ArticleGenes & development2005
Cancer-associated mutations in chromatin remodeler hSNF5 promote chromosomal instability by compromising the mitotic checkpoint.
Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
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Who cites it
51 citing papers in PubMed, 124 citations in OpenAlex.
- Combined inhibition of BETs and HDACs as a potential epigenetics-based therapy for malignant rhabdoid tumor.Cell death & disease · 2026Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Review
- Commentary on: SMARCB1 as a novel diagnostic and prognostic biomarker for osteosarcoma.Bioscience reports · 2022Article
- The SWI/SNF chromatin remodeling assemblies BAF and PBAF differentially regulate cell cycle exit and cellular invasion in vivo.PLoS genetics · 2022Article
- Genetic syndromes predisposing to pediatric brain tumors.Neuro-oncology practice · 2021Review
- Inhibition of MYC by the SMARCB1 tumor suppressor.Nature communications · 2019Article
- The budding yeast RSC complex maintains ploidy by promoting spindle pole body insertion.The Journal of cell biology · 2018Article
- Article
- Loss of CDKN1C in a Recurrent Atypical Teratoid/Rhabdoid Tumor.Journal of pediatric hematology/oncology · 2017Article
- Oncogenic roles of SMARCB1/INI1 and its deficient tumors.Cancer science · 2017Review
- Review
- MYC interaction with the tumor suppressive SWI/SNF complex member INI1 regulates transcription and cellular transformation.Cell cycle (Georgetown, Tex.) · 2016Article
- Contextualizing the Genes Altered in Bladder Neoplasms in Pediatric andTeen Patients Allows Identifying Two Main Classes of Biological ProcessesInvolved and New Potential Therapeutic Targets.Current genomics · 2016Article
- 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
- Mutational dichotomy in desmoplastic malignant melanoma corroborated by multigene panel analysis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015Article
- Atypical ossifying fibromyxoid tumor unusually located in the mediastinum: report of a case showing mosaic loss of INI-1 expression.International journal of clinical and experimental pathology · 2015Article
- Cytoplasmic interaction of the tumour suppressor protein hSNF5 with dynamin-2 controls endocytosis.Oncogene · 2014Article
- ATP-dependent chromatin remodeling complexes as novel targets for cancer therapy.Advances in cancer research · 2014Review
- The chromatin remodelling component SMARCB1/INI1 influences the metastatic behavior of colorectal cancer through a gene signature mapping to chromosome 22.Journal of translational medicine · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hSNF5 subunit of human SWI/SNF ATP-dependent chromatin remodeling complexes is a tumor suppressor that is inactivated in malignant rhabdoid tumors (MRTs). Here, we report that loss of hSNF5 function in MRT-derived cells leads to polyploidization and chromosomal instability. Re-expression of hSNF5 restored the coupling between cell cycle progression and ploidy checkpoints. In contrast, cancer-associated hSNF5 mutants harboring specific single amino acid substitutions exacerbated poly- and aneuploidization, due to abrogated chromosome segregation. We found that hSNF5 activates the mitotic checkpoint through the p16INK4a-cyclinD/CDK4-pRb-E2F pathway. These results establish that poly- and aneuploidy of tumor cells can result from mutations in a chromatin remodeler.
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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.