Compromised telomeric heterochromatin promotes ALTernative lengthening of telomeres

Hsiao P.J. Voon; Philippe Collas; Lee H. Wong

doi:10.1016/j.trecan.2016.02.003

Compromised telomeric heterochromatin promotes ALTernative lengthening of telomeres

Hsiao P.J. Voon, Philippe Collas, Lee H. Wong

Research output: Contribution to journal › Review Article › Other › peer-review

19 Citations (Scopus)

Abstract

Alternative lengthening of telomeres (ALT) is an enigmatic process that allows certain cancers to maintain telomeres in the absence of telomerase. ALT cancers are frequently defective for ATRX/DAXX, a chaperone complex that deposits histone variant H3.3 at telomeres. We propose that mutations in alpha thalassemia-mental retardation syndrome X-linked (ATRX)/death-domain associated protein (DAXX) prime ALT activation by disrupting telomeric heterochromatin.

Original language	English
Pages (from-to)	114-116
Number of pages	3
Journal	Trends In Cancer
Volume	2
Issue number	3
DOIs	https://doi.org/10.1016/j.trecan.2016.02.003
Publication status	Published - 1 Mar 2016

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abstract = "Alternative lengthening of telomeres (ALT) is an enigmatic process that allows certain cancers to maintain telomeres in the absence of telomerase. ALT cancers are frequently defective for ATRX/DAXX, a chaperone complex that deposits histone variant H3.3 at telomeres. We propose that mutations in alpha thalassemia-mental retardation syndrome X-linked (ATRX)/death-domain associated protein (DAXX) prime ALT activation by disrupting telomeric heterochromatin.",

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AU - Voon, Hsiao P.J.

AU - Collas, Philippe

AU - Wong, Lee H.

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Y1 - 2016/3/1

N2 - Alternative lengthening of telomeres (ALT) is an enigmatic process that allows certain cancers to maintain telomeres in the absence of telomerase. ALT cancers are frequently defective for ATRX/DAXX, a chaperone complex that deposits histone variant H3.3 at telomeres. We propose that mutations in alpha thalassemia-mental retardation syndrome X-linked (ATRX)/death-domain associated protein (DAXX) prime ALT activation by disrupting telomeric heterochromatin.

AB - Alternative lengthening of telomeres (ALT) is an enigmatic process that allows certain cancers to maintain telomeres in the absence of telomerase. ALT cancers are frequently defective for ATRX/DAXX, a chaperone complex that deposits histone variant H3.3 at telomeres. We propose that mutations in alpha thalassemia-mental retardation syndrome X-linked (ATRX)/death-domain associated protein (DAXX) prime ALT activation by disrupting telomeric heterochromatin.

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U2 - 10.1016/j.trecan.2016.02.003

DO - 10.1016/j.trecan.2016.02.003

M3 - Review Article

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JO - Trends In Cancer

JF - Trends In Cancer

IS - 3

ER -

Compromised telomeric heterochromatin promotes ALTernative lengthening of telomeres

Abstract

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