ReviewCurrent cancer drug targets2010
Ras-induced senescence and its physiological relevance in cancer.
Review in Current cancer drug targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 74 citations in OpenAlex.
- Novel paradigms in KRAS targeting: Unveiling strategies to combat drug resistance.Chinese medical journal · 2025Review
- PR55α subunit of protein phosphatase 2A supports KRASOncogene · 2025Article
- The complex journey of targeting RAS in oncology.BMC cancer · 2025Review
- Longevity mechanisms in cardiac aging: exploring calcium dysregulation and senescence.Biogerontology · 2025Review
- First molecules to reactivate RASBMC cancer · 2025Article
- A Human Embryonic Stem Cell-derived Neural Stem Cell Senescence Model Triggered by Oxidative Stress.Current stem cell research & therapy · 2025Article
- The Dose Rate of Corpuscular Ionizing Radiation Strongly Influences the Severity of DNA Damage, Cell Cycle Progression and Cellular Senescence in Human Epidermoid Carcinoma Cells.Current issues in molecular biology · 2024Article
- HPV-YAP1 oncogenic alliance drives malignant transformation of fallopian tube epithelial cells.EMBO reports · 2024Article
- MYC and KRAS cooperation: from historical challenges to therapeutic opportunities in cancer.Signal transduction and targeted therapy · 2024Review
- Article
- A Drosophila chemical screen reveals synergistic effect of MEK and DGKα inhibition in Ras-driven cancer.Disease models & mechanisms · 2023Article
- Radiation-induced senescence: therapeutic opportunities.Radiation oncology (London, England) · 2023Review
- TMPRSS2-ERG promotes the initiation of prostate cancer by suppressing oncogene-induced senescence.Cancer gene therapy · 2022Article
- TSPAN6 is a suppressor of Ras-driven cancer.Oncogene · 2022Article
- Genes and Longevity of Lifespan.International journal of molecular sciences · 2022Review
- FGF-2 induces a failure of cell cycle progression in cells harboring amplified K-Ras, revealing new insights into oncogene-induced senescence.Molecular omics · 2021Article
- EGFRAP encodes a new negative regulator of the EGFR acting in both normal and oncogenic EGFR/Ras-driven tissue morphogenesis.PLoS genetics · 2021Article
- Ionizing radiation results in a mixture of cellular outcomes including mitotic catastrophe, senescence, methuosis, and iron-dependent cell death.Cell death & disease · 2020Article
- Epigenetic regulation of miR-29a/miR-30c/DNMT3A axis controls SOD2 and mitochondrial oxidative stress in human mesenchymal stem cells.Redox biology · 2020Article
- Role of p53 in the Regulation of Cellular Senescence.Biomolecules · 2020Review
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
Activated oncogenes like Ras have traditionally been thought as promoting unrestrained proliferation; therefore, the concept of oncogene-induced senescence has been, and still is, controversial. The counter-intuitive notion that activation of oncogenes leads to the prevention of cellular proliferation has initially been fueled by in vitro studies using ectopic expression of activated Ras in primary fibroblasts. While these initial studies demonstrated unambiguously the existence of a new type of cellular senescence, induced by oncogenes in an ex-vivo system, questions were raised about the physiological relevance of this process. Indeed, recent technical advances in mouse modeling for cancer have suggested that the occurrence of Ras-induced senescence is highly dependent on the cellular context, as well as the level of expression of activated Ras, and may not be pertinent to the study of human cancer initiation and/or progression. However, our increased knowledge of the molecular basis for cellular senescence has led to a better understanding of the molecular events modulating cancer progression in vivo. Recent studies have not only clearly established the incidence of cellular senescence in pre-neoplasic lesions, but also its role as a potential tumor-suppressor mechanism in vivo. Here, we review the recent and exciting new findings regarding the physiological relevance of Ras-induced senescence, and discuss their implications in terms of cancer therapy.
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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.