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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“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
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“In Ras-provoked senescent cells, retinoblastoma (Rb) protein– mediated senescence-associated heterochromatin foci have been identified as sites of local transcriptional repression, where heterochromatin proteins are recruited to E2F-responsive promoters (7).”
BackgroundBRAFE600-associated senescence-like cell cycle arrest of human naevi
Michaloglou, C., Vredeveld, L. C. W., Soengas, M. S., Denoyelle, C., Kuilman, T., van der Horst, C. M. A. M., Majoor, D. M., Shay, J. W., Mooi, W. J., & Peeper, D. S. (2005) · Nature · doi:10.1038/nature03890 · Cited by 2,160
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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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