Evidence map›Paper›PMID 31463864›Full record

ReviewCurrent hematologic malignancy reports2019

Molecular Mechanisms of Resistance to Tyrosine Kinase Inhibitors.

Marjan Yaghmaie, Cecilia Cs Yeung

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hematologic malignancy reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Chronic Myeloid Leukemia and the T315IInternational journal of molecular sciences · 2025
    Review
  2. Article
  3. Article
  4. Getting the right combination to break the epigenetic code.Nature reviews. Clinical oncology · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Association ofThe Indian journal of medical research · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Resistance Mechanisms in Pediatric B-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 2 countries.

Marjan YaghmaieHematology, Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran. marjix58@gmail.com.
Cecilia Cs YeungFred Hutchinson Cancer Research Center, Clinical Research Division, Seattle, WA, USA.
Tehran University of Medical Sciences · IRUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewChronic myeloid leukemia (CML) patients with constitutive activity of BCR-ABL1 oncoprotein frequently derive significant clinical benefits from tyrosine kinase inhibitors (TKIs). Point mutations in the ABL1 kinase domain (KD) are an important mechanism of TKI resistance in CML. In this review, we present molecular mechanisms of TKI resistance paying particular attention to drug resistance which allows for a survival advantage in CML. RECENT

findingsSensitive disease monitoring is a required standard of care for management of CML. Screening of these mutations fail to explain 20-40% of resistant cases where activation of different survival pathways must be the main reason for resistance. Eliminating TKI resistance appears to be the most successful therapeutic way to decrease leukemic disease burden and potentiate cure. Advances on novel strategies for identifying and confronting drug resistance are rapidly altering management of CML that are resistant to TKI and expanding the landscape of available therapies.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsFusion Proteins, bcr-ablGene Expression Regulation, LeukemicHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMutationProtein Kinase InhibitorsTreatment OutcomeAntineoplastic AgentsFusion Proteins, bcr-ablImatinib MesylateProtein Kinase InhibitorsChronic myeloid leukemiaMolecular mechanismResistance mutationsTyrosine kinase inhibitor

Identifiers

PMID31463864
OpenAlexW2970976867

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.