Evidence map›Paper›PMID 25079338›Full record

ArticleBritish journal of haematology2014

Apoptosis repressor with caspase recruitment domain modulates second mitochondrial-derived activator of caspases mimetic-induced cell death through BIRC2/MAP3K14 signalling in acute myeloid leukaemia.

Po Y Mak, Duncan H Mak, Vivian Ruvolo, Rodrigo Jacamo, Steven M Kornblau, Hagop Kantarjian, Michael Andreeff, Bing Z Carter

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in British journal of haematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

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  14. A myeloid tumor suppressor role forThe Journal of experimental medicine · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Po Y MakSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Duncan H Mak
Vivian Ruvolo
Rodrigo Jacamo
Steven M Kornblau
Hagop Kantarjian
Michael Andreeff
Bing Z Carter
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KONOPLEVA, MARINA Y · 2003 to 2023
$43.7M
THE THERAPY OF AMLP01CA055164 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMAS, MATTIE J · 1992 to 2011
$25.3M
NCI NIH HHS CA016672NCI NIH HHS CA100632NCI NIH HHS P01 CA055164NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA100632
6 · The paper itself

Abstract

Overexpression of the apoptosis repressor with caspase recruitment domain (ARC, also termed NOL3) protein predicts adverse outcome in patients with acute myeloid leukaemia (AML) and confers drug resistance to AML cells. The second mitochondrial-derived activator of caspases (SMAC, also termed DIABLO) mimetic, birinapant, promotes extrinsic apoptosis in AML cells. SMAC mimetics induce cleavage of cellular inhibitor of apoptosis (cIAP) proteins, leading to stabilization of the nuclear factor-κB (NF-κB)-inducing kinase (MAP3K14, also termed NIK) and activation of non-canonical NF-κB signalling. To enhance the therapeutic potential of SMAC mimetics in AML, we investigated the regulation and role of ARC in birinapant-induced apoptosis. We showed that birinapant increases ARC in AML and bone marrow-derived mesenchymal stromal cells (MSCs). Downregulation of MAP3K14 by siRNA decreased ARC levels and suppressed birinapant-induced ARC increase. Reverse-phase protein array analysis of 511 samples from newly diagnosed AML patients showed that BIRC2 (also termed cIAP1) and ARC were inversely correlated. Knockdown of ARC sensitized, while overexpression attenuated, birinapant-induced apoptosis. Furthermore, ARC knockdown in MSCs sensitized co-cultured AML cells to birinapant-induced apoptosis. Our data demonstrate that ARC is regulated via BIRC2/MAP3K14 signalling and its overexpression in AML or MSCs can function as a resistant factor to birinapant-induced leukaemia cell death, suggesting that strategies to inhibit ARC will improve the therapeutic potential of SMAC mimetics.

Indexed as

Gene Expression Regulation, LeukemicAgedAntimetabolites, AntineoplasticApoptosisApoptosis Regulatory ProteinsCoculture TechniquesDipeptidesDrug DesignDrug Resistance, NeoplasmHumansIndolesInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsLeukemia, Myeloid, AcuteMAP Kinase Signaling SystemMesenchymal Stem CellsAntimetabolites, AntineoplasticApoptosis Regulatory ProteinsBIRC2 protein, humanbirinapantDIABLO protein, humanDipeptidesIndolesInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsMuscle ProteinsNF-kappa BNF-kappaB-Inducing KinaseNOL3 protein, humanProtein Serine-Threonine KinasesRNA, Small InterferingTumor Necrosis Factor-alphaUbiquitin-Protein Ligasesacute myeloid leukaemiaapoptosis repressor with caspaseBIRC2birinapantMAP3K14

Identifiers

PMID25079338
PMCPMC4357400
OpenAlexW2127362505

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.