Randomized trial defines core vulnerabilities in esophageal and gastric cancers through condensate-driven mechanisms, suggesting new therapeutic targets.
Key Points
The study aims to investigate the role of biomolecular condensates in the transcriptional landscape of esophageal and gastric cancers.
Normalized RNA-seq data analyzed for differential expression from GTEx and TCGA
Condensate-related genes identified using GO terms and DepMap dependency data
Machine-learning predictors and coarse-grained molecular dynamics simulations employed to assess intrinsic disorder and condensate formation.
Transcriptomic analyses revealed a hyperactive transcriptional state with upregulation of TOPBP1 and CHERP in tumors.
Dependency mapping indicated that condensate scaffolds are essential for tumor cell viability.
Expression profiling showed that TOPBP1 and CHERP are activated during tumorigenesis but downregulated in metastasis.