ArticleOncogene2006
Decreased Mdm2 expression inhibits tumor development induced by loss of ARF.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Molecularly Targeted Therapy for Neuroblastoma.Children (Basel, Switzerland) · 2018Review
- Neuroblastoma treatment in the post-genomic era.Journal of biomedical science · 2017Review
- Role of Mdm2 and Mdmx in DNA repair.Journal of molecular cell biology · 2017Review
- Genome Stability Requires p53.Cold Spring Harbor perspectives in medicine · 2016Review
- Oncogenic protein MTBP interacts with MYC to promote tumorigenesis.Cancer research · 2014Article
- The Mdm network and its regulation of p53 activities: a rheostat of cancer risk.Human mutation · 2014Review
- NIAM-deficient mice are predisposed to the development of proliferative lesions including B-cell lymphomas.PloS one · 2014Article
- RABL6A, a novel RAB-like protein, controls centrosome amplification and chromosome instability in primary fibroblasts.PloS one · 2013Article
- Review
- Protecting the genome from mdm2 and mdmx.Genes & cancer · 2012Article
- The Many Faces of MDM2 Binding Partners.Genes & cancer · 2012Article
- Article
- Decreased Mdm2 expression inhibits tumor development and extends survival independent of Arf and dependent on p53.PloS one · 2012Article
- MicroRNA biogenesis is required for Myc-induced B-cell lymphoma development and survival.Cancer research · 2010Article
- Residues in the alternative reading frame tumor suppressor that influence its stability and p53-independent activities.Experimental cell research · 2009Article
- Mdm2 promotes genetic instability and transformation independent of p53.Molecular and cellular biology · 2008Article
- Elevated Mdm2 expression induces chromosomal instability and confers a survival and growth advantage to B cells.Oncogene · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressor p14/p19(ARF) regulates Mdm2, which is known for controlling the p53 tumor suppressor. Here we report that loss of one allele of Mdm2 in cells that lack ARF resulted in a decreased rate of proliferation, fewer chromosomal aberrations, and suppression of Ras-induced transformation. Moreover, a haploinsufficiency of Mdm2 inhibited spontaneous tumor development in ARF-null mice. Remarkably, Mdm2(+/-)ARF(-/-) mice survived an average of 6 months longer than Mdm2(+/+)ARF(-/-) mice. The spectrum of tumors that arose in Mdm2(+/-)ARF(-/-) mice did not significantly differ from those that developed in mice lacking only ARF. However, the extended tumor latency allowed for the emergence of multiple primary tumors in a third of the Mdm2(+/-)ARF(-/-) mice, as compared to the single tumor type that arose in ARF-null only mice. Therefore, a decrease in Mdm2 levels restored regulation of critical cellular processes that are altered during transformation and that occur in the absence of ARF. Our findings also indicate that Mdm2 can function independently from ARF and imply that targeting Mdm2 in tumors that lack ARF expression should be an effective therapeutic approach.
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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.