Hung-Ying Kao

Abstract The mechanisms that mediate endocrine therapy resistance remain incompletely understood. We identified promyelocytic leukemia protein isoform 1 (PML1) as a central node of this resistance. We established a PML1 gene signature that strongly correlates with PI3K, MAPK, and endocrine resistance signatures across multiple patient cohorts, predicting poor clinical outcomes.

Abstract The oestrogen receptor (ER or ERα), a nuclear hormone receptor that drives most breast cancer1, is commonly activated by phosphorylation at serine 118 within its intrinsically disordered N-terminal transactivation domain2,3. Although this modification enables oestrogen-independent ER function, its mechanism has remained unclear despite ongoing clinical trials of kinase inhibitors targeting this region4,5,6.