ReviewPLoS genetics2016
Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.
Review in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed, 35 citations in OpenAlex.
- Loss of fragile WWOX gene leads to senescence escape and genome instability.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Transcription-Replication Coordination.Life (Basel, Switzerland) · 2022Review
- Neonatal neuronal WWOX gene therapy rescues Wwox null phenotypes.EMBO molecular medicine · 2021Article
- Review
- Modeling genetic epileptic encephalopathies using brain organoids.EMBO molecular medicine · 2021Article
- Deletion of a pseudogene within a fragile site triggers the oncogenic expression of the mitotic CCSER1 gene.Life science alliance · 2021Article
- WWOX Loses the Ability to Regulate Oncogenic AP-2γ and Synergizes with Tumor Suppressor AP-2α in High-Grade Bladder Cancer.Cancers · 2021Article
- Development and Validation of a 5-Gene Autophagy-Based Prognostic Index in Endometrial Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Roles of Farnesyl-Diphosphate Farnesyltransferase 1 in Tumour and Tumour Microenvironments.Cells · 2020Review
- Role of tumor suppressor molecules in genomic perturbations and damaged DNA repair involved in the pathogenesis of cancer and neurodegeneration (Review).Biomedical reports · 2020Review
- Review
- Impact of Replication Stress in Human Papillomavirus Pathogenesis.Journal of virology · 2019Review
- SUMO2 conjugation of PCNA facilitates chromatin remodeling to resolve transcription-replication conflicts.Nature communications · 2018Article
- WWOX controls hepatic HIF1α to suppress hepatocyte proliferation and neoplasia.Cell death & disease · 2018Article
- Differential clinicopathological and molecular features within late-onset colorectal cancer according to tumor location.Oncotarget · 2018Article
- Phosphorylation/de-phosphorylation in specific sites of tumor suppressor WWOX and control of distinct biological events.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Teneurins: An Integrative Molecular, Functional, and Biomedical Overview of Their Role in Cancer.Frontiers in neuroscience · 2018Review
- Modeling WWOX Loss of FunctionFrontiers in oncology · 2018Review
- Caloric restriction delays early phases of carcinogenesis via effects on the tissue microenvironment.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of common fragile sites (CFSs) in cancer remains controversial. Two main views dominate the discussion: one suggests that CFS loci are hotspots of genomic instability leading to inactivation of genes encoded within them, while the other view proposes that CFSs are functional units and that loss of the encoded genes confers selective pressure, leading to cancer development. The latter view is supported by emerging evidence showing that expression of a given CFS is associated with genome integrity and that inactivation of CFS-resident tumor suppressor genes leads to dysregulation of the DNA damage response (DDR) and increased genomic instability. These two viewpoints of CFS function are not mutually exclusive but rather coexist; when breaks at CFSs are not repaired accurately, this can lead to deletions by which cells acquire growth advantage because of loss of tumor suppressor activities. Here, we review recent advances linking some CFS gene products with the DDR, genomic instability, and carcinogenesis and discuss how their inactivation might represent a selective advantage for cancer cells.
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What OpenQuestion holds
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.