Evidence map›Paper›PMID 39085680›Full record

ReviewInternational journal of hematology2024

Precision medicine in AML: overcoming resistance.

Samuel Urrutia, Koichi Takahashi

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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.

Samuel UrrutiaDivision of Cancer Medicine, The University of Texas MD Anderson Cancer Center, 1901 East Road, 4SCR6.2085, Houston, TX, 77030-4009, USA.
Koichi TakahashiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, USA. ktakahashi@mdanderson.org.ORCID http://orcid.org/0000-0002-8027-9659

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of molecularly targeted therapy for acute myeloid leukemia is progressing at an accelerated pace. Therapies targeting FLT3, IDH1, IDH2, and BCL2 have been approved in the last 5 years. As we exploit these biological vulnerabilities, various mechanisms of resistance arise. Emergence of competing clones with different genetic drivers and acquisition of constitutional mutations in the target renders therapies ineffective, and enzymatic isoform changes can lead to reappearance of the disease phenotype. Understanding the timing and circumstances of resistance origination will allow clinicians to develop combinatorial and sequential therapeutic approaches to deepen responses and improve survival. The objective of this review is to illustrate the biological underpinnings of each therapy and the landscape of resistance mechanisms and discuss strategies to overcome on- and off-target resistance.

Indexed as

Drug Resistance, NeoplasmLeukemia, Myeloid, AcuteMolecular Targeted TherapyMutationPrecision Medicinefms-Like Tyrosine Kinase 3HumansIsocitrate DehydrogenaseProto-Oncogene Proteins c-bcl-2FLT3 protein, humanfms-Like Tyrosine Kinase 3IDH1 protein, humanIDH2 protein, humanIsocitrate DehydrogenaseProto-Oncogene Proteins c-bcl-2Acute myeloid leukemiaResistance mechanismsTargeted therapy

Identifiers

PMID39085680

What OpenQuestion holds

Textmetadata
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.