Response to SMAC mimetics in patient-derived models of triple-negative breast cancer relies on RIPK1 activation
Elisabeth Brown, Paige Jensen, Chieh-Hsiang Yang, Emilio Cortes Sanchez, Zhengtao Chu, Hui Yang, Yi Qiao, 義行 高橋, Apurva Srivastava, Bryan Welm, Jaime Fornetti, Alana L. Welm
This study identifies RIPK1 activation as a key determinant of response to SMAC mimetics in TNBC, showing that resistance is linked to impaired RIPK1 autophosphorylation and HOIP overexpression.
bioRxiv · Oct 28, 2026 · PreprintCancer Biology