Barbara Mair

The paper develops a method to quantify genetic interactions from CRISPR-Cas9 screens and identifies systematic variations in screen data.

The paper constructs a genome-scale genetic interaction network from 4 million double mutants in HAP1 cells, revealing conserved genetic network principles across species and uncovering novel gene functions and cancer dependencies.

This study shows that the SOS1 inhibitor BI-3406 effectively reduces tumor growth in KRAS mutant cancers, similar to genetic SOS1 ablation, with comparable efficacy to another KRAS inhibitor.

The paper identifies genetic vulnerabilities linked to transcription factor activities in cancer cell lines using CRISPR knockout data and validates targets associated with TEAD1.

The paper identifies three types of chromatin boundaries that regulate cohesin traffic, which guides enhancer-promoter interactions and affects gene regulation.

The paper identifies novel paralog gene dependencies in cancer, including sex chromosome-encoded gene pairs, suggesting therapeutic strategies for tumors with Y-chromosome loss.

The paper presents a high-throughput CRISPR-Cas9 screening method for identifying CD47 modulators, identifying QPCTL as a key enzyme involved in its pyroglutamyl modification.