Evidence map›Paper›PMID 33980611›Full record

ArticleMolecular cancer research : MCR2021

EGR1 Addiction in Diffuse Large B-cell Lymphoma.

Shuichi Kimpara, Li Lu, Nguyet M Hoang, Fen Zhu, Paul D Bates, Anusara Daenthanasanmak, Shanxiang Zhang, David T Yang, Amanda Kelm, Yunxia Liu and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 14 citations in OpenAlex.

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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

18 authors at 3 institutions in 1 country.

Shuichi Kimpara *Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Li Lu *Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Nguyet M Hoang *Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Fen ZhuDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Paul D BatesDepartment of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Anusara DaenthanasanmakLymphoid Malignancies Branch, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.ORCID 0000-0002-6404-7444
Shanxiang ZhangDepartment of Pathology and Laboratory Medicine, Indiana University, Indianapolis, Indiana.
David T YangCarbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Amanda KelmDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Yunxia LiuDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Yangguang LiDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Alexander RosiejkaDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Apoorv KondapelliDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Samantha BebelDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Madelyn ChenDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin.
Thomas A WaldmannLymphoid Malignancies Branch, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Christian M CapitiniCarbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin. lrui@medicine.wisc.edu ccapitini@pediatrics.wisc.edu.ORCID 0000-0002-2276-6731
Lixin RuiDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin. lrui@medicine.wisc.edu ccapitini@pediatrics.wisc.edu.
University of Wisconsin–Madison · USCenter for Cancer Research · USIndiana University Health · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
IL-2:IL-15 : implications for cancer therapy (Investigator -Initiated Project)ZIASC004002 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI WALDMANN, THOMAS · 2009 to 2022
$22.9M
Epigenetic Gene Regulation by JAK1 Kinase in Diffuse Large B-Cell LymphomaR01CA187299 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RUI, LIXIN · 2015 to 2019
$1.7M
Inhibiting STAT1 as a novel graft-versus-host/graft-versus-leukemia therapyK08CA174750 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI CAPITINI, CHRISTIAN · 2014 to 2017
$715k
NCI NIH HHS K08 CA174750NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA187299
6 · The paper itself

Abstract

Early growth response gene (EGR1) is a transcription factor known to be a downstream effector of B-cell receptor signaling and Janus kinase 1 (JAK1) signaling in diffuse large B-cell lymphoma (DLBCL). While EGR1 is characterized as a tumor suppressor in leukemia and multiple myeloma, the role of EGR1 in lymphoma is unknown. Here we demonstrate that EGR1 is a potential oncogene that promotes cell proliferation in DLBCL. IHC analysis revealed that EGR1 expression is elevated in DLBCL compared with normal lymphoid tissues and the level of EGR1 expression is higher in activated B cell-like subtype (ABC) than germinal center B cell-like subtype (GCB). EGR1 expression is required for the survival and proliferation of DLBCL cells. Genomic analyses demonstrated that EGR1 upregulates expression of MYC and E2F pathway genes through the CBP/p300/H3K27ac/BRD4 axis while repressing expression of the type I IFN pathway genes by interaction with the corepressor NAB2. Genetic and pharmacologic inhibition of EGR1 synergizes with the BRD4 inhibitor JQ1 or the type I IFN inducer lenalidomide in growth inhibition of ABC DLBCL both in cell cultures and xenograft mouse models. Therefore, targeting oncogenic EGR1 signaling represents a potential new targeted therapeutic strategy in DLBCL, especially for the more aggressive ABC DLBCL. IMPLICATIONS: The study characterizes EGR1 as a potential oncogene that promotes cell proliferation and defines EGR1 as a new molecular target in DLBCL, the most common non-Hodgkin lymphoma.

Indexed as

AnimalsCell Line, TumorCell ProliferationCell SurvivalEarly Growth Response Protein 1FemaleGene Expression Regulation, NeoplasticHumansLymphoma, Large B-Cell, DiffuseMaleMiceMice, Inbred NODSignal TransductionUp-RegulationEarly Growth Response Protein 1EGR1 protein, human

Identifiers

PMID33980611
PMCPMC8349889
OpenAlexW3162961592

What OpenQuestion holds

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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.