Oncogene-Induced Senescence: Putting the Brakes on Tumor Development

Braig, Melanie; Schmitt, Clemens A.

doi:10.1158/0008-5472.can-05-4006

Cited by 274Telomeres, Telomerase, and SenescenceCancer-related Molecular PathwaysGenetics, Aging, and Longevity in Model Organisms

Oncogene-Induced Senescence: Putting the Brakes on Tumor Development

Braig, Melanie, Schmitt, Clemens A.·2006·Cancer Research

DOI 10.1158/0008-5472.can-05-4006

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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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Cellular senescence is one consequence of mitochondrial dysfunction.
“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
Senescence is a key mechanism by which p53 suppresses tumorigenesis.
“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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Authors: Braig, M., & Schmitt, C. A.
Affiliations: Charité – Universitätsmedizin Berlin (DE)
Max Delbrück Center (DE)
ORCID: Schmitt, Clemens A.
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2006-03-15
Volume: 66
Issue: 6
Pages: 2881-2884
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-05-4006
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: Health Sciences › Medicine › Physiology › 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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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development

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