Evidence map›Paper›PMID 38164178›Full record

ReviewInternational journal of biological sciences2024

Mechanisms underlying therapeutic resistance of tyrosine kinase inhibitors in chronic myeloid leukemia.

Jingnan Sun, Ruiping Hu, Mengyuan Han, Yehui Tan, Mengqing Xie, Sujun Gao, Ji-Fan Hu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
9.9field-weighted citation impact, top 2% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
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  5. The silent players: AtypicalOncology reports · 2025
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  10. Allele-Specific PCR for Detection of Missense Mutations in the ChimericInternational journal of molecular sciences · 2025
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  15. Advances in pyrazolo[1,5-RSC advances · 2025
    Review
  16. Article
  17. Molecular medicine reports · 2024
    Article
  18. Imatinib‑induced gynecomastia: A case report.Experimental and therapeutic medicine · 2024
    Article
  19. Review
  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

7 authors at 2 institutions in 2 countries.

Jingnan SunHematology Department, First hospital of Jilin University, Changchun, Jilin, 130021, P.R. China.
Ruiping HuHematology Department, First hospital of Jilin University, Changchun, Jilin, 130021, P.R. China.
Mengyuan HanHematology Department, First hospital of Jilin University, Changchun, Jilin, 130021, P.R. China.
Yehui TanHematology Department, First hospital of Jilin University, Changchun, Jilin, 130021, P.R. China.
Mengqing XieHematology Department, First hospital of Jilin University, Changchun, Jilin, 130021, P.R. China.
Sujun GaoHematology Department, First hospital of Jilin University, Changchun, Jilin, 130021, P.R. China.
Ji-Fan HuHematology Department, First hospital of Jilin University, Changchun, Jilin, 130021, P.R. China.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a malignant clonal disease involving hematopoietic stem cells that is characterized by myeloid cell proliferation in bone marrow and peripheral blood, and the presence of the Philadelphia (Ph) chromosome with BCR-ABL fusion gene. Treatment of CML has dramatically improved since the advent of tyrosine kinase inhibitors (TKI). However, there are a small subset of CML patients who develop resistance to TKI. Mutations in the ABL kinase domain (KD) are currently recognized as the leading cause of TKI resistance in CML. In this review, we discuss the concept of resistance and summarize recent advances exploring the mechanisms underlying CML resistance. Overcoming TKI resistance appears to be the most successful approach to reduce the burden of leukemia and enhance cures for CML. Advances in new strategies to combat drug resistance may rapidly change the management of TKI-resistant CML and expand the prospects for available therapies.

Indexed as

Leukemia, Myelogenous, Chronic, BCR-ABL PositiveTyrosine Kinase InhibitorsDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansProtein Kinase InhibitorsFusion Proteins, bcr-ablProtein Kinase InhibitorsTyrosine Kinase InhibitorsABL mutationchronic myeloid leukemiamechanismTKI Resistance

Identifiers

PMID38164178
PMCPMC10750272
OpenAlexW4388699736

What OpenQuestion holds

Textmetadata
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.