Evidence map›Paper›PMID 35039904›Full record

ArticleCancer immunology, immunotherapy : CII2022

Novel inhibitor of hematopoietic cell kinase as a potential therapeutic agent for acute myeloid leukemia.

Fernanda Marconi Roversi, Maura Lima Pereira Bueno, Juliete Aparecida Francisco da Silva, Guilherme Rossi Assis-Mendonça, Cristiane Okuda Torello, Rodrigo Nato Shiraishi, Fernando Viera Pericole, Karla Priscila Ferro, Adriana Santos Silva Duarte, Eduardo Magalhães Rego and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  5. The antitumor effects of WNT5A against hematological malignancies.Journal of cell communication and signaling · 2023
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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 3 institutions in 2 countries.

Fernanda Marconi RoversiHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil.ORCID http://orcid.org/0000-0002-8285-918X
Maura Lima Pereira BuenoHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil.
Juliete Aparecida Francisco da SilvaDepartment of Ophthalmology and Visual Sciences, University of Alabama at Birmingham-UAB, Birmingham, AL, USA.
Guilherme Rossi Assis-MendonçaDepartment of Pathology, Faculty of Medical Sciences, University of Campinas-Unicamp, Campinas, São Paulo, Brazil.
Cristiane Okuda TorelloHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil.
Rodrigo Nato ShiraishiHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil.
Fernando Viera PericoleHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil.
Karla Priscila FerroHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil.
Adriana Santos Silva DuarteHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil.
Eduardo Magalhães RegoDivision of Hematology, Hospital das Clínicas da Faculdade de Medicina (HCFMUSP), University of São Paulo Medical School, University of São Paulo, São Paulo, Brazil.
Sara Teresinha Olalla SaadHematology and Transfusion Medicine Center, University of Campinas/Hemocentro-Unicamp, Universitária Zeferino Vaz - Barão Geraldo, Rua Carlos Chagas, 480 - Cidade Campinas, São Paulo, Brazil. sara@unicamp.br.
Universidade Estadual de Campinas (UNICAMP) · BRHospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRUniversity of Alabama at Birmingham · US

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2011/22376-7Fundação de Amparo à Pesquisa do Estado de São Paulo 2017/21801-2
6 · The paper itself

Abstract

Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are characterized by risk of relapses, poor survival, unwanted side effects and high toxicity with the current therapies. In light of these facts, there are efforts to develop new drugs specific for deregulated molecules that participate in leukemia pathogenesis. Hematopoietic cell kinase (HCK), an Src kinase family member, is overexpressed on hematopoietic stem cells of MDS and de novo AML patients and involved in the oncogenic process. Thus, we investigated in vitro, ex vivo and in vivo effects of a novel chemical compound targeting HCK inhibition (iHCK-37), in combination with the most used drugs for the treatment of MDS and de novo AML, 5-Azacytidine and Cytarabine. Herein, the combination treatment with iHCK-37 and 5-Azacytidine or Cytarabine demonstrated additive effects against leukemia cells, compared to either drug alone. iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression. Moreover, treatment with iHCK-37 reduced MDS and AML CD34-positive cell numbers inside a 3D-structure but did not affect normal CD34-positive cell numbers. In vivo analysis showed that leukemic mice treated with iHCK-37 had reduced ERK and AKT proteins phosphorylation levels and leukocyte numbers. In conclusion, the iHCK-37 inhibitor has anti-neoplastic activity in leukemia cells without altering apoptosis and survival rate of normal cells, suggesting on-target malignant cell killing activity as a single agent or in combination with 5-Azacytidine or Cytarabine.

Indexed as

Leukemia, Myeloid, AcuteMyelodysplastic SyndromesAnimalsAzacitidineCytarabineMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-hckAzacitidineCytarabinePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-hckDe novo acute myeloid leukemiaDrug inhibitionHematopoietic cell kinaseiHCK-37Myelodysplastic syndrome

Identifiers

PMID35039904
PMCPMC10992478
OpenAlexW4205940652

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.