KDM1A is strongly overexpressed in human medulloblastomas, cell lines derived from them and murine medulloblastic tumors. a Data from a representative cohort of 62 medulloblastomas (MB) and normal cerebellar tissue (CB) used in a published microarray analysis [22, 23] were re-analyzed for KDM1A expression. ***p < 0.0001 b KDM1A protein expresion was evaluated immunohistochemically in a tissue microarray of 70 medulloblastomas (MB) and 9 tissue samples of normal cerebellum (CB). Micrograph showing KDM1A-positive staining in a representative MB sample, and KDM1A-negative staining in CB, scale bar = 100 μm. c Bars reflect the proportion of cells with strong (black), moderate (dark grey), weak (light grey) or no (white) nuclear KDM1A staining. A two-tailed student’s t-test revealed a significant upregulation of KDM1A protein in the medulloblastomas represented in the tissue microarrays. ***p < 0.0001 d Bars represent KDM1A expression measured using real-time RT-PCR and normalized to the geometric mean of GAPDH, UBC and HPRT expression in a panel of human medulloblastoma cell lines derived from diverse histological tumor subtypes and the SK-N-BE human neuroblastoma cell line, known to express high levels of KDM1A as a reference. e Bars represent KDM1A expression measured using real-time RT-PCR in medulloblastic tumors (black) spontaneously arising in genetically engineered mice with activating mutations in the sonic hedgehog pathway, SmoA1 MB (p = 0.014) and Ptch+/− MB (p = 0.037), compared to normal murine cerebellum (CB, white). f Strong KDM1A protein expression was confirmed in the medulloblastic tumors from SmoA1- and Ptch+/−-mice relative to KDM1A expression in cerebellar tissue (CB) using western blotting of tissue lysates. β-actin expression was used as a loading control.