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. 2022 Jun 6;2(6):402–416. doi: 10.1158/2767-9764.CRC-22-0124

FIGURE 1.

FIGURE 1

SMOi-induced mutations to SHH pathway genes only occur in medulloblastomas in which CSCs depend on the SHH signaling. A, A schematic of the major hypothesis tested in the study. B, Gross images of vehicle- and LDE225-treated fSmoM2;hGFAP-cre brains at harvest. C, Kaplan–Meier survival curve analysis showing no significant survival benefit of LDE225 treatment. D, GLI1 protein level is reduced in LDE-treated fSmoM2;GFAPcre tumors in vivo. E, A summary of high impact mutations in vehicle- and LDE225-treated fSmoM2;hGFAP-cre medulloblastomas. F, A summary of identified mutations and copy-number alterations in SHH pathway genes in SMOi-resistant SI-CSC and SD-CSC Ptch;p53 medulloblastoma. G, LDE225-induced SMO mutation in Ptch;p53 SD-CSC tumor. H, LDE225-induced Gli2 amplification observed in two SD-CSC tumors from the same cohort, which is not observed in any SI-CSC medulloblastomas. Copy-number variation compared with vehicle-treated tumor from the same cohort.