Alice H. Berger

EZHIP, a PRC2 inhibitor, arose on the placental mammal X chromosome, evolves under positive selection in primates, and duplicated, including a testis-expressed primate paralog, EZHIP2, whose gorilla copy inhibits H3K27me3.

The paper measures variant effects across the MAPK pathway in human cells, revealing how cell context influences variant function and identifying 14,412 previously unknown dominant negative variants.

The paper investigates transcriptional adaptation in paralog gene families using Perturb-seq, finding six paralog pairs show adaptation and identifying mechanisms like nonsense-mediated decay and nuclear import.

The paper constructs a unified transcriptomic landscape of lung cancer using RNA-seq data from 1,824 tumors, identifying nine molecular clusters with distinct biological and clinical features.

This paper develops a mouse model of RIT1M90I-driven lung cancer and identifies YAP/TEAD as a therapeutic target for RIT1-mutant lung cancer.

This study shows that USP9X stabilizes RIT1 protein and that its depletion reduces RIT1 abundance and sensitizes cells to EGFR inhibitors.

This paper introduces prime-SGE, a prime editing framework for assessing drug resistance variants across multiple oncogenes in a single experiment.

The paper compares somatic mutations and aneuploidy in lung adenocarcinomas from never-smokers and smokers, finding that mutations, not copy number changes, distinguish the two groups.

This study identifies unique vulnerabilities of oncogenic EGFR, KRAS, and RIT1 in lung cancer through integrative analysis of CRISPR screens and drug sensitivity data.

The paper identifies synthetic lethal and tumor suppressive paralog pairs in the human genome using a CRISPR-based approach, revealing new drug targets and essential gene families.

The paper introduces eVIP2, a tool to predict the functional impact of gene variants using gene expression data, and validates its predictions with experimental assays.

The paper uses Perturb-seq to assess the phenotypic impact of somatic variants in cancer, revealing a continuum of gain-of-function KRAS variants.

The paper introduces the L1000 platform, a high-throughput gene expression profiling method, and reports 1.3 million perturbational profiles expanding the Connectivity Map for drug mechanism discovery and functional annotation.