ATRX represses alternative lengthening of telomeres.
Sydney, Australia. In Oncotarget, 15 May 2015
Mutations in the ATRX/DAXX chromatin remodeling complex have been reported in tumors and cell lines that use the ALT mechanism, suggesting that ATRX may be an ALT repressor.
Integrated genomic characterization of adrenocortical carcinoma.
Paris, France. In Nat Genet, Jun 2014
We performed exome sequencing and SNP array analysis of 45 ACCs and identified recurrent alterations in known driver genes (CTNNB1, TP53, CDKN2A, RB1 and MEN1) and in genes not previously reported in ACC (ZNRF3, DAXX, TERT and MED12), which we validated in an independent cohort of 77 ACCs.
Molecular genetics of gliomas.
Atlanta, United States. In Cancer J, 2014
Pediatric GBMs have a distinctive molecular pathogenesis, as H3F3A and DAXX mutations are frequent, and their gene expression profile is different than adult GBMs.
Virion factors that target Daxx to overcome intrinsic immunity.
Hamburg, Germany. In J Virol, 2013
A number of recent reports suggest that several virion proteins may also play vital roles in gene activation processes, in particular by counteracting intrinsic immune mechanisms mediated by the PML nuclear body-associated cellular factors Daxx, ATRX, and Sp100.
Neuroendocrine tumours: cracking the epigenetic code.
London, United Kingdom. In Endocr Relat Cancer, 2013
Recent progress has been facilitated by development of high-throughput tools including second-generation sequencing and arrays for analysis of the 'epigenome' of tumour and normal tissue, permitting unbiased approaches such as exome sequencing that identified mutations of chromatin-remodelling genes ATRX/DAXX in 44% of pancreatic NETs.
Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma.
Montréal, Canada. In Nature, 2012
Mutations in ATRX (α-thalassaemia/mental retardation syndrome X-linked) and DAXX (death-domain associated protein), encoding two subunits of a chromatin remodelling complex required for H3.3 incorporation at pericentric heterochromatin and telomeres, were identified in 31% of samples overall, and in 100% of tumours harbouring a G34R or G34V H3.3 mutation.