Pancreas organoids resulted in neoplastic
发表于 ： 周二 3月 28, 2023 6:55 am
Induced pluripotent stem cells (iPSCs) (Figure 1), which accounts for another major advantage of organoid technology, allowing screening for compounds which specifically target tumor cells while leaving wild type cells intact. Targeting oncogenes with gene engineering methods, such as Crispr-Cas9 or shRNA, researchers can produce cancer organoids in a dish. Double K.O of Cdh1 and Tp53 in stomach organoids enables the organoids to demonstrate invasive phenotypes in vitro and robust metastasis in vivo (Li et al., 2014). Modeling of colorectal carcinoma has been achieved using organoids.
In the reverse experiment, expression of mutated KRAS and/or TP53 in transformation in culture and in vivo (Boj et al., 2015). Furthermore, two independent studies have Spain phone number list achieved to model the “adeno-carcinoma sequence”, a stepwise activation pattern of oncogenes, with simultaneous inactivation of tumor suppressor genes, introduced in human colon organoids (Drost et al., 2015; Matano et al., 2015). In addition, Crispr-Cas9 was utilized to introduce combinations of CRC driver mutations to generate accurate CRC progression models.
Surprisingly, those models showed that growth happens independently from intestinal stem cell niche factors like EGF, WNT, R-spondin and Noggin (Matano et al., 2015). Organoid technology can also be utilized to study cancer-related processes and signaling pathways. Using intestinal organoids, it was shown that mutations in RHOA, a gene involved in gastric cancer, were able to induce resistance to commonly used anticancer drugs (Wang K. et al., 2014). Finally, human colon organoids were used to show that CDX2 loss and BRAF mutations are the driving force in serrated colon carcinoma.
In the reverse experiment, expression of mutated KRAS and/or TP53 in transformation in culture and in vivo (Boj et al., 2015). Furthermore, two independent studies have Spain phone number list achieved to model the “adeno-carcinoma sequence”, a stepwise activation pattern of oncogenes, with simultaneous inactivation of tumor suppressor genes, introduced in human colon organoids (Drost et al., 2015; Matano et al., 2015). In addition, Crispr-Cas9 was utilized to introduce combinations of CRC driver mutations to generate accurate CRC progression models.
Surprisingly, those models showed that growth happens independently from intestinal stem cell niche factors like EGF, WNT, R-spondin and Noggin (Matano et al., 2015). Organoid technology can also be utilized to study cancer-related processes and signaling pathways. Using intestinal organoids, it was shown that mutations in RHOA, a gene involved in gastric cancer, were able to induce resistance to commonly used anticancer drugs (Wang K. et al., 2014). Finally, human colon organoids were used to show that CDX2 loss and BRAF mutations are the driving force in serrated colon carcinoma.