Evidence map›Paper›PMID 28368403›Full record

ArticleOncogene2017

HBEGF promotes gliomagenesis in the context of Ink4a/Arf and Pten loss.

C H Shin, J P Robinson, J A Sonnen, A E Welker, D X Yu, M W VanBrocklin, S L Holmen

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Manganese-Templated Nontrivial Structures for MRI and Therapy.Journal of the American Chemical Society · 2026
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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

7 authors at 3 institutions in 1 country.

C H ShinHuntsman Cancer Institute, University of Utah Health Sciences Center, University of Utah, Salt Lake City, UT, USA.
J P RobinsonHormel Institute, University of Minnesota, Austin, MN, USA.
J A SonnenDepartment of Pathology, University of Utah Health Sciences Center, Salt Lake City, UT, USA.
A E WelkerHuntsman Cancer Institute, University of Utah Health Sciences Center, University of Utah, Salt Lake City, UT, USA.
D X YuHuntsman Cancer Institute, University of Utah Health Sciences Center, University of Utah, Salt Lake City, UT, USA.
M W VanBrocklinHuntsman Cancer Institute, University of Utah Health Sciences Center, University of Utah, Salt Lake City, UT, USA.
S L HolmenHuntsman Cancer Institute, University of Utah Health Sciences Center, University of Utah, Salt Lake City, UT, USA.
University of Utah · USHuntsman Cancer Institute · USHormel (United States) · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Defining the role of mutant IDH in glioma initiation and maintenanceR01NS075155 · NINDS · UNIVERSITY OF UTAH · PI HOLMEN, SHERI L · 2011 to 2016
$1.7M
Defining the role of BRAF in glioma initiation and maintenanceR01NS073870 · NINDS · UNIVERSITY OF UTAH · PI HOLMEN, SHERI L · 2011 to 2016
$1.7M
The role of stromal APC haploinsufficiency in colorectal tumorigenesisR00CA175690 · NCI · UNIVERSITY OF MINNESOTA · PI ROBINSON, JAMES PETER · 2015 to 2017
$747k
Characterizing HBEGF in glioma formation and maintenanceF30CA203096 · NCI · UNIVERSITY OF UTAH · PI SHIN, CLIFFORD · 2016 to 2018
$94k
NCI NIH HHS F30 CA203096NCI NIH HHS P30 CA042014NCI NIH HHS R00 CA175690NINDS NIH HHS R01 NS073870NINDS NIH HHS R01 NS075155
6 · The paper itself

Abstract

Heparin-binding epidermal growth factor (EGF)-like growth factor (HBEGF) is a ligand for the EGF receptor (EGFR), one of the most commonly amplified receptor tyrosine kinases (RTKs) in glioblastoma (GBM). While HBEGF has been found to be expressed in a subset of malignant gliomas, its sufficiency for glioma initiation has not been evaluated. In this study, we demonstrate that HBEGF can initiate GBM in mice in the context of Ink4a/Arf and Pten loss, and that these tumors are similar to the classical GBM subtype observed in patients. Isogenic astrocytes from these mice showed activation not only of Egfr but also the RTK Axl in response to HBEGF stimulation. Deletion of either Egfr or Axl decreased the tumorigenic properties of HBEGF-transformed cells; however, only EGFR was able to rescue the phenotype in cells lacking both RTKs indicating that Egfr is required for activation of Axl in this context. Silencing of HBEGF in vivo resulted in tumor regression and significantly increased survival, suggesting that HBEGF may be a clinically relevant target.

Indexed as

ADP-Ribosylation Factor 1AnimalsAstrocytesBrain NeoplasmsCarcinogenesisCohort StudiesCyclin-Dependent Kinase Inhibitor p16ErbB ReceptorsGlioblastomaHeparin-binding EGF-like Growth FactorHumansKaplan-Meier EstimateMiceMice, KnockoutPTEN PhosphohydrolaseReceptor Protein-Tyrosine KinasesADP-Ribosylation Factor 1Cyclin-Dependent Kinase Inhibitor p16EGFR protein, mouseErbB ReceptorsHBEGF protein, humanHeparin-binding EGF-like Growth FactorPTEN PhosphohydrolaseReceptor Protein-Tyrosine Kinases

Identifiers

PMID28368403
PMCPMC5552427
OpenAlexW2604129195

What OpenQuestion holds

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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.