Tails of a Super Histone

Patrick Sin-Chan; Iqra Mumal; Annie Huang

doi:10.1016/j.ccell.2018.12.005

Tails of a Super Histone

Cancer Cell. 2019 Jan 14;35(1):7-9. doi: 10.1016/j.ccell.2018.12.005.

Authors

Patrick Sin-Chan¹, Iqra Mumal², Annie Huang³

Affiliations

¹ Arthur and Sonia Labatt Brain Tumour Research Centre, Department of Pediatrics/Division of Haematology/Oncology, Hospital for Sick Children, Toronto, ON M5G1X8, Canada.
² Arthur and Sonia Labatt Brain Tumour Research Centre, Department of Pediatrics/Division of Haematology/Oncology, Hospital for Sick Children, Toronto, ON M5G1X8, Canada; Department of Medical Biophysics, Faculty of Medicine, University of Toronto, Toronto, ON M5S3H7, Canada.
³ Arthur and Sonia Labatt Brain Tumour Research Centre, Department of Pediatrics/Division of Haematology/Oncology, Hospital for Sick Children, Toronto, ON M5G1X8, Canada; Department of Medical Biophysics, Faculty of Medicine, University of Toronto, Toronto, ON M5S3H7, Canada; Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Toronto, ON M5S3H7, Canada. Electronic address: annie.huang@sickkids.ca.

PMID: 30645977
DOI: 10.1016/j.ccell.2018.12.005

Abstract

Diffuse intrinsic brain stem gliomas (DIPGs) with characteristic K27M mutation of H3.3 are lethal and poorly understood childhood cancers. In this issue of Cancer Cell, Larson et al. exploit a unique murine DIPG model with inducible, endogenous K27M expression to reveal insights into mechanisms of K27M-mediated transformation in DIPG.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Animals
Brain Stem Neoplasms*
Glioma*
Histones / genetics
Mice
Mutation

Substances

Histones

Grants and funding

327030/CIHR/Canada