ArticleOncogene2002
Loss of neurofibromatosis-1 and p19(ARF) cooperate to induce a multiple tumor phenotype.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Malignant Peripheral Nerve Sheath Tumor, a Heterogeneous, Aggressive Cancer with Diverse Biomarkers and No Targeted Standard of Care: Review of the Literature and Ongoing Investigational Agents.Targeted oncology · 2024Review
- Translating current basic research into future therapies for neurofibromatosis type 1.British journal of cancer · 2020Review
- Cdkn2a (Arf) loss drives NF1-associated atypical neurofibroma and malignant transformation.Human molecular genetics · 2019Article
- The Challenge of Cancer Genomics in Rare Nervous System Neoplasms: Malignant Peripheral Nerve Sheath Tumors as a Paradigm for Cross-Species Comparative Oncogenomics.The American journal of pathology · 2016Review
- Article
- NF1 deletion generates multiple subtypes of soft-tissue sarcoma that respond to MEK inhibition.Molecular cancer therapeutics · 2013Article
- Genetically engineered mouse models shed new light on the pathogenesis of neurofibromatosis type I-related neoplasms of the peripheral nervous system.Brain research bulletin · 2012Review
- Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms.Acta neuropathologica · 2012Review
- Nf1 mutant mice with p19ARF gene loss develop accelerated hematopoietic disease resembling acute leukemia with a variable phenotype.American journal of hematology · 2011Article
- Article
- The loss of Nf1 transiently promotes self-renewal but not tumorigenesis by neural crest stem cells.Cancer cell · 2008Article
- Transcriptional repression of the Neurofibromatosis-1 tumor suppressor by the t(8;21) fusion protein.Molecular and cellular biology · 2005Article
- Emerging mechanism and therapeutic potential of neurofibromatosis type 1-related nerve system tumor: Advancing insights into tumor development.Neuro-oncology advancesReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inactivation of the neurofibromatosis-1 (NF1) gene de-regulates RAS and cooperates with mutation or loss of the p53 tumor suppressor to induce tumorigenesis. p19(ARF) acts upstream of p53 in an oncogene checkpoint to induce apoptosis in response to activated RAS and other factors that stimulate proliferation. Therefore, we bred p19(ARF-/-) to NF1(+/-) mice to determine if loss of these genes collaborates in tumorigenesis. As expected from the embryonic lethality of NF1 null mice, no mice lacking both p19(ARF) and NF1 were born. Unexpectedly, the loss of one allele of NF1 did not greatly shorten the time to tumor formation in a p19(ARF) null background. The tumor types observed were characteristic of p19(ARF) null animals, not those associated with neurofibromatosis or those observed with NF1(+/-)/p53(+/-) mice. However, seven out of 12 animals developed multiple tumors, some with metastases. This multiple tumor phenotype was not previously observed with p19(ARF)-null mice and suggests a distinct form of cooperation between the loss of these tumor suppressors.
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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.