ArticleOncogene2003
Both products of the mouse Ink4a/Arf locus suppress melanoma formation in vivo.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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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.
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Who cites it
39 citing papers in PubMed, 98 citations in OpenAlex.
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- Telomerase reactivation induces progression of mouse BrafbioRxiv : the preprint server for biology · 2023Article
- Review
- Current Molecular Markers of Melanoma and Treatment Targets.International journal of molecular sciences · 2020Review
- Genetically engineered mouse models of melanoma.Cancer · 2017Review
- Absence of germline CDKN2A mutation in Sicilian patients with familial malignant melanoma: Could it be a population-specific genetic signature?Cancer biology & therapy · 2016Article
- CDKN2B Loss Promotes Progression from Benign Melanocytic Nevus to Melanoma.Cancer discovery · 2015Article
- Circadian clock, cancer, and chemotherapy.Biochemistry · 2015Article
- Establishment and characterization of a primary and a metastatic melanoma cell line from Grey horses.In vitro cellular & developmental biology. Animal · 2014Article
- Loss of ARF sensitizes transgenic BRAFV600E mice to UV-induced melanoma via suppression of XPC.Cancer research · 2013Article
- Melanoma: from melanocyte to genetic alterations and clinical options.Scientifica · 2013Review
- Melanoma: from mutations to medicine.Genes & development · 2012Review
- Ubiquitin proteasomal pathway mediated degradation of p53 in melanoma.Archives of biochemistry and biophysics · 2011Article
- Topical application of bleaching phenols; in-vivo studies and mechanism of action relevant to melanoma treatment.Melanoma research · 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
- Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasis.Oncogene · 2010Article
- Cooperative interactions of PTEN deficiency and RAS activation in melanoma metastasis.Small GTPases · 2010Article
- Somatic p16(INK4a) loss accelerates melanomagenesis.Oncogene · 2010Article
- Article
- Pathways of oncogene-induced senescence in human melanocytic cells.Cell cycle (Georgetown, Tex.) · 2010Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deletion of the INK4a/ARF locus at 9p21 is detected with high frequency in human melanoma. Within a short genomic distance, this locus encodes several proteins with established tumor-suppressor roles in a broad spectrum of cancer types. Several lines of evidence support the view that p16INK4a and p19ARF exert the tumor-suppressor activities of this locus, although their relative importance in specific cancer types such as melanoma has been less rigorously documented on the genetic level. Here, we exploit a well-defined mouse model of RAS-induced melanomas to examine the impact of germline p16INK4a or p19ARF nullizygosity on melanoma formation. We demonstrate that loss of either Ink4a/Arf product can cooperate with RAS activation to produce clinically indistinguishable melanomas. In line with the common phenotypic end point, we further show that RAS+ p16INK4a-/- melanomas sustain somatic inactivation of p19ARF-p53 and, correspondingly, that RAS+ p19ARF-/- melanomas experience high-frequency loss of p16INK4a. These genetic studies provide definitive proof that p16INK4a and p19ARF cooperate to suppress the development of melanoma in vivo.
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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.