Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMC

Fibroblast subtypes in pancreatic cancer and pancreatitis: from mechanisms to therapeutic strategies

Huang H., Lu W., Zhang X., Pan J., Cao F., Wen L.

Narrative Review, published in Cell Oncol (Dordr) (2024) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Cell Oncol (Dordr) (2024)
Reported sample size
—
Source database
Europe PMC
PMID
37721678
PMCID
PMC12974079
DOI
10.1007/s13402-023-00874-x
Citations
6

Abstract (original English)

Excessive fibrosis is a predominant feature of pancreatic stroma and plays a crucial role in the development and progression of pancreatic ductal adenocarcinoma (PDAC) and chronic pancreatitis (CP). Emerging evidence showed diversity and heterogeneity of fibroblasts play crucial and somewhat contradictory roles, the interactions between fibroblasts and pancreatic cells or infiltrating immune cells are of great importance during PDAC and CP progression, with some promising therapeutic strategies being tested. Therefore, in this review, we describe the classification of fibroblasts and their functions in PDAC and pancreatitis, the mechanisms by which fibroblasts mediate the development and progression of PDAC and CP through direct or indirect interaction between fibroblast and pancreatic parenchymal cells, or by remodeling the pancreatic immune microenvironment mediates the development and progression of PDAC and CP. Finally, we summarized the current therapeutic strategies and agents that directly target subtypes of fibroblasts or interfere with their essential functions.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
PancreasFibroblastsAnimalsHumansCarcinoma, Pancreatic DuctalPancreatic NeoplasmsPancreatitisPancreatitis, ChronicTumor Microenvironment

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