The functional role of cytoskeletal dysregulation in activated B cell-like diffuse large B cell lymphoma

Chronic active BCR signaling is the key survival pathway in activated B-cell-like (ABC) DLBCL. In this project we will study how cytoskeleton dynamics influence BCR signaling and lymphoma cell survival. We will particularly focus on the GTPase RhoA which is recurrently mutated in DLBCL. In ABC-DLBCL cell lines and mouse models we will study i) the molecular function of mutant RhoA including its interplay with BCR signaling, ii) the role of mutant RhoA in lymphomagenesis, and iii) the possibilities to therapeutically target mutant RhoA signaling, particularly with regard to mechanisms of non-oncogene addiction induced by altered RhoA signaling.