ArticleLife science alliance2021
Deletion of a pseudogene within a fragile site triggers the oncogenic expression of the mitotic CCSER1 gene.
Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 2 citations in OpenAlex.
- Genomic Variability of the HCT116 Cell Line Identified Using Oxford Nanopore Sequencing.International journal of molecular sciences · 2026Article
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- Proteogenomic characterization of primary colorectal cancer and metastatic progression identifies proteome-based subtypes and signatures.Cell reports · 2024Article
- Genetic Elements at the Alpha-Synuclein Locus.Frontiers in neuroscience · 2022Review
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Authors and funding
16 authors at 4 institutions in 2 countries.
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Abstract
The oncogenic role of common fragile sites (CFS), focal and pervasive gaps in the cancer genome arising from replicative stress, remains controversial. Exploiting the TCGA dataset, we found that in most CFS the genes residing within the associated focal deletions are down-regulated, including proteins involved in tumour immune recognition. In a subset of CFS, however, the residing genes are surprisingly overexpressed. Within the most frequent CFS in this group, FRA4F, which is deleted in up to 18% of cancer cases and harbours the CCSER1 gene, we identified a region which includes an intronic, antisense pseudogene, TMSB4XP8. TMSB4XP8 focal ablation or transcriptional silencing elicits the overexpression of
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