Altered Telomeres in Tumors with ATRX and DAXX Mutations

By C. Heaphy, R. D. de Wilde, Y. Jiao, A. Klein, B. Edil, C. Shi, C. Bettegowda, F. Rodriguez, C. Eberhart, Sachidanand Hebbar and 15 more. Science, 2011

1,029 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/bfb7ca4159aca69a5d2a5c547afda69c76ccd52e

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Citations in the corpus

Recent progress in pancreatic cancer (2013, background): “DAXX and ATRX mutations have been associated with “alternative lengthening of telomeres,” establishing a new cancer pathway in PanNETs.100 The mTOR pathway gene mutations are particularly interesting because the drug everolimus targets the mTOR pathway and everolimus has been shown to be effective i”
Epigenetic plasticity and the hallmarks of cancer (2017, background): “3 or its chaperone proteins that promote telomerase-independent telomere lengthening (57, 94), or by nongenetic mechanisms that simulate self-renewing stem cell states (9, 95).”
Epidemiologic and Molecular Prognostic Review of Glioblastoma (2014, background): “I-X tumors are a genetically heterogeneous group, associated with poor patient survival 13 months, advanced patient age, and are similar to primary GBMs (133, 134).”
Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma. (2012, methodology): “Telomere-specific FISH was done using a standard formalin-fixed paraffin-embedded FISH protocol (Heaphy et al., 2011) using a FITC peptide nucleic acid telomere probe from Dako (Glostrup, Denmark).”
TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal (2013, background): “Why would cancer cells need ALT if telomerase activity was already constitutively active in their precursors? This question was highlighted by the discovery that many ALT cancers harbor mutations in alpha thalassemia/mental retardation syndrome X-linked (ATRX) or death-domain associated protein (DAX”
Glioblastoma: pathology, molecular mechanisms and markers (2015, background): “3/ ATRX/DAXX and consequent alternative lengthening of telomeres (ALT) [59, 145].”
Pathology and Genetics (2010, background): “Furthermore, the loss of ATRX/DAXX seems to be associated with ALT (alternative telomere lengthening), a crucial mechanism by which PanNENs maintain telomere length [35].”