We also show that LOH of a shared TP53 mutation was restricted to the NEC components of both mixed tumors, while deep deletion of RB1 was exclusive to the NEC component in one, again suggesting a role for TP53/RB1 co-inactivation in the pathogenesis of the NEC phenotype in the breast, including at least a subset of LCNEC. This evidence concerns the gene TP53 and large cell neuroendocrine carcinoma.