ArticlePloS one2009
High mutability of the tumor suppressor genes RASSF1 and RBSP3 (CTDSPL) in cancer.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Research Trends in C-Terminal Domain Nuclear Envelope Phosphatase 1.Life (Basel, Switzerland) · 2023Review
- Zinc finger myeloid Nervy DEAF-1 type (ZMYND) domain containing proteins exert molecular interactions to implicate in carcinogenesis.Discover oncology · 2022Review
- Identification of Pan-Cancer Biomarkers Based on the Gene Expression Profiles of Cancer Cell Lines.Frontiers in cell and developmental biology · 2021Article
- The effects of mutant Ras proteins on the cell signalome.Cancer metastasis reviews · 2020Review
- Tumor suppressor properties of the small C-terminal domain phosphatases in non-small cell lung cancer.Bioscience reports · 2019Article
- Facets of Communication: Gap Junction Ultrastructure and Function in Cancer Stem Cells and Tumor Cells.Cancers · 2019Review
- The miR-181 family promotes cell cycle by targeting CTDSPL, a phosphatase-like tumor suppressor in uveal melanoma.Journal of experimental & clinical cancer research : CR · 2018Article
- *K-means and cluster models for cancer signatures.Biomolecular detection and quantification · 2017Article
- Integration of ALV intoOncotarget · 2017Article
- Excess of a Rassf1-targeting microRNA, miR-193a-3p, perturbs cell division fidelity.British journal of cancer · 2017Article
- Ras signaling through RASSF proteins.Seminars in cell & developmental biology · 2016Review
- Understanding thrombocytopenia: physiological role of microRNA in survival of neonatal megakaryocytes.Journal of thrombosis and thrombolysis · 2015Article
- Lentivirus-mediated silencing of USO1 inhibits cell proliferation and migration of human colon cancer cells.Medical oncology (Northwood, London, England) · 2015Article
- Clusters of Multiple Mutations: Incidence and Molecular Mechanisms.Annual review of genetics · 2015Review
- MiR-99a may serve as a potential oncogene in pediatric myeloid leukemia.Cancer cell international · 2013Article
- Article
- NotI microarrays: novel epigenetic markers for early detection and prognosis of high grade serous ovarian cancer.International journal of molecular sciences · 2012Article
- A RASSF1A polymorphism restricts p53/p73 activation and associates with poor survival and accelerated age of onset of soft tissue sarcoma.Cancer research · 2012Article
- MiR-100 regulates cell differentiation and survival by targeting RBSP3, a phosphatase-like tumor suppressor in acute myeloid leukemia.Oncogene · 2012Article
- RASSF1 Polymorphisms in Cancer.Molecular biology international · 2012Article
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Authors and funding
23 authors at 7 institutions in 5 countries.
Funding
Abstract
backgroundMany different genetic alterations are observed in cancer cells. Individual cancer genes display point mutations such as base changes, insertions and deletions that initiate and promote cancer growth and spread. Somatic hypermutation is a powerful mechanism for generation of different mutations. It was shown previously that somatic hypermutability of proto-oncogenes can induce development of lymphomas. METHODOLOGY/PRINCIPAL
findingsWe found an exceptionally high incidence of single-base mutations in the tumor suppressor genes RASSF1 and RBSP3 (CTDSPL) both located in 3p21.3 regions, LUCA and AP20 respectively. These regions contain clusters of tumor suppressor genes involved in multiple cancer types such as lung, kidney, breast, cervical, head and neck, nasopharyngeal, prostate and other carcinomas. Altogether in 144 sequenced RASSF1A clones (exons 1-2), 129 mutations were detected (mutation frequency, MF = 0.23 per 100 bp) and in 98 clones of exons 3-5 we found 146 mutations (MF = 0.29). In 85 sequenced RBSP3 clones, 89 mutations were found (MF = 0.10). The mutations were not cytidine-specific, as would be expected from alterations generated by AID/APOBEC family enzymes, and appeared de novo during cell proliferation. They diminished the ability of corresponding transgenes to suppress cell and tumor growth implying a loss of function. These high levels of somatic mutations were found both in cancer biopsies and cancer cell lines. CONCLUSIONS/SIGNIFICANCE: This is the first report of high frequencies of somatic mutations in RASSF1 and RBSP3 in different cancers suggesting it may underlay the mutator phenotype of cancer. Somatic hypermutations in tumor suppressor genes involved in major human malignancies offer a novel insight in cancer development, progression and spread.
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