ArticlePloS one2009
Limited role of murine ATM in oncogene-induced senescence and p53-dependent tumor suppression.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
38 citing papers in PubMed, 57 citations in OpenAlex.
- ATM and p53 in aging and cancer: a double-edged sword in genomic integrity.Biogerontology · 2025Review
- TRIP13 protects pancreatic cancer cells against intrinsic and therapy-induced DNA replication stress.NAR cancer · 2025Article
- Correction: Limited Role of Murine ATM in Oncogene-Induced Senescence and p53-Dependent Tumor Suppression.PloS one · 2024Article
- ERK5 Is a Major Determinant of Chemical Sarcomagenesis: Implications in Human Pathology.Cancers · 2022Article
- Preclinical Models for the Study of Lung Cancer Pathogenesis and Therapy Development.Cold Spring Harbor perspectives in medicine · 2021Review
- Genetic Determinants of EGFR-Driven Lung Cancer Growth and Therapeutic ResponseCancer discovery · 2021Article
- Targeting sphingosine kinase 1 (SK1) enhances oncogene-induced senescence through ceramide synthase 2 (CerS2)-mediated generation of very-long-chain ceramides.Cell death & disease · 2021Article
- CD9 induces cellular senescence and aggravates atherosclerotic plaque formation.Cell death and differentiation · 2020Article
- A prototypical non-malignant epithelial model to study genome dynamics and concurrently monitor micro-RNAs and proteins in situ during oncogene-induced senescence.BMC genomics · 2018Article
- ATM-deficiency increases genomic instability and metastatic potential in a mouse model of pancreatic cancer.Scientific reports · 2017Article
- A step-by-step microRNA guide to cancer development and metastasis.Cellular oncology (Dordrecht, Netherlands) · 2017Review
- A quantitative and multiplexed approach to uncover the fitness landscape of tumor suppression in vivo.Nature methods · 2017Article
- Mechanisms of oncogene-induced genomic instability.Biophysical chemistry · 2017Review
- Essential Roles of E3 Ubiquitin Ligases in p53 Regulation.International journal of molecular sciences · 2017Review
- Article
- Altered telomere homeostasis and resistance to skin carcinogenesis in Suv39h1 transgenic mice.Cell cycle (Georgetown, Tex.) · 2015Article
- Effects of TP53 mutational status on gene expression patterns across 10 human cancer types.The Journal of pathology · 2014Article
- The Mre11 complex suppresses oncogene-driven breast tumorigenesis and metastasis.Molecular cell · 2013Article
- Functional interplay between the DNA-damage-response kinase ATM and ARF tumour suppressor protein in human cancer.Nature cell biology · 2013Article
- Tumor suppressor activity of the ERK/MAPK pathway by promoting selective protein degradation.Genes & development · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies in human fibroblasts have provided a new general paradigm of tumor suppression according to which oncogenic signaling produces DNA damage and this, in turn, results in ATM/p53-dependent cellular senescence. Here, we have tested this model in a variety of murine experimental systems. Overexpression of oncogenic Ras in murine fibroblasts efficiently induced senescence but this occurred in the absence of detectable DNA damage signaling, thus suggesting a fundamental difference between human and murine cells. Moreover, lung adenomas initiated by endogenous levels of oncogenic K-Ras presented abundant senescent cells, but undetectable DNA damage signaling. Accordingly, K-Ras-driven adenomas were also senescent in Atm-null mice, and the tumorigenic progression of these lesions was only modestly accelerated by Atm-deficiency. Finally, we have examined chemically-induced fibrosarcomas, which possess a persistently activated DNA damage response and are highly sensitive to the activity of p53. We found that the absence of Atm favored genomic instability in the resulting tumors, but did not affect the persistent DNA damage response and did not impair p53-dependent tumor suppression. All together, we conclude that oncogene-induced senescence in mice may occur in the absence of a detectable DNA damage response. Regarding murine Atm, our data suggest that it plays a minor role in oncogene-induced senescence or in p53-dependent tumor suppression, being its tumor suppressive activity probably limited to the maintenance of genomic stability.
Indexed as
Identifiers
What OpenQuestion holds
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.