Regulation of metaplasia and dysplasia in the stomach by the stromal microenvironment.


Journal

Experimental & molecular medicine
ISSN: 2092-6413
Titre abrégé: Exp Mol Med
Pays: United States
ID NLM: 9607880

Informations de publication

Date de publication:
03 Jun 2024
Historique:
received: 30 11 2023
accepted: 03 03 2024
revised: 03 03 2024
medline: 3 6 2024
pubmed: 3 6 2024
entrez: 2 6 2024
Statut: aheadofprint

Résumé

Research on the microenvironment associated with gastric carcinogenesis has focused on cancers of the stomach and often underestimates premalignant stages such as metaplasia and dysplasia. Since epithelial interactions with T cells, macrophages, and type 2 innate lymphoid cells (ILC2s) are indispensable for the formation of precancerous lesions in the stomach, understanding the cellular interactions that promote gastric precancer warrants further investigation. Although various types of immune cells have been shown to play important roles in gastric carcinogenesis, it remains unclear how stromal cells such as fibroblasts influence epithelial transformation in the stomach, especially during precancerous stages. Fibroblasts exist as distinct populations across tissues and perform different functions depending on the expression patterns of cell surface markers and secreted factors. In this review, we provide an overview of known microenvironmental components in the stroma with an emphasis on fibroblast subpopulations and their roles during carcinogenesis in tissues including breast, pancreas, and stomach. Additionally, we offer insights into potential targets of tumor-promoting fibroblasts and identify open areas of research related to fibroblast plasticity and the modulation of gastric carcinogenesis.

Identifiants

pubmed: 38825636
doi: 10.1038/s12276-024-01240-z
pii: 10.1038/s12276-024-01240-z
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : CA009592
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : CA272687
Organisme : U.S. Department of Veterans Affairs (Department of Veterans Affairs)
ID : IBX000930
Organisme : U.S. Department of Defense (United States Department of Defense)
ID : CA190172
Organisme : U.S. Department of Health & Human Services | National Institutes of Health (NIH)
ID : DK101332

Informations de copyright

© 2024. The Author(s).

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Auteurs

Jared D Rhodes (JD)

Program in Cancer Biology, Nashville, TN, USA.
Epithelial Biology Center, Vanderbilt University School of Medicine, Nashville, TN, USA.

James R Goldenring (JR)

Program in Cancer Biology, Nashville, TN, USA. jim.goldenring@vumc.org.
Epithelial Biology Center, Vanderbilt University School of Medicine, Nashville, TN, USA. jim.goldenring@vumc.org.
Section of Surgical Sciences, Nashville, TN, USA. jim.goldenring@vumc.org.
Department of Cell and Developmental Biology, Nashville, TN, USA. jim.goldenring@vumc.org.
Nashville VA Medical Center, Nashville, TN, USA. jim.goldenring@vumc.org.

Su-Hyung Lee (SH)

Epithelial Biology Center, Vanderbilt University School of Medicine, Nashville, TN, USA. su-hyung.lee@vumc.org.
Section of Surgical Sciences, Nashville, TN, USA. su-hyung.lee@vumc.org.

Classifications MeSH