Hugo Guillen-Ramirez

This study uses CRISPR-Cas9 to identify functional exons in lncRNAs, finding most exons are non-functional and functionality is enriched at the 5' end.

The paper identifies 121 lncRNA driver mutations across 19 cancer types using 12,631 genomes, showing mutations disrupt RNA-binding protein interactions to promote oncogenesis.

The paper introduces TransCistor, a framework to identify cis-regulatory lncRNAs with controlled false discovery rates, finding that only a minority of lncRNAs are cis-acting, primarily as activators.

The paper identifies mutated long noncoding RNAs (lncRNAs) as contributors to tumour cell fitness through experimental validation of their oncogenic effects.

The paper identifies 60 high-confidence oncogenic lncRNAs in NSCLC using CRISPR deletion screens and ASO validation, revealing therapeutic vulnerabilities.

This paper shows that temporarily inhibiting DNA-PK increases CRISPR-Cas9 deletion efficiency by delaying NHEJ, improving experimental outcomes across multiple cell lines and guide RNAs.