The role of BCR in lymphocyte polarity and leukemia development

The BCR (Breakpoint Cluster Region) protein is a multifunctional molecule expressed in a wide range of cell types. It contains several interaction domains that allow it to localize to the plasma membrane and participate in protein complexes involved in the control of cell polarity. In particular, BCR forms a functional complex with the GEF Tiam1, playing a key role in regulating the activity of the small GTPase Rac1. Despite these potentially crucial roles, the precise physiological functions of BCR remain poorly understood. Our team investigates the molecular mechanisms that govern its localization, protein interactions, and impact on membrane-associated signaling.

Understanding these mechanisms is especially important given that numerous genetic alterations of BCR lead to the formation of pathogenic fusion proteins, such as BCR-ABL in chronic myeloid leukemia (CML) or in certain cases of acute lymphoblastic leukemia (ALL). In these pathological contexts, the normal function of BCR is lost or hijacked, which may contribute to disrupted polarity, signaling, and uncontrolled cell proliferation.

By dissecting the fundamental functions of BCR, our goal is to better understand how its perturbation contributes to leukemogenic processes.