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

Non-small cell lung cancer is susceptible to induction of DNA damage responses and inhibition of angiogenesis by telomere overhang oligonucleotides.

Cancer letters - 1 Feb 2014

Puri Neelu, Pitman Ryan T, Mulnix Richard E, Erickson Terrianne, Iness Audra N, Vitali Connie, Zhao Yutong, Salgia Ravi

Abstract excerpt

Exposure of the telomere overhang acts as a DNA damage signal, and exogenous administration of an 11-base oligonucleotide homologous to the 3'-telomere overhang sequence (T-oligo) mimics the effects of overhang exposure by inducing senescence and cell death in non-small cell lung cancer (NSCLC) cells, but not in normal bronchial epithelial cells. T-oligo-induced decrease in cellular proliferation in NSCLC is...

Read the complete abstract on PubMed

Topics

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

Share to Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Share to Bronchi

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cellular Senescence

Share to Cyclin-Dependent Kinase Inhibitor p21

Share to Cyclin-Dependent Kinase Inhibitor p27

Share to Neoplasm Transplantation

Share to Neovascularization, Pathologic

Share to Oligonucleotides

Source

Open in PubMed Open full text

Identifiers

PMID: 24041868
DOI: 10.1016/j.canlet.2013.09.010
PMCID: PMC5839143

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Non-small cell lung cancer is susceptible to induction of DNA damage responses and inhibition of angiogenesis by telomere overhang oligonucleotides.PMID 24041868Read ↗

Telomere homolog oligonucleotides induce apoptosis in malignant but not in normal lymphoid cells: Mechanism and therapeutic potentialSemantic proximity Read ↗

Telomerase inhibitors and ‘T-oligo’ as cancer therapeutics: contrasting molecular mechanisms of cytotoxicitySemantic proximity Read ↗

Evidence that exposure of the telomere 3′ overhang sequence induces senescenceSemantic proximity Read ↗

Telomeric DNA induces apoptosis and senescence of human breast carcinoma cellsSemantic proximity Read ↗

Oligonucleotides Targeting Telomeres and Telomerase in CancerSemantic proximity Read ↗

Telomerase deficiency and dysfunctional telomeres in the lung tumor microenvironment impair tumor progression in NSCLC mouse models and patient-derived xenograftsSemantic proximity Read ↗

Induction of a p95/Nbs1‐mediated S phase checkpoint by telomere 3′ overhang specific DNASemantic proximity Read ↗

Telomere‐based DNA damage responses: a new approach to melanomaSemantic proximity Read ↗

Treating Cancer by Targeting Telomeres and TelomeraseSemantic proximity Read ↗

PARP inhibitors induce a senescence phenotype in non-small cell lung carcinoma cell lines.Semantic proximity Read ↗

SRSF3 knockdown-induced cellular senescence as a possible therapeutic strategy for non-small cell lung cancer.Semantic proximity Read ↗

Induction of Telomere Dysfunction Mediated by the Telomerase Substrate Precursor 6-Thio-2′-DeoxyguanosineSemantic proximity Read ↗

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