Elizabeth Lieschke

The paper shows that pre-existing levels of pro-survival proteins and BCL-XL induction determine cell fate after p53 activation, with implications for cancer therapy.

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

This study identifies secondary splice-site mutations in BRCA1 that drive exon skipping and PARP inhibitor resistance in ovarian and breast cancer.