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.