Evidence map›Paper›PMID 34233924›Full record

ArticleCancer research2021

Metabolic Enzyme DLST Promotes Tumor Aggression and Reveals a Vulnerability to OXPHOS Inhibition in High-Risk Neuroblastoma.

Nicole M Anderson, Xiaodan Qin, Jennifer M Finan, Andrew Lam, Jacob Athoe, Rindert Missiaen, Nicolas Skuli, Annie Kennedy, Amandeep S Saini, Ting Tao and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 65 citations in OpenAlex.

  1. 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

16 authors at 7 institutions in 2 countries.

Nicole M AndersonAbramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Xiaodan QinDepartments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, The Center for Cancer Research, Boston University School of Medicine, Boston, Massachusetts.
Jennifer M FinanAbramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.ORCID 0000-0001-7706-1643
Andrew LamDepartments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, The Center for Cancer Research, Boston University School of Medicine, Boston, Massachusetts.
Jacob AthoeDepartments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, The Center for Cancer Research, Boston University School of Medicine, Boston, Massachusetts.
Rindert MissiaenAbramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Nicolas SkuliAbramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Annie KennedyAbramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
Amandeep S SainiDepartments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, The Center for Cancer Research, Boston University School of Medicine, Boston, Massachusetts.ORCID 0000-0003-4032-0562
Ting TaoNational Clinical Research Center for Child Health, National Children's Regional Medical Center, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.ORCID 0000-0003-1260-2351
Shizhen ZhuDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Mayo Clinic Cancer Center, Rochester, Minnesota.ORCID 0000-0002-2929-3279
Itzhak NissimDivision of Genetics and Metabolism, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.
A Thomas LookDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.ORCID 0000-0001-7851-8617
Guoliang QingFrontier Science Center for Immunology & Metabolism, Medical Research Institute, Wuhan University, Wuhan, Hubei, China.
M Celeste SimonAbramson Family Cancer Research Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania. huifeng@bu.edu celeste2@pennmedicine.upenn.edu.ORCID 0000-0001-9106-447X
Hui FengDepartments of Pharmacology and Medicine, Section of Hematology and Medical Oncology, The Center for Cancer Research, Boston University School of Medicine, Boston, Massachusetts. huifeng@bu.edu celeste2@pennmedicine.upenn.edu.
University of Pennsylvania · USBoston Medical Center · USChildren's Hospital of Philadelphia · USChildren's Hospital of Zhejiang University · CNDana-Farber Cancer Institute · USMayo Clinic · USWuhan University of Science and Technology · CN

Funding

Project-005UL1TR001430 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BAIR-MERRITT, MEGAN H, CENTER, DAVID M. · 2015 to 2024
$52.3M
TRANSLATIONAL CONTROL IN ADAPTATION TO HYPOXIAP01CA104838 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SIMON, M. CELESTE · 2004 to 2018
$17.6M
Mechanisms and Vulnerabilities of Aberrant Transcriptional Enhancers in CancerR35CA210064 · NCI · DANA-FARBER CANCER INST · PI LOOK, A. THOMAS · 2016 to 2022
$7.3M
The Role of DLST in LeukemogenesisR01CA215059 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FENG, HUI · 2018 to 2022
$2.0M
"Oncorequisite" Genes in MYC-mediated TransformationR00CA134743 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FENG, HUI · 2012 to 2014
$712k
The Role of DLST in LeukemogenesisR56CA215059 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FENG, HUI · 2017 to 2017
$376k
"Oncorequisite" Genes in MYC-mediated TransformationK99CA134743 · NCI · DANA-FARBER CANCER INST · PI FENG, HUI · 2009 to 2010
$282k
NCATS NIH HHS UL1 TR001430NCI NIH HHS K99 CA134743NCI NIH HHS P01 CA104838NCI NIH HHS R00 CA134743NCI NIH HHS R01 CA215059NCI NIH HHS R35 CA210064NCI NIH HHS R56 CA215059
6 · The paper itself

Abstract

High-risk neuroblastoma remains therapeutically challenging to treat, and the mechanisms promoting disease aggression are poorly understood. Here, we show that elevated expression of dihydrolipoamide S-succinyltransferase (DLST) predicts poor treatment outcome and aggressive disease in patients with neuroblastoma. DLST is an E2 component of the α-ketoglutarate (αKG) dehydrogenase complex, which governs the entry of glutamine into the tricarboxylic acid cycle (TCA) for oxidative decarboxylation. During this irreversible step, αKG is converted into succinyl-CoA, producing NADH for oxidative phosphorylation (OXPHOS). Utilizing a zebrafish model of MYCN-driven neuroblastoma, we demonstrate that even modest increases in DLST expression promote tumor aggression, while monoallelic

Indexed as

Oxidative PhosphorylationAcyltransferasesAnimalsApoptosisBrain NeoplasmsCell Line, TumorCollagenDisease Models, AnimalDrug CombinationsFemaleGene Expression ProfilingHEK293 CellsHumansInhibitory Concentration 50Ketoglutarate Dehydrogenase ComplexLamininAcyltransferasesCollagendihydrolipoamide succinyltransferaseDrug CombinationsKetoglutarate Dehydrogenase ComplexLamininmatrigelOxygenProteoglycansTricarboxylic Acids

Identifiers

PMID34233924
PMCPMC8577318
OpenAlexW3180723792

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.