Evidence map›Paper›PMID 32434219›Full record

ArticleThe Journal of experimental medicine2020

Distinct fibroblast functional states drive clinical outcomes in ovarian cancer and are regulated by TCF21.

Ali Hussain, Veronique Voisin, Stephanie Poon, Christina Karamboulas, Ngoc Hoang Bao Bui, Jalna Meens, Julia Dmytryshyn, Victor W Ho, Kwan Ho Tang, Joshua Paterson and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 99 citations in OpenAlex.

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  11. Modeling CAF-tumor interactions to overcome therapy resistance.Journal of experimental & clinical cancer research : CR · 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

15 authors at 3 institutions in 2 countries.

Ali HussainDepartment of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Veronique VoisinThe Donnelly Centre, University of Toronto, Toronto, Ontario, Canada.
Stephanie PoonDepartment of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Christina KaramboulasPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Ngoc Hoang Bao BuiPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Jalna MeensPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Julia DmytryshynPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Victor W HoPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Kwan Ho TangLaura and Isaac Perlmutter Cancer Center, New York Langone Health, New York, NY.
Joshua PatersonPrincess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
Blaise A ClarkeDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Marcus Q BernardiniDivision of Gynaecologic Oncology, University Health Network, Toronto, Ontario, Canada.
Gary D BaderThe Donnelly Centre, University of Toronto, Toronto, Ontario, Canada.
Benjamin G NeelDepartment of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Laurie E AillesDepartment of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
University Health Network · CAUniversity of Toronto · CANYU Langone Health · US

Funding

CIHR PJT153147
6 · The paper itself

Abstract

Recent studies indicate that cancer-associated fibroblasts (CAFs) are phenotypically and functionally heterogeneous. However, little is known about CAF subtypes, the roles they play in cancer progression, and molecular mediators of the CAF "state." Here, we identify a novel cell surface pan-CAF marker, CD49e, and demonstrate that two distinct CAF states, distinguished by expression of fibroblast activation protein (FAP), coexist within the CD49e+ CAF compartment in high-grade serous ovarian cancers. We show for the first time that CAF state influences patient outcomes and that this is mediated by the ability of FAP-high, but not FAP-low, CAFs to aggressively promote proliferation, invasion and therapy resistance of cancer cells. Overexpression of the FAP-low-specific transcription factor TCF21 in FAP-high CAFs decreases their ability to promote invasion, chemoresistance, and in vivo tumor growth, indicating that it acts as a master regulator of the CAF state. Understanding CAF states in more detail could lead to better patient stratification and novel therapeutic strategies.

Indexed as

Cell ProliferationDrug Resistance, NeoplasmTumor MicroenvironmentBasic Helix-Loop-Helix ProteinsCancer-Associated FibroblastsCell Line, TumorFemaleHumansNeoplasm InvasivenessNeoplasm ProteinsOvarian NeoplasmsBasic Helix-Loop-Helix ProteinsNeoplasm ProteinsTCF21 protein, human

Identifiers

PMID32434219
PMCPMC7398174
OpenAlexW3026934713

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.