Andrew H. Wei

This study identifies heme biosynthesis as a selective dependency in AML, showing that its inhibition triggers cuproptosis via copper accumulation and reveals synthetic lethal pathways for therapeutic strategies.

This study shows DNMT3A mutations reduce DNA methylation and disrupt p53 pathway, increasing self-renewal and cancer risk in hematopoietic cells.

This study identifies a small molecule that differentially regulates BAX and BAK apoptotic activity by modulating their interaction with VDAC2, revealing therapeutic potential for overcoming drug resistance in leukemia.

This study identifies ATM-driven DNA repair and ROS addiction as mechanisms of resistance to FLT3 inhibitors in AML and shows ATM inhibition can overcome resistance in vitro and in vivo.

The paper introduces scRaCH-seq, a method for single-cell long-read sequencing that improves detection of isoform usage and mutations in targeted genes, demonstrating its application in CLL samples.