Evidence map›Paper›PMID 32404407›Full record

ArticleMolecular cancer therapeutics2020

Combinatorial Inhibition of Focal Adhesion Kinase and BCL-2 Enhances Antileukemia Activity of Venetoclax in Acute Myeloid Leukemia.

Xiangmeng Wang, Po Yee Mak, Hong Mu, Wenjing Tao, Arvind Rao, Ravikumar Visweswaran, Vivian Ruvolo, Jonathan A Pachter, David T Weaver, Michael Andreeff and 2 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cancer therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 21 citations in OpenAlex.

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  9. BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021
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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

12 authors at 3 institutions in 2 countries.

Xiangmeng WangSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Po Yee MakSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Hong MuSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Wenjing TaoSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Arvind RaoThe Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Ravikumar VisweswaranThe Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Vivian RuvoloSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jonathan A PachterVerastem, Inc., Needham, Massachusetts.ORCID 0000-0002-0263-474X
David T WeaverVerastem, Inc., Needham, Massachusetts.
Michael AndreeffSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas. mandreef@mdanderson.org bicarter@mdanderson.org xubingzhangjian@126.com.ORCID 0000-0002-1144-1958
Bing XuDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China. mandreef@mdanderson.org bicarter@mdanderson.org xubingzhangjian@126.com.
Bing Z CarterSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas. mandreef@mdanderson.org bicarter@mdanderson.org xubingzhangjian@126.com.
The University of Texas MD Anderson Cancer Center · USVerastem (United States) · USFirst Affiliated Hospital of Xiamen University · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Focal adhesion kinase (FAK) promotes cancer cell growth and metastasis. We previously reported that FAK inhibition by the selective inhibitor VS-4718 exerted antileukemia activities in acute myeloid leukemia (AML). The mechanisms involved, and whether VS-4718 potentiates efficacy of other therapeutic agents, have not been investigated. Resistance to apoptosis inducted by the BCL-2 inhibitor ABT-199 (venetoclax) in AML is mediated by preexisting and ABT-199-induced overexpression of MCL-1 and BCL-XL. We observed that VS-4718 or silencing FAK with siRNA decreased MCL-1 and BCL-XL levels. Importantly, VS-4718 antagonized ABT-199-induced MCL-1 and BCL-XL. VS-4718 markedly synergized with ABT-199 to induce apoptosis in AML cells, including primary AML CD34

Indexed as

AnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorBridged Bicyclo Compounds, HeterocyclicCell ProliferationFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticHumansLeukemia, Myeloid, AcuteMaleMiceMice, Inbred NODMice, SCIDNucleophosminProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsBCL2 protein, humanBiomarkers, TumorBridged Bicyclo Compounds, HeterocyclicFocal Adhesion Kinase 1NPM1 protein, humanNpm1 protein, mouseNucleophosminProto-Oncogene Proteins c-bcl-2PTK2 protein, humanSulfonamidesvenetoclax

Identifiers

PMID32404407
PMCPMC7416436
OpenAlexW3025975123

What OpenQuestion holds

Textmetadata
LicenceTDM
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.