HNF4A and GATA6 Loss Reveals Therapeutically Actionable Subtypes in Pancreatic Cancer

Published: 12 May 2020| Version 1 | DOI: 10.17632/74s7crj7xj.1
Contributor:
Holly Brunton

Description

SUPPLEMENTAL TABLE LIST Table S1. Related to Figure 1: PDCL normalized RNA-seq expression analysis. PDCL consensus clustering using Bailey classification (Squamous Vs Classical) differential gene expression analysis and PDCL class designation (Squamous or Classical). Bulk tumor signature scores of enriched gene expression pathways. Table S2. Related to Figure 1: Untargeted metabolomics and enriched metabolic pathways in Squamous vs Classical PDCLs. Table S3. Related to Figure 1: Seahorse assay: Glycolysis stress test (ECAR values) and Fatty acid Oxidation (Mitochondrial Stress Test, OCR values) in PDCLs. Lactate production and glucose uptake in PDCLs. Table S4. Related to Figure 6 and Figure S1: PDCL point mutations, germline mutations, structural variants and copy number variants. Table S5. Related to Figure 2, Figure 3 and Figure S3: siHNF4A and siGATA6 RNA-seq in Mayo 5289 PDCL. ECAR values after HNF4A knockdown in Classical PDCLs. Table S6: Related to Figure 4 and Figure S4: PDCL siRNA screen, GSK3Bi IC50 (72hr vs 144hr) and GSK3Bi ECAR values. Table S7: Related to Figure 6, Figure 7 and Figure S7: PDCL ATAC-seq analysis. ATAC-seq analysis comparing GSK3Bi initial-responders vs GSK3Bi responders. Survival analysis of PDCLs treated with GSK3Bi + ULKi + PORCNi triple inhibitor treatments. In vivo WNT7A RNAscope analysis.

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