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. 2022 Jul 7;17(8):1874–1888. doi: 10.1016/j.stemcr.2022.06.003

Figure 4.

Figure 4

Transcriptome of patient-derived FLC organoids

(A) Principal-component analysis comparing normal cholangiocyte and hepatocyte organoids derived from normal tissue compared with FLC tumor organoids (in cholangiocyte and hepatocyte media) derived from their corresponding patient FLC tumor tissue.

(B) Heatmap organized by closest similarity between FLC patient normal tissue, FLC patient tumor tissue, patient-derived normal organoids, and FLC organoids in cholangiocyte or hepatocyte media.

(C) Heatmap with known FLC-dysregulated genes comparing FLC patient normal tissue, FLC patient tumor tissue, patient-derived normal organoids, and FLC organoids in cholangiocyte or hepatocyte media. Both heatmaps show unsupervised clustering. N, normal; M, metastasis; L, primary liver tumor; O, organoid; T, tissue; H, grown in hepatocyte medium; C, grown in cholangiocyte medium. When multiple independent metastases were resected and analyzed, we used a subscript. Sample 14∗ was isolated in an alternative medium for liver tumors, which replaced the Noggin, Rspo-1, and Wnt3a with 3 nM dexamethasone (Broutier et al., 2017).

(D) We have generated a “fibrolamellar signature” representing 509 transcripts (Lalazar et al., 2021). The change in expression of these genes in the FLC-derived organoids relative to organoids derived from non-transformed liver tissue was plotted as a function of the expression in FLC tumor relative to the adjacent non-transformed tissue. The Pearson correlation coefficient is > 0.8.