ArticleOncogene2014
Pleiotropic effect of somatic mutations in the E2F subunit DP-1 gene in human cancer.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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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
6 citing papers in PubMed, 11 citations in OpenAlex.
- Upregulation ofCanadian respiratory journal · 2025Article
- TFDP1 transcriptionally activates KIF22 to enhance aggressiveness and stemness in endometrial cancer: implications for prognosis and targeted therapy.Journal of molecular histology · 2024Article
- Effects of cancer-testis antigen, TFDP3, on cell cycle regulation and its mechanism in L-02 and HepG2 cell lines in vitro.PloS one · 2017Article
- An RB-EZH2 Complex Mediates Silencing of Repetitive DNA Sequences.Molecular cell · 2016Article
- Intra-tumor heterogeneity in TP53 null High Grade Serous Ovarian Carcinoma progression.BMC cancer · 2015Article
- To live or let die - complexity within the E2F1 pathway.Molecular & cellular oncologyReview
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 1 institution in 1 country.
Funding
Abstract
Transcription factor E2F-1 and its interaction with pRb provide a key point of control in cell proliferation. E2F-1 participates in both cell cycle progression and apoptosis, and in cells exists with a DP dimerization partner protein, the most prominent being DP-1. By mining the tumor tissue and cancer cell line encyclopedia genomic databases, we identified the first somatic mutations in the DP-1 gene and describe 53 distinct mutation events here. The mutations are mostly missense mutations, but also include nonsense and frame-shift mutations that result in truncated DP-1 derivatives. Mutation occurs throughout the DP-1 gene but generally leaves protein dimerization activity intact. This allows the mutant derivatives to affect the properties of the E2F-1/DP-1 heterodimer through a transdominant mechanism, which changes the DNA binding, transcriptional activation and pRb-binding properties of the heterodimer. In particular, many DP-1 mutants were found to impair E2F-1-dependent apoptosis. Our results establish that somatic mutations in DP-1 uncouple normal control of the E2F pathway, and thus define a new mechanism that could contribute to aberrant proliferation in tumor cells.
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Registered trials
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