BRAF^V600E accelerates disease progression and enhances immune suppression in a mouse model of B-cell leukemia.

ABSTRACT: Mutated mitogen-activated protein kinase (MAPK) pathway components promote tumor survival, proliferation, and immune evasion in solid tumors. MAPK mutations occur in hematologic cancers as well, but their role is less clear and few models are available to study this. We developed an in vivo model of disseminated BRAF^V600E B-cell leukemia to determine the effects of this mutation on tumor development and immune evasion. Mice with B-cell-restricted BRAF^V600E expression crossed with the Eµ-TCL1 model of chronic lymphocytic leukemia (CLL) developed leukemia significantly earlier (median, 4.9 vs 8.1 months; P < .001) and had significantly shorter lifespan (median, 7.3 vs 12.1 months; P < .001) versus BRAF wild-type counterparts. BRAF^V600E expressio

SUBMITTER: Tsai YT 

PROVIDER: S-EPMC5737117 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature