Evidence map›Paper›PMID 22834780›Full record

ReviewExpert opinion on therapeutic targets2012

Ron receptor tyrosine kinase signaling as a therapeutic target.

Nancy M Benight, Susan E Waltz

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Genetic Influences in Cancer-Associated Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2023
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. NanoString technology distinguishes anti-TIF-1γBrain pathology (Zurich, Switzerland) · 2021
    Article
  9. The HNRNPA2B1-MST1R-Akt axis contributes to epithelial-to-mesenchymal transition in head and neck cancer.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  10. Article
  11. 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

2 authors at 2 institutions in 1 country.

Nancy M BenightUniversity of Cincinnati College of Medicine, Cincinnati Veterans Affairs Medical Center, Department of Cancer and Cell Biology, OH 45267-0521, USA.
Susan E Waltz
University of Cincinnati Medical Center · USWeatherford College · US

Funding

Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
RON Receptor in Pancreatic Cancer Biology and TherapyR01CA155620 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LOWY, ANDREW M · 2011 to 2021
$2.9M
The Ron Receptor/Chemokine Axis in Prostate CancerR01CA125379 · NCI · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E · 2008 to 2012
$1.3M
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 CA125379NCI NIH HHS CA155620NCI NIH HHS R01 CA125379NCI NIH HHS R01 CA155620NCI NIH HHS T32 CA117846
6 · The paper itself

Abstract

introductionSince its discovery nearly 20 years ago, the Ron receptor tyrosine kinase has been extensively studied. These studies have elucidated many of the major signaling pathways activated by Ron. In the context of the inflammation and cancer, studies have shown that Ron plays differential roles; Ron activation limits the inflammatory response, whereas in cancer, Ron activation is associated with increased metastases and poor prognosis. AREAS COVERED: This review discusses the current literature with regard to Ron signaling and consequences of its activation in cancer as well as its role in cancer therapy. Further, we discuss the mechanisms by which Ron influences the inflammatory response and its role in chronic inflammatory diseases. Finally, we discuss Ron's connection between chronic inflammation and progression to cancer. EXPERT OPINION: The complex nature of Ron's signaling paradigm necessitates additional studies to understand the pathways by which Ron is functioning and how these differ in inflammation and cancer. This will be vital to understanding the impact that Ron signaling has in disease states. Additional studies of targeted therapies, either alone or in conjunction with current therapies are needed to determine if inhibition of Ron signaling will provide long-term benefits to cancer patients.

Indexed as

Antineoplastic AgentsGene Expression Regulation, NeoplasticHumansNeoplasmsReceptor Protein-Tyrosine KinasesSignal TransductionAntineoplastic AgentsReceptor Protein-Tyrosine KinasesRON protein

Identifiers

PMID22834780
PMCPMC4075176
OpenAlexW1980532029

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.