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Genomic profiling of biliary tract cancer cell lines reveals molecular subtypes and actionable drug targets

ABSTRACT: Genomic profiling of biliary tract cancer cell lines reveals molecular subtypes and actionable drug targets

PROVIDER: PRJNA577107 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10267509.fastq.gz	Fastqsanger.gz
	SRR10267510.fastq.gz	Fastqsanger.gz
	SRR10267511.fastq.gz	Fastqsanger.gz
	SRR10267512.fastq.gz	Fastqsanger.gz
	SRR10267513.fastq.gz	Fastqsanger.gz

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Genomic profiling of biliary tract cancer cell lines reveals molecular subtypes and actionable drug targets

Project description:Purpose: Biliary tract cancers (BTCs) carry a very poor prognosis and have no approved targeted therapies. Recent genomic profiling of primary BTCs identified a number of potentially actionable drug targets, however accurate model systems to evaluate these targets are currently lacking. The purpose of this study was to compare the genomic landscape of commonly used BTC cell lines to primary BTCs, and to utilize these models for drug target evaluation. Design: Twenty BTC cell lines were profiled by RNA-seq analysis. Results: Transcriptomic profiling of BTC cell lines identified two subtypes, enriched for epithelial and mesenchymal genes respectively, which were also identified in primary BTC. Conclusions: Cell lines harbor similar genomic alterations to primary BTCs. Integration of cell line and primary cancer data identify novel molecular subsets, and highlight specific molecular vulnerabilities in BTC.

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Project description:Biliary tract cancers (BTCs) are aggressive malignancies encompassing intrahepatic and extrahepatic cholangiocarcinoma, gallbladder carcinoma, and ampullary carcinoma. Here, we report integrative analysis of 63 BTC cell lines via multi-omics and genome-scale CRISPR screens. We identify widespread EGFR dependency in BTC, alongside dependencies selective to anatomic subtypes. Additionally, we delineate strategies to overcome therapeutic resistance, with combined EGFR inhibition potentiating targeting of KRAS-mutant and FGFR2-fusion-driven models, and SHP2 inhibition effective in the latter context. Clustering RNA/protein expression and dependencies data revealed functional relationships transcending single-gene alterations, with biliary, squamous, or dual biliary/hepatocyte lineage signatures stratifying BTC models. These subtypes exhibit distinct dependency profiles— including cell fate transcription factors GRHL2, TP63, and HNF1B, respectively— and demonstrate prognostic significance in patient samples. Potential subtype-specific targetable vulnerabilities include Integrin-a3 and the detoxification enzyme UXS1. This cell line atlas reveals therapeutic targets in molecularly-defined BTCs, unveils disease subtypes, and provides a resource for therapeutic development.

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Project description:Biliary tract cancers (BTCs) currently have no approved targeted therapies. Although genomic profiling of primary BTCs has identified multiple potential drug targets, accurate models are needed for their evaluation. Genomic profiling of 22 BTC cell lines revealed they harbor similar mutational signatures, recurrently mutated genes, and genomic alterations to primary tumors. Transcriptomic profiling identified two major subtypes, enriched for epithelial and mesenchymal genes, which were also evident in patient-derived organoids and primary tumors. Interrogating these models revealed multiple mechanisms of MAPK signaling activation in BTC, including co-occurrence of low-activity BRAF and MEK mutations with receptor tyrosine kinase overexpression. Finally, BTC cell lines with altered ERBB2 or FGFRs were exquisitely sensitive to specific targeted agents, whereas surprisingly, IDH1-mutant lines did not respond to IDH1 inhibitors in vitro. These findings establish BTC cell lines as robust models of primary disease, reveal specific molecular disease subsets, and highlight specific molecular vulnerabilities in these cancers.

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