Evidence map›Paper›PMID 35532877›Full record

ReviewInternational journal of hematology2022

FLT3-targeted treatment for acute myeloid leukemia.

Yasuyuki Arai, SungGi Chi, Yosuke Minami, Masamitsu Yanada

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of hematology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. A Review of FLT3 Kinase Inhibitors in AML.Journal of clinical medicine · 2023
    Review
  11. Article
  12. Flavones, Flavonols, Lignans, and Caffeic Acid Derivatives fromInternational journal of molecular sciences · 2022
    Article
  13. Article
  14. Binding Studies and Lead Generation of Pteridin-7(8International journal of molecular sciences · 2022
    Article
  15. 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

4 authors at 3 institutions in 1 country.

Yasuyuki AraiDepartment of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
SungGi ChiDepartment of Hematology, National Cancer Center Hospital East, Kashiwa, Japan.
Yosuke MinamiDepartment of Hematology, National Cancer Center Hospital East, Kashiwa, Japan.
Masamitsu YanadaDepartment of Hematology and Cell Therapy, Aichi Cancer Center, 1-1 Kanokoden, Chikusa-ku, Nagoya, 464-8681, Japan. myanada@aichi-cc.jp.ORCID http://orcid.org/0000-0003-1602-9775
National Cancer Center Hospital East · JPAichi Cancer Center · JPKyoto University · JP

Funding

Aichi Cancer Research Foundation 2021-1-19National Cancer Research and Development 2021-A-11
6 · The paper itself

Abstract

Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene are detected in approximately 30% of acute myeloid leukemia (AML). The high frequency of FLT3 mutations, along with their adverse effect on prognosis, makes FLT3 a promising therapeutic target, and has spurred development of FLT3 inhibitors. First-generation inhibitors, including midostaurin and sorafenib, lack specificity for FLT3 and act on multiple kinases, whereas second-generation inhibitors, including gilteritinib, and quizartinib, are highly specific to FLT3 and are more potent than first-generation inhibitors. Several FLT3 inhibitors have recently gained regulatory approval worldwide, and several others are under development. The advent of FLT3 inhibitors has changed the standard treatment for FLT3-mutated AML in the frontline and relapsed/refractory settings and contributed to improved outcomes for this formidable AML subtype. However, numerous unresolved issues remain owing to rapid changes in practice. These include identification of optimum FLT3 inhibitors and combination therapies, the role of maintenance therapy, and the indication for allogeneic hematopoietic cell transplantation. Furthermore, strategies to overcome resistance to FLT3 inhibitors must be pursued. Results of ongoing and future studies will improve our ability to use FLT3 inhibitors more effectively, which should provide significant benefits to a wider range of patients.

Indexed as

Antineoplastic Agentsfms-Like Tyrosine Kinase 3Hematopoietic Stem Cell TransplantationLeukemia, Myeloid, AcuteProtein Kinase InhibitorsHumansMutationAntineoplastic AgentsFLT3 protein, humanfms-Like Tyrosine Kinase 3Protein Kinase InhibitorsAcute myeloid leukemiaAllogeneic hematopoietic cell transplantationFLT3Targeted therapy

Identifiers

PMID35532877
OpenAlexW4229374919

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.