Evidence map›Paper›PMID 27197262›Full record

ReviewCancer research2016

Carcinoma Cell Hyaluronan as a "Portable" Cancerized Prometastatic Microenvironment.

Eva A Turley, David K Wood, James B McCarthy

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Metastasis-promoting functions of myeloid cells.Cancer metastasis reviews · 2025
    Review
  3. Article
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  5. Biophysical modeling of membrane curvature generation and curvature sensing by the glycocalyx.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Article
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  9. Review
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  15. Cancer-associated fibroblasts-derived HAPLN1 promotes tumour invasion through extracellular matrix remodeling in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022
    Article
  16. Review
  17. Article
  18. Review
  19. 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

3 authors at 3 institutions in 2 countries.

Eva A TurleyCancer Research Laboratories, London Regional Cancer Center, Victoria Hospital, London, Ontario, Canada. Departments of Oncology, Biochemistry and Surgery, Schulich School of Medicine, Western University, London, Ontario, Canada. mccar001@umn.edu eva.turley@lhsc.on.ca.
David K WoodDepartment of Biomedical Engineering, College of Science and Engineering, University of Minnesota, Minneapolis, Minnesota. Masonic Cancer Center, Minneapolis, Minnesota.
James B McCarthyMasonic Cancer Center, Minneapolis, Minnesota. Department of Laboratory Medicine and Pathology, Medical School, University of Minnesota, Minneapolis, Minnesota. mccar001@umn.edu eva.turley@lhsc.on.ca.
University of Minnesota · USUniversity of Minnesota Medical Center · USWestern University · CA

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Jeffrey S. Miller · 1998 to 2026
$100.4M
Hyaluronan Receptors in Prostate Cancer ProgressionR01CA119092 · NCI · UNIVERSITY OF MINNESOTA · PI MCCARTHY, JAMES B. · 2008 to 2012
$2.2M
Carcinoma Cell Hyaluronan as a Therapeutic Target in MetastasisR21CA205455 · NCI · UNIVERSITY OF MINNESOTA · PI WOOD, DAVID KEVIN · 2016 to 2017
$363k
NCI NIH HHS P30 CA077598NCI NIH HHS R01 CA119092NCI NIH HHS R21 CA205455
6 · The paper itself

Abstract

Hyaluronan (HA) is a structurally simple polysaccharide, but its ability to act as a template for organizing pericellular matrices and its regulated synthesis and degradation are key to initiating repair responses. Importantly, these HA functions are usurped by tumor cells to facilitate progression and metastasis. Recent advances have identified the functional complexities associated with the synthesis and degradation of HA-rich matrices. Three enzymes synthesize large HA polymers while multiple hyaluronidases or tissue free radicals degrade these into smaller bioactive fragments. A family of extracellular and cell-associated HA-binding proteins/receptors translates the bioinformation encrypted in this complex polymer mixture to activate signaling networks required for cell survival, proliferation, and migration in an actively remodeling microenvironment. Changes in HA metabolism within both the peritumor stroma and parenchyma are linked to tumor initiation, progression, and poor clinical outcome. We review evidence that metastatic tumor cells must acquire the capability to autonomously synthesize, assemble, and process their own "portable" HA-rich microenvironments to survive in the circulation, metastasize to ectopic sites, and escape therapeutic intervention. Strategies to disrupt the HA machinery of primary tumor and circulating tumor cells may enhance the effectiveness of current conventional and targeted therapies. Cancer Res; 76(9); 2507-12. ©2016 AACR.

Indexed as

AnimalsCarcinomaHumansHyaluronic AcidNeoplasm InvasivenessTumor MicroenvironmentHyaluronic Acid

Identifiers

PMID27197262
PMCPMC4874571
OpenAlexW2337050790

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.