Loss of TNFAIP3 enhances MYD88_L265P-driven signaling in non-Hodgkin lymphoma.

ABSTRACT: MYD88 mutations are one of the most recurrent mutations in hematologic malignancies. However, recent mouse models suggest that MYD88_L265P alone may not be sufficient to induce tumor formation. Interplay between MYD88_L265P and other genetic events is further supported by the fact that TNFAIP3 (A20) inactivation often accompanies MYD88_L265P. However, we are still lacking information about the consequence of MYD88_L265P in combination with TNFAIP3 loss in human B cell lymphoma. Review of our genetic data on diffuse large B cell lymphoma (DLBCL) and Waldenstrom macroglobulinemia (WM), found that a large percentage of DLBCL and WM cases that have a MYD88 mutation also harbor a TNFAIP3 loss, 55% DLBCL and 28% of WM, respectively. To mimic this combinati

SUBMITTER: Wenzl K 

PROVIDER: S-EPMC6177394 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature