ReviewJournal of biomedicine & biotechnology2011
Common fragile site tumor suppressor genes and corresponding mouse models of cancer.
Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
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- Replication of [AT/TA]Biochemistry · 2024Article
- Replication of [AT/TA]bioRxiv : the preprint server for biology · 2023Article
- Review
- SUMO2 conjugation of PCNA facilitates chromatin remodeling to resolve transcription-replication conflicts.Nature communications · 2018Article
- Deciphering splenic marginal zone lymphoma pathogenesis: the proposed role of microRNA.Oncotarget · 2018Review
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- Remarkably Long-Tract Gene Conversion Induced by Fragile Site Instability in Saccharomyces cerevisiae.Genetics · 2016Article
- Murine Models of Splenic Marginal Zone Lymphoma: A Role forFrontiers in oncology · 2016Review
- A novel canine kidney cell line model for the evaluation of neoplastic development: karyotype evolution associated with spontaneous immortalization and tumorigenicity.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2015Article
- High Prevalence and Clinical Relevance of Genes Affected by Chromosomal Breaks in Colorectal Cancer.PloS one · 2015Article
- Causes and consequences of replication stress.Nature cell biology · 2014Review
- Stepwise activation of the ATR signaling pathway upon increasing replication stress impacts fragile site integrity.PLoS genetics · 2013Article
- Sites of genetic instability in mitosis and cancer.Annals of the New York Academy of Sciences · 2012Article
- Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer.Genome biology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
Abstract
Chromosomal common fragile sites (CFSs) are specific mammalian genomic regions that show an increased frequency of gaps and breaks when cells are exposed to replication stress in vitro. CFSs are also consistently involved in chromosomal abnormalities in vivo related to cancer. Interestingly, several CFSs contain one or more tumor suppressor genes whose structure and function are often affected by chromosomal fragility. The two most active fragile sites in the human genome are FRA3B and FRA16D where the tumor suppressor genes FHIT and WWOX are located, respectively. The best approach to study tumorigenic effects of altered tumor suppressors located at CFSs in vivo is to generate mouse models in which these genes are inactivated. This paper summarizes our present knowledge on mouse models of cancer generated by knocking out tumor suppressors of CFS.
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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.