Evidence map›Paper›PMID 35626096›Full record

ArticleCancers2022

RON (

Brian G Hunt, Angelle Jones, Carissa Lester, James C Davis, Nancy M Benight, Susan E Waltz

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Breast cancer (Dove Medical Press) · 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

6 authors at 2 institutions in 1 country.

Brian G HuntDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Angelle JonesDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Carissa LesterDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
James C DavisDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.ORCID 0000-0002-8645-9247
Nancy M BenightDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Susan E WaltzDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.ORCID 0000-0003-3572-4642
University of Cincinnati Medical Center · USVeterans Health Administration · US

Funding

Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Defining genetic and metabolic requirements of aggressive breast cancerR01CA239697 · NCI · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E, WELLS, SUSANNE I · 2020 to 2024
$2.4M
Targeting glycolytic metabolism in RON-driven breast cancerF31CA228373 · NCI · UNIVERSITY OF CINCINNATI · PI HUNT, BRIAN GREGORY · 2018 to 2021
$169k
Ron Receptor Tyrosine Kinase Signaling in Breast CancerI01BX000803 · VA · CINCINNATI VA MEDICAL CENTER RESEARCH · PI WALTZ, SUSAN E · 2011 to 2025
–
BLRD VA I01 BX000803NCI NIH HHS CA117846NCI NIH HHS CA228373NCI NIH HHS CA239697NCI NIH HHS F31 CA228373NCI NIH HHS R01 CA239697NCI NIH HHS T32 CA117846
6 · The paper itself

Abstract

backgroundAberrant RON signaling is present in numerous cancers including breast cancer. Evidence suggests that the ligand, hepatocyte growth factor-like (HGFL), is also overexpressed in breast cancer. RON (

methodsMouse models were used to establish the functional significance of RON and HGFL co-overexpression on the activation of tumor cells and tumor-associated macrophages in breast cancer. TCGA and METABRIC gene expression and alteration data were used to query the relationships between

resultsIn tumor models, physiologic sources of HGFL modestly improve Arginase-1

conclusionsCo-overexpression of RON and HGFL in breast cancer cells (augmented by physiologic sources of HGFL) promotes tumorigenesis through autocrine-mediated RON activation/RON-dependent secretome changes and paracrine activation of macrophage RON to promote breast cancer stem cell self-renewal.

Indexed as

breast tumorigenesismacrophage activationreceptor tyrosine kinasestumor microenvironment

Identifiers

PMID35626096
PMCPMC9140067
OpenAlexW4280534002

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.