Evidence map›Paper›PMID 39614924›Full record

ArticleAnnals of hematology2024

FLT3 inhibitors and hematopoietic cell transplantation prolong survival in patients with FLT3-ITD-positive AML.

Toshihiro Matsukawa, Masahiro Onozawa, Takeshi Kondo, Minoru Kanaya, Daisuke Hidaka, Shuichi Ota, Akio Mori, Akio Shigematsu, Takuto Miyagishima, Yasutaka Kakinoki and 20 more

Abstract read
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Article in Annals 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. Leukemia cutis as the first manifestation of acute myeloid leukemia.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2026
    Article
  2. Novel juxtamembraneFrontiers in oncology · 2026
    Article
  3. Observational
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

30 authors.

Toshihiro MatsukawaDepartment of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan. toshimatsukawa@med.hokudai.ac.jp.
Masahiro OnozawaDepartment of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan.
Takeshi KondoBlood Disorders Center, Aiiku Hospital, Sapporo, Japan.
Minoru KanayaBlood Disorders Center, Aiiku Hospital, Sapporo, Japan.
Daisuke HidakaDepartment of Hematology, Sapporo Hokuyu Hospital, Sapporo, Japan.
Shuichi OtaDepartment of Hematology, Sapporo Hokuyu Hospital, Sapporo, Japan.
Akio MoriBlood Disorders Center, Aiiku Hospital, Sapporo, Japan.
Akio ShigematsuDepartment of Hematology, Kushiro Rosai Hospital, Kushiro, Japan.
Takuto MiyagishimaDepartment of Hematology, Kushiro Rosai Hospital, Kushiro, Japan.
Yasutaka KakinokiDepartment of Hematology, Asahikawa City Hospital, Asahikawa, Japan.
Junichi HashiguchiInternal Medicine/General Medicine, Kitami Red Cross Hospital, Kitami, Japan.
Satoshi YamamotoDepartment of Hematology, Sapporo City General Hospital, Sapporo, Japan.
Masayo YamamotoDivision of Hematology, Department of Internal Medicine, Asahikawa Medical University, Asahikawa, Japan.
Kentaro WakasaDepartment of Hematology, Obihiro Kosei Hospital, Obihiro, Japan.
Mutsumi TakahataDepartment of Hematology, Sapporo Kosei Hospital, Sapporo, Japan.
Toshimichi IshiharaDepartment of Hematology, Kin-ikyo Chuo Hospital, Sapporo, Japan.
Yoshihito HaseyamaDepartment of Hematology, Tonan Hospital, Sapporo, Japan.
Akihito FujimiDepartment of Hematology, Sapporo Kiyota Hospital, Sapporo, Japan.
Tetsuya IgarashiDepartment of Hematology, Tenshi Hospital, Sapporo, Japan.
Takehiro SarashinaDepartment of Pediatrics, Asahikawa Medical University Hospital, Asahikawa, Japan.
Satoshi IyamaDepartment of Medical Oncology and Hematology, Sapporo Medical University Hospital, Sapporo, Japan.
Ryoji KobayashiDepartment of Hematology/Oncology for Children and Adolescents, Sapporo Hokuyu Hospital, Sapporo, Japan.
Hajime SakaiDepartment of Hematology, Teine Keijinkai Hospital, Sapporo, Japan.
Katsuya FujimotoDepartment of Hematology, NHO Hokkaido Cancer Center, Sapporo, Japan.
Junki InamuraDepartment of Hematology/Oncology, Asahikawa Kosei General Hospital, Asahikawa, Japan.
Yuji KanisawaDepartment of Hematology/Oncology, Oji General Hospital, Tomakomai, Japan.
Shinsuke HirabayashiDepartment of Pediatrics, Hokkaido University Faculty of Medicine, Sapporo, Japan.
Tomoyuki EndoDepartment of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan.
Daigo HashimotoDepartment of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan.
Takanori TeshimaDepartment of Hematology, Hokkaido University Faculty of Medicine, Sapporo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is an aggressive hematological malignancy with genetic alterations. The FMS-like tyrosine kinase 3 (FLT3) gene is frequently mutated in adult de novo AML, with two types of mutations: internal tandem duplication (ITD) and point mutations in the tyrosine kinase domain. This study aimed to investigate the impact of FLT3 inhibitors and hematopoietic cell transplantation (HCT) on survival outcomes in patients with FLT3-ITD AML in a real-world setting. We retrospectively analyzed 139 patients with FLT3-ITD-positive AML between 2012 and 2021. The median age was 63 years. In the propensity score-matched cohort, FLT3 inhibitors improved overall survival (OS) compared with patients treated without FLT3 inhibitors (3-year OS: 33.7% vs. 25.8%, p = 0.021). Patients who underwent HCT had superior outcomes to those without HCT (3-year OS: 45.3% vs. 2.2%, p < 0.0001). The combination of FLT3 inhibitors and HCT resulted in the highest OS and relapse-free survival (RFS) rates (3-year OS: 62.4%; 3-year RFS: 44.4%). Disease status before transplantation did not predict the prognosis, but use of FLT3 inhibitors increased survival in patients without complete remission before HCT. These results demonstrate the clinical impact of FLT3 inhibitors on survival outcomes in patients with FLT3-ITD-positive AML, particularly when combined with HCT. FLT3 inhibitors can improve the prognosis of AML with FLT3 mutations, especially in patients who undergo HCT.

Indexed as

fms-Like Tyrosine Kinase 3Hematopoietic Stem Cell TransplantationLeukemia, Myeloid, AcuteProtein Kinase InhibitorsAdultAgedDisease-Free SurvivalFemaleHumansMaleMiddle AgedRetrospective StudiesSurvival RateTandem Repeat SequencesFLT3 protein, humanfms-Like Tyrosine Kinase 3Protein Kinase InhibitorsAcute myeloid leukemiaFLT3 inhibitorFLT3-ITDHematopoietic cell transplantation

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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.