ArticleOncogene2008
Telomere attrition induces a DNA double-strand break damage signal that reactivates p53 transcription in HTLV-I leukemic cells.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Review
- The critical role of ferroptosis in virus-associated hematologic malignancies and its potential value in antiviral-antitumor therapy.Virulence · 2025Review
- BCL-2 family dysregulation in HTLV-1 and BLV pathogenesis and its implications for leukemogenesis and therapy.Molecular biology reports · 2025Review
- Cellular Senescence in Immunity against Infections.International journal of molecular sciences · 2022Review
- Senescence and Host-Pathogen Interactions.Cells · 2020Review
- Telomere Dynamics in Immune Senescence and Exhaustion Triggered by Chronic Viral Infection.Viruses · 2017Review
- Tax impairs DNA replication forks and increases DNA breaks in specific oncogenic genome regions.Molecular cancer · 2014Article
- "Antivirals" in the treatment of adult T cell leukaemia- lymphoma (ATLL).Current hematologic malignancy reports · 2012Review
- Human T-lymphotropic virus proteins and post-translational modification pathways.World journal of virology · 2012Review
- HTLV-I tax increases genetic instability by inducing DNA double strand breaks during DNA replication and switching repair to NHEJ.PloS one · 2012Article
- Human T-lymphotropic type 1 virus p30 inhibits homologous recombination and favors unfaithful DNA repair.Blood · 2011Article
- Aliphatic hyperbranched polyester: a new building block in the construction of multifunctional nanoparticles and nanocomposites.Langmuir : the ACS journal of surfaces and colloids · 2010Article
- HTLV-I Tax-dependent and -independent events associated with immortalization of human primary T lymphocytes.Blood · 2010Article
- HTLV-1 and apoptosis: role in cellular transformation and recent advances in therapeutic approaches.Apoptosis : an international journal on programmed cell death · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Persistent inhibition of telomerase induces a severe telomere shortening in human T-cell leukemia virus type-1-infected cells which signals a DNA double-strand break damage response, formation of telomere dysfunction-induced foci and activates the ATM pathway. In turn, activation of ATM and its downstream effectors led to an increased phosphorylation and acetylation on specific residues of p53 known to be involved in transcriptional activation. Disruption of Mdm2-p53 complexes coupled with increased proteasomal degradation of MDMX further enhanced reactivation of p53 transcription, ultimately leading to senescence of tumor cells. Induction of senescence in these T-cells was associated with an increased expression of p21, p16 and activation of GSK3beta. Our results support the cancer-aging model and demonstrate that the halt of aging in cancer cells can be reversed through reactivation of p53.
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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.