Evidence map›Paper›PMID 27648825›Full record

ArticleMolecular carcinogenesis2017

Exploiting agonist biased signaling of chemokines to target cancer.

Ishan Roy, Anthony E Getschman, Brian F Volkman, Michael B Dwinell

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Physiology of chemokines in the cancer microenvironment.American journal of physiology. Cell physiology · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. The role of CXCL chemokine family in the development and progression of gastric cancer.International journal of clinical and experimental pathology · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Potential Role of Chemokines in Fracture Repair.Frontiers in endocrinology · 2017
    Review
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

4 authors.

Ishan RoyDepartment of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin.
Anthony E GetschmanDepartment of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin.
Brian F VolkmanDepartment of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin.
Michael B DwinellDepartment of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin.

Funding

Medical Scientist Training ProgramT32GM080202 · NIGMS · MEDICAL COLLEGE OF WISCONSIN · PI BARBIERI, JOSEPH T, SALZMAN, NITA H · 2010 to 2024
$5.7M
Structural Basis for Chemokine FunctionR01AI058072 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI VOLKMAN, BRIAN F · 2004 to 2019
$4.1M
Structural Basis for Chemokine FunctionR37AI058072 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI Brian F Volkman · 2020 to 2026
$2.8M
Targeting pancreatic cancer energy metabolism, tumor growth, and metastasisU01CA178960 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI DWINELL, MICHAEL B, KALYANARAMAN, BALARAMAN · 2014 to 2018
$2.6M
NCI NIH HHS U01 CA178960NIAID NIH HHS R01 AI058072NIAID NIH HHS R37 AI058072NIGMS NIH HHS T32 GM080202
6 · The paper itself

Abstract

As knowledge of growth-independent functions of cancer cells is expanding, exploration into the role of chemokines in modulating cancer pathogenesis, particularly metastasis, continues to develop. However, more study into the mechanisms whereby chemokines direct the migration of cancer cells is needed before specific therapies can be generated to target metastasis. Herein, we draw attention to the longstanding conundrum in the field of chemokine biology that chemokines stimulate migration in a biphasic manner; and explore this phenomenon's impact on chemokine function in the context of cancer. Typically, low concentrations of chemokines lead to chemotactic migration and higher concentrations halt migration. The signaling mechanisms that govern this phenomenon remain unclear. Over the last decade, we have defined a novel signaling mechanism for regulation of chemokine migration through ligand oligomerization and biased agonist signaling. We provide insight into this new paradigm for chemokine signaling and discuss how it will impact future exploration into chemokine function and biology. In the pursuit of producing more novel cancer therapies, we suggest a framework for pharmaceutical application of the principles of chemokine oligomerization and biased agonist signaling in cancer. © 2016 Wiley Periodicals, Inc.

Indexed as

AnimalsAntineoplastic AgentsCell MovementChemokinesDisease ProgressionHumansModels, MolecularNeoplasmsProtein MultimerizationReceptors, G-Protein-CoupledSignal TransductionAntineoplastic AgentsChemokinesReceptors, G-Protein-Coupledbiased agonistfunctional selectivityG protein coupled receptor

Identifiers

PMID27648825
PMCPMC5479419

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.