Research Paper Volume 16, Issue 5 pp 4396—4422
A pair of primary colorectal cancer-derived and corresponding synchronous liver metastasis-derived organoid cell lines
Figure 5. Drug treatment sensitivities of different organoids to KRAS G12C, KRAS G12D and pan-KRAS inhibitors. (A) Dose-response curves of KRAS G12D-mutated organoids (CRC1-Org and CRC16-Org) and RAS-unmutated organoid (CRC27-Org) exposed to increasing concentrations of sotorasib (a KRAS G12C inhibitor), and the corresponding IC50 values. (B) Representative images of CWH22, CLM22, CRC1-Org, and CRC16-Org organoids exposed to sotorasib at concentrations of 10 μM and 20 μM (scale bars, 200 μm). (C) Quantitative analysis of the viability of CWH22, CLM22, CRC1-Org, CRC16-Org and CRC27-Org (with different KRAS mutation backgrounds) following exposure to 10 μM and 20 μM sotorasib (n = 3, data represented as the mean ± SD, **p < 0.01). (D, E) Dose-response curves and IC50 values for (D) the KRAS G12D inhibitor (MRTX1133) and (E) the pan-KRAS inhibitor (BI-2865) for organoids with different KRAS mutation statuses.