Evidence map›Paper›PMID 36793444›Full record

ReviewFrontiers in cell and developmental biology2023

Cancer-associated fibroblasts: The chief architect in the tumor microenvironment.

Mrinmoy Sarkar, Tristan Nguyen, Esheksha Gundre, Olajumoke Ogunlusi, Mohanad El-Sobky, Biplab Giri, Tapasree Roy Sarkar

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
26.0field-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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
  2. Cell identity competes with surface tension to determine stromal organization in tumor spheroids beyond the CAF shell paradigm.Proceedings of the National Academy of Sciences of the United States of America · 2026
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42 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

7 authors at 3 institutions in 2 countries.

Mrinmoy SarkarDepartment of Biology, Texas A&M University, College Station, TX, United States.
Tristan NguyenDepartment of Biology, Texas A&M University, College Station, TX, United States.
Esheksha GundreDepartment of Biology, Texas A&M University, College Station, TX, United States.
Olajumoke OgunlusiDepartment of Biology, Texas A&M University, College Station, TX, United States.
Mohanad El-SobkyDepartment of Biology, Texas A&M University, College Station, TX, United States.
Biplab GiriDepartment of Physiology, University of Gour Banga, English Bazar, India.
Tapasree Roy SarkarDepartment of Biology, Texas A&M University, College Station, TX, United States.
Texas A&M University · USIndian Institute of Chemical Biology · INUniversity of Gour Banga · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stromal heterogeneity of tumor microenvironment (TME) plays a crucial role in malignancy and therapeutic resistance. Cancer-associated fibroblasts (CAFs) are one of the major players in tumor stroma. The heterogeneous sources of origin and subsequent impacts of crosstalk with breast cancer cells flaunt serious challenges before current therapies to cure triple-negative breast cancer (TNBC) and other cancers. The positive and reciprocal feedback of CAFs to induce cancer cells dictates their mutual synergy in establishing malignancy. Their substantial role in creating a tumor-promoting niche has reduced the efficacy of several anti-cancer treatments, including radiation, chemotherapy, immunotherapy, and endocrine therapy. Over the years, there has been an emphasis on understanding CAF-induced therapeutic resistance in order to enhance cancer therapy results. CAFs, in the majority of cases, employ crosstalk, stromal management, and other strategies to generate resilience in surrounding tumor cells. This emphasizes the significance of developing novel strategies that target particular tumor-promoting CAF subpopulations, which will improve treatment sensitivity and impede tumor growth. In this review, we discuss the current understanding of the origin and heterogeneity of CAFs, their role in tumor progression, and altering the tumor response to therapeutic agents in breast cancer. In addition, we also discuss the potential and possible approaches for CAF-mediated therapies.

Indexed as

breast cancerCAFheterogeneitytargetingtumor microenvironment

Identifiers

PMID36793444
PMCPMC9923123
OpenAlexW4318473304

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.