New Publication by Flümann et al. in Blood Cancer Discovery
Our current study on an improved model of Myd88- and BCL2-driven DLBCL has just been published in Blood Cancer Discovery. In this model, we incorporate a loss of Prdm1, a recurrent feature of MCD/C5 DLBCL that blocks plasmacytic differentiation. This refined autochthonous MCD DLBCL model provides an ideal platform for immune checkpoint studies and is responsive to CAR-T cell therapy. We additionally show that these mice are responsive to a combination treatment with ibrutinib and venetoclax, a regimen that is also effective in a small set of heavily pretreated non-GCB DLBCL patients.
More details: Distinct genetically-determined origins of Myd88/Bcl2-driven aggressive lymphoma rationalize targeted therapeutic intervention strategies.