ArticleProceedings of the National Academy of Sciences of the United States of America2019
Proteomic and genomic signatures of repeat instability in cancer and adjacent normal tissues.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed.
- Compensatory relationship between low-complexity regions and gene paralogy in the evolution of prokaryotes.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Variation within major internal repeats of KSHV in vivo.Virus evolution · 2023Article
- Article
- Analysis of lineage-specific protein family variability in prokaryotes combined with evolutionary reconstructions.Biology direct · 2022Article
- Kaiso Regulates DNA Methylation Homeostasis.International journal of molecular sciences · 2021Article
- Mutation-selection balance and compensatory mechanisms in tumour evolution.Nature reviews. Genetics · 2021Review
- Amino acid homorepeats in proteins.Nature reviews. Chemistry · 2020Review
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Repetitive sequences are hotspots of evolution at multiple levels. However, due to difficulties involved in their assembly and analysis, the role of repeats in tumor evolution is poorly understood. We developed a rigorous motif-based methodology to quantify variations in the repeat content, beyond microsatellites, in proteomes and genomes directly from proteomic and genomic raw data. This method was applied to a wide range of tumors and normal tissues. We identify high similarity between repeat instability patterns in tumors and their patient-matched adjacent normal tissues. Nonetheless, tumor-specific signatures both in protein expression and in the genome strongly correlate with cancer progression and robustly predict the tumorigenic state. In a patient, the hierarchy of genomic repeat instability signatures accurately reconstructs tumor evolution, with primary tumors differentiated from metastases. We observe an inverse relationship between repeat instability and point mutation load within and across patients independent of other somatic aberrations. Thus, repeat instability is a distinct, transient, and compensatory adaptive mechanism in tumor evolution and a potential signal for early detection.
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