Evidence map›Paper›PMID 32811837›Full record

ArticleNature communications2020

Chlorpromazine eliminates acute myeloid leukemia cells by perturbing subcellular localization of FLT3-ITD and KIT-D816V.

Shinya Rai, Hirokazu Tanaka, Mai Suzuki, J Luis Espinoza, Takahiro Kumode, Akira Tanimura, Takafumi Yokota, Kenji Oritani, Toshio Watanabe, Yuzuru Kanakura and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  7. Nuclear Control of Mitochondrial Homeostasis and Venetoclax Efficacy in AML via COX4I1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Importance of PTM of FLT3 in acute myeloid leukemia.Acta biochimica et biophysica Sinica · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. A platform utilizingProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Article
  16. Article
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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

11 authors at 4 institutions in 1 country.

Shinya Rai *Department of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.ORCID http://orcid.org/0000-0003-3929-9751
Hirokazu Tanaka *Department of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan. htanaka@med.kindai.ac.jp.ORCID http://orcid.org/0000-0002-7192-525X
Mai SuzukiDivision of Hematological Malignancy, National Cancer Center Research Institute, Chuo, Tokyo, Japan.
J Luis EspinozaDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.ORCID http://orcid.org/0000-0002-1794-6666
Takahiro KumodeDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.
Akira TanimuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Takafumi YokotaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Kenji OritaniDepartment of Hematology, International University of Health and Welfare, Narita, Chiba, Japan.
Toshio WatanabeDepartment of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Nara, Japan.
Yuzuru KanakuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Itaru MatsumuraDepartment of Hematology and Rheumatology, Kindai University Faculty of Medicine, Osaka-sayama, Osaka, Japan.ORCID http://orcid.org/0000-0003-2818-4270
Kindai University · JPThe University of Osaka · JPInternational University of Health and Welfare · JPNara Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutated receptor tyrosine kinases (MT-RTKs) such as internal tandem duplication of FMS-like tyrosine kinase 3 (FLT3 ITD) and a point mutation KIT D816V are driver mutations for acute myeloid leukemia (AML). Clathrin assembly lymphoid myeloid leukemia protein (CALM) regulates intracellular transport of RTKs, however, the precise role for MT-RTKs remains elusive. We here show that CALM knock down leads to severely impaired FLT3 ITD- or KIT D814V-dependent cell growth compared to marginal influence on wild-type FLT3- or KIT-mediated cell growth. An antipsychotic drug chlorpromazine (CPZ) suppresses the growth of primary AML samples, and human CD34

Indexed as

AdolescentAdultAgedAged, 80 and overAnimalsAntineoplastic AgentsApoptosisCell ProliferationCell SurvivalChlorpromazineFemalefms-Like Tyrosine Kinase 3HL-60 CellsHumansLeukemia, Myeloid, AcuteMaleAntineoplastic AgentsChlorpromazineFLT3 protein, humanfms-Like Tyrosine Kinase 3Monomeric Clathrin Assembly ProteinsPICALM protein, humanProto-Oncogene Proteins c-kit

Identifiers

PMID32811837
PMCPMC7434901
OpenAlexW3056247019

What OpenQuestion holds

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Registered trials

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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.