Abstract
Th e potential of molecularly targeted therapy has been propagated to improve overall outcome in diff use large B-cell lymphoma (DLBCL) [1]. Recent whole-exome sequencing data revealed BRAF and KRAS mutations as likely drivers and potentially targetable mutations [2] in a clinically relevant fraction (4%) of patients with DLBCL [3]. Interestingly, for primary mediastinal B-cell lymphoma (PMBL), a genetically distinct variant of DLBCL [4,5], the prevalence of BRAF and KRAS hotspot mutations has not been elucidated. Given the widespread clinical availability of sensitive molecular genetic BRAF / KRAS assays, screening by genotyping might be a feasible option to identify a subset of patients with PMBL
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