한빛사논문
- 조회213
Jared D. Rhodes1,2, James R. Goldenring1,2,3,4,5 and Su-Hyung Lee2,3
1Program in Cancer Biology, Nashville, TN, USA.
2Epithelial Biology Center, Vanderbilt University School of Medicine, Nashville, TN, USA.
3Section of Surgical Sciences, Nashville, TN, USA.
4Department of Cell and Developmental Biology, Nashville, TN, USA.
5Nashville VA Medical Center, Nashville, TN, USA.
Corresponding authors
Correspondence to James R. Goldenring or Su-Hyung Lee.
Abstract
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.
논문정보
- Research article
- 2024년 06월 (BRIC 등록일 2024-06-03)
- 국외 연구진
- 의약학 > 종양의학
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