ArticleMolecular carcinogenesis2009
Inactivation of SNF5 cooperates with p53 loss to accelerate tumor formation in Snf5(+/-);p53(+/-) mice.
Article in Molecular carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Telomeres: Dysfunction, Maintenance, Aging and Cancer.Aging and disease · 2023Review
- Atypical teratoid rhabdoid tumor (ATRT): disease mechanisms and potential drug targets.Expert opinion on therapeutic targets · 2022Article
- SWI/SNF chromatin remodeling complex is required for initiation of sex-dependent differentiation in mouse germline.Scientific reports · 2021Article
- Preclinical In Vivo Modeling of Pediatric Sarcoma-Promises and Limitations.Journal of clinical medicine · 2021Review
- Article
- p53 Is Not Required for High CIN to Induce Tumor Suppression.Molecular cancer research : MCR · 2021Article
- EWS-FLI1 modulated alternative splicing of ARID1A reveals novel oncogenic function through the BAF complex.Nucleic acids research · 2019Article
- Case-based review: atypical teratoid/rhabdoid tumor.Neuro-oncology practice · 2019Review
- High Frequency of Ovarian Cyst Development in VhlThe American journal of pathology · 2018Article
- Generation of a mouse model of atypical teratoid/rhabdoid tumor of the central nervous system through combined deletion of Snf5 and p53.Cancer research · 2015Article
- The clinicopathologic significance of p53 and BAF-250a (ARID1A) expression in clear cell carcinoma of the endometrium.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2013Article
- Establishment and characterization of MRT cell lines from genetically engineered mouse models and the influence of genetic background on their development.International journal of cancer · 2013Article
- The role of genetics in the establishment and maintenance of the epigenome.Cellular and molecular life sciences : CMLS · 2013Review
- p16INK4A and p14ARF tumor suppressor pathways are deregulated in malignant rhabdoid tumors.Journal of neuropathology and experimental neurology · 2011Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Malignant rhabdoid tumors (MRTs) are poorly differentiated pediatric cancers that arise in various anatomical locations and have a very poor outcome. The large majority of these malignancies are caused by loss of function of the SNF5/INI1 component of the SWI/SNF chromatin remodeling complex. However, the mechanism of tumor development associated with SNF5 loss remains unclear. Multiple studies have demonstrated a role for SNF5 in the regulation of cyclin D1, p16(INK4A), and pRb(f) activities suggesting it functions through the SWI/SNF complex to affect transcription of genes involved in cell cycle control. Previous studies in genetically engineered mouse models (GEMM) have shown that loss of SNF5 on a p53-null background significantly accelerates tumor development. Here, we use established GEMM to further define the relationship between the SNF5 and p53 tumor suppressor pathways. Combined haploinsufficiency of p53 and Snf5 leads to decreased latency for MRTs arising in alternate anatomical locations but not for the standard facial MRTs. We also observed acceleration in the appearance of T-cell lymphomas in the p53(+/-);Snf5(+/-) mice. Our studies suggest that loss of SNF5 activity does not bestow a selective advantage on the p53 spectrum of tumors in the p53(+/-);Snf5(+/-) mice. However, reduced p53 expression specifically accelerated the growth of a subset of MRTs in these mice.
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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.