPMC7372828
OpenAlexW3045364226

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.