Our findings suggest that TRAF3-regulated choline metabolism has diagnostic and therapeutic value for B cell malignancies with <i>TRAF3</i> deletions or relevant mutations.
Results from both approaches showed that LMP1-expressing B cells display a phenotype highly similar to that of B cells lacking <i>TRAF</i><i>3</i> genes, indicating that LMP1 can render B cells functionally TRAF3 deficient without <i>TRAF3</i> gene mutations, a finding of significant relevance to selecting pathway-targeted therapies for B-cell malignancies.
Our results identify a new mechanism by which nuclear TRAF3 regulates B-cell survival via inhibition of CREB stability, information highly relevant to the role of TRAF3 in B-cell malignancies.
In addition, TRAF3 mice develop autoimmunity and are predisposed to cancer, particularly squamous cell carcinomas of the tongue ( approximately 50% incidence) and salivary gland tumors.