ArticleCell cycle (Georgetown, Tex.)2010
Cooperativity of Cdk4R24C and Ras in melanoma development.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Establishment of Stable Immortalized Human Choroidal Melanocytes for Ocular Research.Investigative ophthalmology & visual science · 2026Article
- Modeling rare melanoma subtypes: mechanisms, microenvironments and translational opportunities.Frontiers in oncology · 2026Review
- Cyclins and cyclin-dependent kinases: from biology to tumorigenesis and therapeutic opportunities.Journal of cancer research and clinical oncology · 2023Review
- CDK4: a master regulator of the cell cycle and its role in cancer.Genes & cancer · 2022Review
- Intrinsic and acquired resistance to CDK4/6 inhibitors and potential overcoming strategies.Acta pharmacologica Sinica · 2021Review
- Targeting cyclin-dependent kinases in human cancers: from small molecules to Peptide inhibitors.Cancers · 2015Review
- Melanoma: from melanocyte to genetic alterations and clinical options.Scientifica · 2013Review
- CDK4: A Key Player in the Cell Cycle, Development, and Cancer.Genes & cancer · 2012Article
- Article
- Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Oncotarget · 2011Article
- Animal models of melanoma: a somatic cell gene delivery mouse model allows rapid evaluation of genes implicated in human melanoma.Chinese journal of cancer · 2011Review
- Therapeutic strategies for targeting ras proteins.Genes & cancer · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The importance of the CDK4 protein in human cancer first became evident following the identification of a germ line mutation in the Cdk4 locus that predisposes humans to melanoma. This mutation results in substitution of arginine with cysteine at position 24 (R24C). In an earlier study, we introduced the R24C mutation into the Cdk4 locus of mice using Cre-loxP-mediated "knock-in" technology and observed a very low incidence of spontaneous melanomas in Cdk4(R24C/R24C) mice. This suggested that additional oncogenic mutations might be required for development of melanomas. Here we report an increased incidence of spontaneous cutaneous melanoma in mice expressing the oncogene HRAS(G12V) in melanocytes on a Cdk4(R24C) background. Treatment of Tyr-HRas:Cdk4(R24C/R24C) mice with the carcinogen, DMBA/TPA resulted in a further increase in the number of nevi and melanomas developed when compared with Tyr-HRas:Cdk4(+/+) mice. In summary, in Tyr-HRas:Cdk4(R24C/R24C) mice, we observed that activated CDK4 cooperates with the oncogenic HRAS(G12V) protein to increase the susceptibility of melanoma development in vivo.
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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.