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Review
. 2023 Jun 15;26(2):328.
doi: 10.3892/ol.2023.13914. eCollection 2023 Aug.

Tumor organoid model of colorectal cancer (Review)

Affiliations
Review

Tumor organoid model of colorectal cancer (Review)

Chi Yang et al. Oncol Lett. .

Abstract

The establishment of self-organizing 'mini-gut' organoid models has brought about a significant breakthrough in biomedical research. Patient-derived tumor organoids have emerged as valuable tools for preclinical studies, offering the retention of genetic and phenotypic characteristics of the original tumor. These organoids have applications in various research areas, including in vitro modelling, drug discovery and personalized medicine. The present review provided an overview of intestinal organoids, focusing on their unique characteristics and current understanding. The progress made in colorectal cancer (CRC) organoid models was then delved into, discussing their role in drug development and personalized medicine. For instance, it has been indicated that patient-derived tumor organoids are able to predict response to irinotecan-based neoadjuvant chemoradiotherapy. Furthermore, the limitations and challenges associated with current CRC organoid models were addressed, along with proposed strategies for enhancing their utility in future basic and translational research.

Keywords: colorectal cancer; drug therapy; organoids; tumor microenvironment; tumor model.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1.
Figure 1.
Schematic depicting the establishment of organoid cultures. Tissues, stem cells or activin-treated human pluripotent stem cells from different organs of humans or mice are embedded in a basement membrane matrix and maintained in a medium containing niche factors important for proliferation. ESCs, embryonic stem cells; iPSCs, induced pluripotent stem cells.
Figure 2.
Figure 2.
Strengths and weaknesses of tumor organoids. PDX, patient-derived xenograft.
Figure 3.
Figure 3.
Composition of intestinal crypts. Intestinal stem cells initiate crypt renewal and generate TA cells, and Paneth cells provide essential niche factors [Wnt, RSPO, EGF, Notch, Noggin]. RSPO, R-spondin; EGF, epidermal growth factor; TA cell, transit-amplifying cell.
Figure 4.
Figure 4.
Schematic representation of the uses of normal and tumor organoids for CRC basic and clinical research. CRC, colorectal cancer; PDCO, patient-derived cancer organoids; CAF, cancer-associated fibroblast.

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