Evidence map›Paper›PMID 36612058›Full record

ReviewCancers2022

Cancer-Associated Fibroblast Diversity Shapes Tumor Metabolism in Pancreatic Cancer.

Raphaël Peiffer, Yasmine Boumahd, Charlotte Gullo, Rebekah Crake, Elisabeth Letellier, Akeila Bellahcène, Olivier Peulen

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  11. Transcriptome analysis of key genes and pathways associated with cisplatin resistance in oral squamous cell carcinoma Cal27 cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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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

7 authors at 2 institutions in 2 countries.

Raphaël PeifferMetastasis Research Laboratory, GIGA-Cancer, University of Liège, 4000 Liège, Belgium.
Yasmine BoumahdMetastasis Research Laboratory, GIGA-Cancer, University of Liège, 4000 Liège, Belgium.
Charlotte GulloMetastasis Research Laboratory, GIGA-Cancer, University of Liège, 4000 Liège, Belgium.
Rebekah CrakeLaboratory of Tumor and Development Biology, GIGA-Cancer, University of Liège, 4000 Liège, Belgium.
Elisabeth LetellierMolecular Disease Mechanisms Group, University of Luxembourg, Campus Belval, 4367 Esch-sur-Alzette, Luxembourg.ORCID 0000-0001-8242-9393
Akeila BellahcèneMetastasis Research Laboratory, GIGA-Cancer, University of Liège, 4000 Liège, Belgium.ORCID 0000-0001-9154-7631
Olivier PeulenMetastasis Research Laboratory, GIGA-Cancer, University of Liège, 4000 Liège, Belgium.ORCID 0000-0002-6933-0134
University of Liège · BEUniversity of Luxembourg · LU

Funding

Fondation Léon FredericqFund for Scientific Research 40000551
6 · The paper itself

Abstract

Despite extensive research, the 5-year survival rate of pancreatic cancer (PDAC) patients remains at only 9%. Patients often show poor treatment response, due partly to a highly complex tumor microenvironment (TME). Cancer-associated fibroblast (CAF) heterogeneity is characteristic of the pancreatic TME, where several CAF subpopulations have been identified, such as myofibroblastic CAFs (myCAFs), inflammatory CAFs (iCAFs), and antigen presenting CAFs (apCAFs). In PDAC, cancer cells continuously adapt their metabolism (metabolic switch) to environmental changes in pH, oxygenation, and nutrient availability. Recent advances show that these environmental alterations are all heavily driven by stromal CAFs. CAFs and cancer cells exchange cytokines and metabolites, engaging in a tight bidirectional crosstalk, which promotes tumor aggressiveness and allows constant adaptation to external stress, such as chemotherapy. In this review, we summarize CAF diversity and CAF-mediated metabolic rewiring, in a PDAC-specific context. First, we recapitulate the most recently identified CAF subtypes, focusing on the cell of origin, activation mechanism, species-dependent markers, and functions. Next, we describe in detail the metabolic crosstalk between CAFs and tumor cells. Additionally, we elucidate how CAF-driven paracrine signaling, desmoplasia, and acidosis orchestrate cancer cell metabolism. Finally, we highlight how the CAF/cancer cell crosstalk could pave the way for new therapeutic strategies.

Indexed as

acidosisCAFcancer-associated fibroblastdesmoplasiahypoxiametabolismpancreatic cancerparacrine signalingPDAC

Identifiers

PMID36612058
PMCPMC9817728
OpenAlexW4313415296

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.