Rachel M. Nakagawa

This study uses single-cell RNA-sequencing to track how Pik3caH1047R mutation drives mammary tumor progression by altering epithelial and fibroblast transcriptional states.

The paper identifies synthetic lethality between POLE exonuclease deficiency and high aneuploidy in cancer cells, suggesting POLE inhibition as a therapeutic strategy for aneuploid tumors.

The paper shows that gap junctions between breast cancer cells and adipocytes transfer cAMP, activating lipolysis in the tumor microenvironment to support tumor growth.

This study shows that YAP activation in monolayer cultures causes resistance to EGFR/KRAS/BRAF pathway inhibitors, while spheroids are more sensitive, highlighting differences in culture systems for modeling cancer progression.