ArticleGenes & development2004
Increased gene dosage of Ink4a/Arf results in cancer resistance and normal aging.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
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Who cites it
63 citing papers in PubMed, 135 citations in OpenAlex.
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Variable Gene Copy Number in Cancer-Related Pathways Is Associated With Cancer Prevalence Across Mammals.Molecular biology and evolution · 2025Article
- Review
- P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022Review
- The Senescence Markers p16INK4A, p14ARF/p19ARF, and p21 in Organ Development and Homeostasis.Cells · 2022Review
- Transcriptional regulation of INK4/ARF locus by cis and trans mechanisms.Frontiers in cell and developmental biology · 2022Review
- Endothelial sprouting, proliferation, or senescence: tipping the balance from physiology to pathology.Cellular and molecular life sciences : CMLS · 2021Review
- Chronic expression of p16Nature communications · 2020Article
- IKKβ overexpression together with a lack of tumour suppressor genes causes ameloblastic odontomas in mice.International journal of oral science · 2020Article
- Testis-specific Arf promoter expression in a transposase-aided BAC transgenic mouse model.Molecular biology reports · 2019Article
- p53 Isoforms in Cellular Senescence- and Ageing-Associated Biological and Physiological Functions.International journal of molecular sciences · 2019Review
- Review
- CDKN2B upregulation prevents teratoma formation in multipotent fibromodulin-reprogrammed cells.The Journal of clinical investigation · 2019Article
- p16Ink4a Prevents the Activation of Aged Quiescent Dentate Gyrus Stem Cells by Physical Exercise.Frontiers in cellular neuroscience · 2019Article
- From humans to hydra: patterns of cancer across the tree of life.Biological reviews of the Cambridge Philosophical Society · 2018Review
- Senescence in Health and Disease.Cell · 2017Review
- Increased Arf/p53 activity in stem cells, aging and cancer.Aging cell · 2017Review
- A role for cellular senescence in birth timing.Cell cycle (Georgetown, Tex.) · 2017Review
- Dynamics of ARF regulation that control senescence and cancer.BMB reports · 2016Review
- p53 and the Carcinogenicity of Chronic Inflammation.Cold Spring Harbor perspectives in medicine · 2016Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian genes frequently present allelic variants that differ in their expression levels and that, in the case of tumor suppressor genes, can be of relevance for cancer susceptibility and aging. We report here the characterization of a novel mouse model with increased activity for the Ink4a and Arf tumor suppressors. We have generated a "super Ink4a/Arf" mouse strain carrying a transgenic copy of the entire Ink4a/Arf locus. Cells derived from super Ink4a/Arf mice have increased resistance to in vitro immortalization and oncogenic transformation. Importantly, super Ink4a/Arf mice manifest higher resistance to cancer compared to normal, nontransgenic, mice. Finally, super Ink4a/Arf mice have normal aging and lifespan. Together, these results indicate that modest increases in the activity of the Ink4a/Arf tumor suppressor result in a beneficial cancer-resistant phenotype without affecting normal viability or aging.
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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.