ArticleCell2012
Antitelomerase therapy provokes ALT and mitochondrial adaptive mechanisms in cancer.
Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
187 citing papers in PubMed, 287 citations in OpenAlex.
- Redox regulation of telomerase and telomeres in cancer: a critical appraisal of exposure, causality and molecular directness.Molecular biology reports · 2026Review
- Patient-partnered multiomics reveals the molecular architecture of angiosarcoma.Nature communications · 2026Article
- Selective killing of ALT-cancer cells by Withaferin-A involves destabilization of Rad51 and disruption of DNA repair.Cell death & disease · 2026Article
- Review
- Epigenetic control of telomeric RNA maintains heterochromatin in telomerase-driven cancers.Signal transduction and targeted therapy · 2026Article
- Highly mutagenic copying of telomeric circles promotes ALT establishment.Nature communications · 2026Article
- The role of telomeres in leukemic stem cells function.Regenerative therapy · 2025Review
- Cellular adaptations impact the biological activity of naphthalene diimide G-quadruplex ligands in ALT-positive osteosarcoma cells.Cell death & disease · 2025Article
- Loss of function ofiScience · 2025Article
- Alternative lengthening of telomeres confers favorable prognosis in chondrosarcomas.Journal of translational medicine · 2025Article
- Identification of telomere maintenance-driven molecular subtypes in hepatocellular carcinoma: implications for prognosis and targeted therapy via KPNA2.Discover oncology · 2025Article
- Telomere function and regulation from mouse models to human ageing and disease.Nature reviews. Molecular cell biology · 2025Review
- A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches.Cancers · 2025Review
- Telomerase-based vaccines: a promising frontier in cancer immunotherapy.Cancer cell international · 2024Review
- Beginning at the ends: telomere and telomere-based cancer therapeutics.Molecular genetics and genomics : MGG · 2024Review
- Exploring the role of alternative lengthening of telomere-related genes in diagnostic modeling for non-alcoholic fatty liver disease.Scientific reports · 2024Article
- Aggregation-Induced Emission Luminogen: Role in Biopsy for Precision Medicine.Chemical reviews · 2024Review
- NRF2 signaling pathway and telomere length in aging and age-related diseases.Molecular and cellular biochemistry · 2024Review
- Understanding, diagnosing, and treating pancreatic cancer from the perspective of telomeres and telomerase.Cancer gene therapy · 2024Review
- TRF1 and TRF2: pioneering targets in telomere-based cancer therapy.Journal of cancer research and clinical oncology · 2024Review
127 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
Abstract
To assess telomerase as a cancer therapeutic target and determine adaptive mechanisms to telomerase inhibition, we modeled telomerase reactivation and subsequent extinction in T cell lymphomas arising in Atm(-/-) mice engineered with an inducible telomerase reverse transcriptase allele. Telomerase reactivation in the setting of telomere dysfunction enabled full malignant progression with alleviation of telomere dysfunction-induced checkpoints. These cancers possessed copy number alterations targeting key loci in human T cell lymphomagenesis. Upon telomerase extinction, tumor growth eventually slowed with reinstatement of telomere dysfunction-induced checkpoints, yet growth subsequently resumed as tumors acquired alternative lengthening of telomeres (ALT) and aberrant transcriptional networks centering on mitochondrial biology and oxidative defense. ALT+ tumors acquired amplification/overexpression of PGC-1β, a master regulator of mitochondrial biogenesis and function, and they showed marked sensitivity to PGC-1β or SOD2 knockdown. Genetic modeling of telomerase extinction reveals vulnerabilities that motivate coincidental inhibition of mitochondrial maintenance and oxidative defense mechanisms to enhance antitelomerase cancer therapy.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.