Evidence map›Paper›PMID 30871956›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2019

The double edge sword of fibrosis in cancer.

Chelsea Chandler, Tianshi Liu, Ronald Buckanovich, Lan G Coffman

Abstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers.

0numbers the graph read from it
0cells of the map it votes in
150citing 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

150 citing papers in PubMed.

  1. Article
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  9. Review
  10. Growth Hormone, Not Simply Just a Hormone for Growth.Endocrinology and metabolism (Seoul, Korea) · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  17. Review
  18. Article
  19. Article
  20. Review

90 more citing papers are in PubMed but not listed here.

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.

Chelsea ChandlerDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Pittsburgh, Pittsburgh, Pennsylvania.
Tianshi LiuDepartment of Internal Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.
Ronald BuckanovichDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Pittsburgh, Pittsburgh, Pennsylvania; Division of Hematology Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania.
Lan G CoffmanDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Pittsburgh, Pittsburgh, Pennsylvania; Division of Hematology Oncology, University of Pittsburgh, Pittsburgh, Pennsylvania. Electronic address: coffmanl@upmc.edu.

Funding

Developing a Human in Mouse Cancer Model with a Completely Humanized StromaR01CA211913 · NCI · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI BUCKANOVICH, RONALD J · 2017 to 2020
$1.9M
Defining the formation and function of carcinoma-associated mesenchymal stem cells in the ovarian cancer microenvironmentK08CA211362 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI COFFMAN, LAN · 2016 to 2021
$918k
NCI NIH HHS K08 CA211362NCI NIH HHS R01 CA211913
6 · The paper itself

Abstract

Cancer-associated fibrosis is a critical component of the tumor microenvironment (TME) which significantly impacts cancer behavior. However, there is significant controversy regarding fibrosis as a predominantly tumor promoting or tumor suppressing factor. Cells essential to the generation of tissue fibrosis such as fibroblasts and mesenchymal stem cells (MSCs) have dual phenotypes dependent upon their independence or association with cancer cells. Cancer-associated fibroblasts and cancer-associated MSCs have unique molecular profiles which facilitate cancer cell cross talk, influence extracellular matrix deposition, and direct the immune system to generate a protumorigenic environment. In contrast, normal tissue fibroblasts and MSCs are important in restraining cancer initiation, influencing epithelial cell differentiation, and limiting cancer cell invasion. We propose this apparent dichotomy of function is due to (1) cancer mediated stromal reprogramming; (2) tissue stromal source; (3) unique subtypes of fibrosis; and (4) the impact of fibrosis on other TME elements. First, as cancer progresses, tumor cells influence their surrounding stroma to move from a cancer restraining phenotype into a cancer supportive role. Second, cancer has specific organ tropism, thus stroma derived from preferred metastatic organs support growth while less preferred metastatic tissues do not. Third, there are subtypes of fibrosis which have unique function to support or inhibit cancer growth. Fourth, depleting fibrosis influences other TME components which drive the cancer response. Collectively, this review highlights the complexity of cancer-associated fibrosis and supports a dual function of fibrosis which evolves during the continuum of cancer growth.

Indexed as

CarcinogenesisDisease ProgressionFibrosisHumansMolecular Targeted TherapyNeoplasmsTumor Microenvironment

Identifiers

PMID30871956
PMCPMC6545239

What OpenQuestion holds

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Registered trials

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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.