Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Switch telomerase to ALT mechanism by inducing telomeric DNA damages and dysfunction of ATRX and DAXX

31 Aug 2016

Abstract excerpt

Activation of telomerase or alternative lengthening of telomeres (ALT) is necessary for tumours to escape from dysfunctional telomere-mediated senescence. Anti-telomerase drugs might be effective in suppressing tumour growth in approximately 85-90% of telomerase-positive cancer cells. However, there are still chances for these cells to bypass drug treatment after switching to the ALT mechanism to maintain their...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Advanced biosensing and bioanalysis techniques
Share to DNA Repair Mechanisms
Share to Telomeres, Telomerase, and Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 27578458
DOI: 10.1038/srep32280

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Switch telomerase to ALT mechanism by inducing telomeric DNA damages and dysfunction of ATRX and DAXXPMID 27578458Read ↗

Compromised Telomeric Heterochromatin Promotes ALTernative Lengthening of Telomeres.Semantic proximity Read ↗

The Role of ATRX in the Alternative Lengthening of Telomeres (ALT) PhenotypeSemantic proximity Read ↗

Telomere Length Maintenance in Cancer: At the Crossroad between Telomerase and Alternative Lengthening of Telomeres (ALT).Semantic proximity Read ↗

Alternative lengthening of telomeres renders cancer cells hypersensitive to ATR inhibitorsSemantic proximity Read ↗

ALT Positivity in Human Cancers: Prevalence and Clinical InsightsSemantic proximity Read ↗

Loss of ATRX, Genome Instability, and an Altered DNA Damage Response Are Hallmarks of the Alternative Lengthening of Telomeres PathwaySemantic proximity Read ↗

A non-genetic switch triggers alternative telomere lengthening and cellular immortalization in ATRX deficient cellsSemantic proximity Read ↗

Alternative Lengthening of Telomeres (ALT) in Tumors and Pluripotent Stem CellsSemantic proximity Read ↗

Alternative lengthening of telomeres: from molecular mechanisms to therapeutic outlooksSemantic proximity Read ↗

Functional Loss of ATRX and TERC Activates Alternative Lengthening of Telomeres (ALT) in LAPC4 Prostate Cancer CellsSemantic proximity Read ↗

Cancer therapy with a CRISPR-assistant telomerase-activating gene expression systemSemantic proximity Read ↗

ALT: A Multi-Faceted Phenomenon.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.