The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Oncogene-Induced Senescence: Putting the Brakes on Tumor Development
Abstract
Cellular senescence, a permanent cell cycle arrest, is considered a safeguard mechanism that may prevent aged or abnormal cells from further expansion. Although the term “replicative senescence” stands for the widely accepted model of a terminal growth arrest due to telomere attrition, the significance of “oncogene-inducible senescence” remained an issue of debate over the years. A number of recent studies now show the effect of this acute and telomere-independent form of senescence as a tumor-protective, fail-safe mechanism in vivo that shares conceptual and possibly therapeutic similarities with the genetically encoded apoptosis machinery. (Cancer Res 2006; 66(6): 2881-4)
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In the citing paper
“One consequence of mitochondrial dysfunction is cellular senescence”
From Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2016) · cites this paper as Braig and Schmitt, 2006
In the citing paper
“It is believed that senescence is a key mechanism by which p53 suppresses tumorigenesis (Braig and Schmitt, 2006; Collado and Serrano, 2010).”
From p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells (2013) · cites this paper as Braig and Schmitt, 2006
Citations
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Cited by
Sorted by citations
The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Cellular senescence: when bad things happen to good cells
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“Several lines of evidence indicate that cellular senescence is a potent tumor-suppressive mechanism [4,9,10].”
BackgroundAging, Cellular Senescence, and Cancer
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Cellular senescence and the senescent secretory phenotype: therapeutic opportunities
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Metadata
- Authors
- Braig, M., & Schmitt, C. A.
- Affiliations
- Charité – Universitätsmedizin Berlin (DE)
- Max Delbrück Center (DE)
- ORCID
- Schmitt, Clemens A.
- Venue
- Cancer Research
- Published
- 2006-03-15
- Volume
- 66
- Issue
- 6
- Pages
- 2881-2884
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2044729521
- Cited by
- 274
- References
- 29
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 7 · 2023: 14 · 2022: 13 · 2021: 9 · 2020: 8 · 2019: 9 · 2018: 7 · 2017: 10 · 2016: 11 · 2015: 13 · 2014: 23 · 2013: 22 · 2012: 19
- FWCI
- 12.08
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- oncogene-induced senescence, cellular senescence, replicative senescence, telomere shortening, tumor suppression, cell cycle arrest, apoptosis, cancer therapy
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Humans, Oncogenes, Precancerous Conditions, Cellular Senescence
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