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Oncogenic Activation of Noncanonical NF-kB in B-cell Lymphomas

Shao-Cong Sun

3 Collaborator(s)

Funding source

University of Texas MD Anderson Cancer Center
The development of B-cell malignancies is often due to deregulation of the signaling events that mediate B-cell activation. Understanding these signaling events in normal and malignant B cells is crucial for targeted therapies. This project focuses on the oncogenic activation of noncanonical NF-κB signaling pathway in B-cell malignancies. This pathway relies on the NF-κB-inducing kinase (NIK), which responds to B-cell surface receptors, CD40 and BAFF receptor (BAFFR), and induces the processing of p100. Since p100 functions as a potent inhibitor of NF-κB, the NIK-induced p100 processing both generates mature NF-κB2, p52, and leads to activation of the p100-sequestered NF- κB members. In normal B cells, NIK is constantly degraded and becomes transiently stabilized in response to CD40 and BAFFR signals. Emerging evidence suggests that deregulated NIK accumulation occurs in B-cell lymphoma cells and is responsible for the constitutive NF-κB activation. However, how NIK is normally controlled and deregulated in lymphoma cells and how the aberrantly activated noncanonical NF-κB contributes to B-cell oncogenesis remain poorly understood.

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