Theme

・(Epi)genetic mechanisms of pediatric brain tumor formation
・Cancer neuroscience: Tumor-neuron communications in the brain
・Preclinical studies with molecular targeting inhibitors

Medulloblastoma, a malignant brain tumor generated in mouse cerebellum using the CRIPSR-Cas9 genome editing technology.

Member

Professor
Daisuke Kawauchi, Ph.D
Associate professor
Kun Zou, Ph.D
Technical staff
Seiko Ukai

Publications

  • Cancer-specific epigenome identifies oncogenic hijacking by nuclear factor I family proteins for medulloblastoma progression. Dev Cell. 59(17):2302-2319.(2024)
  • Cross-species genomics reveals oncogenic dependencies in ZFTA/C11orf95 fusion-positive supratentorial ependymomas. Cancer Discov. 11(9):2230-2247.(2021)
  • Functional loss of a noncanonicalk BCOR-PRC1.1 complex accelerates SHH-driven medulloblastoma formation. Genes Dev. 34(17-18):1161-1176. (2020)
  • YAP1 subgroup supratentorial ependymoma requires TEAD and nuclear factor I-mediated transcriptional programmes for tumorigenesis. Nat Commun. 10(1):3914. (2019)
  • Aberrant ERBB4-SRC Signaling as a Hallmark of Group 4 Medulloblastoma Revealed by Integrative Phosphoproteomic Profiling. Cancer Cell. 34(3):379-395. (2018)
  • Chd7 is indispensable for mammalian brain development through activation of a neuronal differentiation programme. Nat Commun. 8:14758. (2017)
  • Somatic CRISPR/Cas9-mediated tumour suppressor disruption enables versatile brain tumour modelling. Nat Commun. 6:7391. (2015)
  • A mouse model of the most aggressive subgroup of human medulloblastoma. Cancer Cell. 21(2):168-180. (2012)