Dataset Information
EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion ETD, Q Exactive
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Nerve, Cell Culture, Prostate Epithelium
DISEASE(S): Malignant Peripheral Nerve Sheath Tumor,Prostate Cancer
SUBMITTER: 
Pascal Jansen
LAB HEAD: Raphaël Margueron
PROVIDER: PXD012547 | Pride | 2019-03-01
REPOSITORIES: Pride
Publications
EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer.
Proceedings of the National Academy of Sciences of the United States of America 20190313 13
Genetic mutations affecting chromatin modifiers are widespread in cancers. In malignant peripheral nerve sheath tumors (MPNSTs), Polycomb repressive complex 2 (PRC2), which plays a crucial role in gene silencing, is inactivated through recurrent mutations in core subunits embryonic ectoderm development (EED) and suppressor of zeste 12 homolog (SUZ12), but mutations in PRC2's main catalytic subunit enhancer of zeste homolog 2 (EZH2) have never been found. This is in contrast to myeloid and lympho ...[more]
