ReviewBriefings in bioinformatics2018
Mutational signatures and mutable motifs in cancer genomes.
Review in Briefings in bioinformatics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 56 citations in OpenAlex.
- Pharmacologic Resistance in Soft Tissue Sarcomas: Mechanisms, Biomarkers, and Translational Therapeutic Strategies.Cancers · 2026Review
- Mapping DNA glycosylase binding across lesion sequence contexts reveals extended sequence and structural recognition logic.Nature communications · 2026Article
- BASCULE: bayesian inference and clustering of mutational signatures leveraging biological priors.Genome biology · 2025Article
- Three-Dimensional Organization of Telomeres: An Emerging Prognostic Biomarker in Multiple Myeloma.Cells · 2025Review
- CRISPR Technology in Disease Management: An Updated Review of Clinical Translation and Therapeutic Potential.Cell proliferation · 2025Article
- Comprehensive Insights into APOBEC Mutations in Thyroid Cancer: Prognostic and Therapeutic Discoveries.Biological procedures online · 2025Article
- Sequencing of high-frequency mutated genes in breast cancer (BRCA) and associated-functions analysis.International journal of clinical and experimental pathology · 2025Article
- Tumorigenesis Caused by Aberrant Expression of GANP, a Central Component in the Mammalian TREX-2 Complex-Lessons from Transcription-Coupled DNA Damages.International journal of molecular sciences · 2024Review
- Widespread mutagenesis and chromosomal instability shape somatic genomes in systemic sclerosis.Nature communications · 2024Article
- Anisakis extracellular vesicles elicit immunomodulatory and potentially tumorigenic outcomes on human intestinal organoids.Parasites & vectors · 2024Article
- Properties and Mechanisms of Deletions, Insertions, and Substitutions in the Evolutionary History of SARS-CoV-2.International journal of molecular sciences · 2024Review
- DNA damage response alterations in clear cell renal cell carcinoma: clinical, molecular, and prognostic implications.European journal of medical research · 2024Article
- DNA polymerase ε and δ variants drive mutagenesis in polypurine tracts in human tumors.Cell reports · 2024Article
- Utilizing biological experimental data and molecular dynamics for the classification of mutational hotspots through machine learning.Bioinformatics advances · 2024Article
- The Cytotoxic Properties of Extreme Fungi's Bioactive Components-An Updated Metabolic and Omics Overview.Life (Basel, Switzerland) · 2023Review
- Mutational signatures reveal mutual exclusivity of homologous recombination and mismatch repair deficiencies in colorectal and stomach tumors.Scientific data · 2023Article
- Cancer driver mutations: predictions and reality.Trends in molecular medicine · 2023Review
- REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis.Cell death & disease · 2022Article
- A score of DNA damage repair pathway with the predictive ability for chemotherapy and immunotherapy is strongly associated with immune signaling pathway in pan-cancer.Frontiers in immunology · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 7 institutions in 2 countries.
Funding
Abstract
Cancer is a genetic disorder, meaning that a plethora of different mutations, whether somatic or germ line, underlie the etiology of the 'Emperor of Maladies'. Point mutations, chromosomal rearrangements and copy number changes, whether they have occurred spontaneously in predisposed individuals or have been induced by intrinsic or extrinsic (environmental) mutagens, lead to the activation of oncogenes and inactivation of tumor suppressor genes, thereby promoting malignancy. This scenario has now been recognized and experimentally confirmed in a wide range of different contexts. Over the past decade, a surge in available sequencing technologies has allowed the sequencing of whole genomes from liquid malignancies and solid tumors belonging to different types and stages of cancer, giving birth to the new field of cancer genomics. One of the most striking discoveries has been that cancer genomes are highly enriched with mutations of specific kinds. It has been suggested that these mutations can be classified into 'families' based on their mutational signatures. A mutational signature may be regarded as a type of base substitution (e.g. C:G to T:A) within a particular context of neighboring nucleotide sequence (the bases upstream and/or downstream of the mutation). These mutational signatures, supplemented by mutable motifs (a wider mutational context), promise to help us to understand the nature of the mutational processes that operate during tumor evolution because they represent the footprints of interactions between DNA, mutagens and the enzymes of the repair/replication/modification pathways.
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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.