Evidence map›Paper›PMID 32466724›Full record

ReviewPhysiological reviews2021

Diversity and Biology of Cancer-Associated Fibroblasts.

Giulia Biffi, David A Tuveson

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 812 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
812citing papers in PubMed, 1 pooled it
52.7field-weighted citation impact, top 1% 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

812 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,196 citations in OpenAlex.

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752 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

2 authors at 1 institution in 2 countries.

Giulia BiffiCold Spring Harbor Laboratory, Cold Spring Harbor, New York; Lustgarten Foundation Pancreatic Cancer Research Laboratory, Cold Spring Harbor, New York; and Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0003-4592-0970
David A TuvesonCold Spring Harbor Laboratory, Cold Spring Harbor, New York; Lustgarten Foundation Pancreatic Cancer Research Laboratory, Cold Spring Harbor, New York; and Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, United Kingdom.
University of Cambridge · GB

Funding

Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI John Edward Moses · 1987 to 2026
$118.9M
Pancreatic Cancer Detection ConsortiumU01CA210240 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Michael A. Hollingsworth · 2017 to 2026
$12.9M
CSHL-JAX Patient-Derived Models of Pancreatic Cancer as Systems for Investigating Tumor HeterogeneityU01CA224013 · NCI · COLD SPRING HARBOR LABORATORY · PI ROBSON, PAUL, TUVESON, DAVID A · 2018 to 2022
$4.2M
Targeting aberrant enhancer landscapes in pancreatic cancerR01CA229699 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Christopher Vakoc · 2019 to 2026
$3.3M
Nrf2 Regulation of Ductal Pancreatic Cancer Etiology and Treatment ResponseR01CA188134 · NCI · COLD SPRING HARBOR LABORATORY · PI TUVESON, DAVID A · 2017 to 2021
$3.0M
(PQA-4) Organoid Omics To Detect And Defeat Ductal Pancreatic CancerR01CA190092 · NCI · COLD SPRING HARBOR LABORATORY · PI TUVESON, DAVID A · 2014 to 2017
$2.2M
Cancer Research UK A27463NCI NIH HHS P30 CA045508NCI NIH HHS R01 CA188134NCI NIH HHS R01 CA190092NCI NIH HHS R01 CA229699NCI NIH HHS U01 CA210240NCI NIH HHS U01 CA224013NIH HHS 5P30CA045508
6 · The paper itself

Abstract

Efforts to develop anti-cancer therapies have largely focused on targeting the epithelial compartment, despite the presence of non-neoplastic stromal components that substantially contribute to the progression of the tumor. Indeed, cancer cell survival, growth, migration, and even dormancy are influenced by the surrounding tumor microenvironment (TME). Within the TME, cancer-associated fibroblasts (CAFs) have been shown to play several roles in the development of a tumor. They secrete growth factors, inflammatory ligands, and extracellular matrix proteins that promote cancer cell proliferation, therapy resistance, and immune exclusion. However, recent work indicates that CAFs may also restrain tumor progression in some circumstances. In this review, we summarize the body of work on CAFs, with a particular focus on the most recent discoveries about fibroblast heterogeneity, plasticity, and functions. We also highlight the commonalities of fibroblasts present across different cancer types, and in normal and inflammatory states. Finally, we present the latest advances regarding therapeutic strategies targeting CAFs that are undergoing preclinical and clinical evaluation.

Indexed as

AnimalsAntineoplastic AgentsCancer-Associated FibroblastsCell ProliferationHumansNeoplasmsTumor MicroenvironmentAntineoplastic Agentsfibroblastsheterogeneitytumor microenvironment

Identifiers

PMID32466724
PMCPMC7864232
OpenAlexW3031767666

What OpenQuestion holds

Textmetadata
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.