ReviewEMBO molecular medicine2016
The dark matter of the cancer genome: aberrations in regulatory elements, untranslated regions, splice sites, non-coding RNA and synonymous mutations.
Review in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 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
165 citing papers in PubMed, 249 citations in OpenAlex.
- Alternative splicing discriminates molecular subtypes and has prognostic impact in diffuse large B-cell lymphoma.Blood cancer journal · 2017Trial
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- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Integrating single-cell and spatial transcriptomics with pan-cancer bulk sequencing identifies OSR2 as a multifaceted biomarker for prognosis and tumor immunity.Discover oncology · 2026Article
- The SynMall resource for characterizing the functional impact of synonymous variation.Genome research · 2026Article
- Identification of BRCA1 and BRCA2 Germline Mutations in Female Breast Cancer Patients Using Next Generation Sequencing.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Synonymous Variants of Potential Significance Identified by a 52-Gene Clinical Sequencing Panel in Non-Small Cell Lung Cancer.Genes, chromosomes & cancer · 2026Article
- Computational screening of oncogenic genetic variations in tumor suppressor proteins driving gastric cancer pathogenesis.PloS one · 2026Article
- Cancer-associated mutational patterns reshape miRNA regulatory regions and potentially disrupt miRNA-gene interactions.American journal of clinical and experimental immunology · 2026Article
- Novel and recurrent mutations in exon 8 of natural killer group 2D (NKG2D) gene among chronic myeloid leukemia patients and their potential role in pathogenesis.Molecular biology reports · 2025Article
- The dark matter in cancer immunology: beyond the visible- unveiling multiomics pathways to breakthrough therapies.Journal of translational medicine · 2025Review
- Strategies for neoantigen screening and immunogenicity validation in cancer immunotherapy (Review).International journal of oncology · 2025Review
- Mitochondrial Complex I Molecular Alterations in Sapajus apella as a Human Gastric Carcinogenesis Model After MNU Exposure.Journal of medical primatology · 2025Article
- Nonstop mutations cause loss of renal tumor suppressor proteinsScience advances · 2025Article
- Targeting RNA splicing modulation: new perspectives for anticancer strategy?Journal of experimental & clinical cancer research : CR · 2025Review
- Activin A receptor type 1C single nucleotide polymorphisms associated with esophageal squamous cell carcinoma risk in Chinese population.World journal of gastrointestinal oncology · 2025Article
- Activation of Wnt/β-catenin signaling is critical for the tumorigenesis of choroid plexus.Neuro-oncology · 2025Article
- Development of a prognostic model based on the ceRNA network in Triple-Negative Breast cancer.PeerJ · 2025Article
105 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is a disease of the genome caused by oncogene activation and tumor suppressor gene inhibition. Deep sequencing studies including large consortia such as TCGA and ICGC identified numerous tumor-specific mutations not only in protein-coding sequences but also in non-coding sequences. Although 98% of the genome is not translated into proteins, most studies have neglected the information hidden in this "dark matter" of the genome. Malignancy-driving mutations can occur in all genetic elements outside the coding region, namely in enhancer, silencer, insulator, and promoter as well as in 5'-UTR and 3'-UTR Intron or splice site mutations can alter the splicing pattern. Moreover, cancer genomes contain mutations within non-coding RNA, such as microRNA, lncRNA, and lincRNA A synonymous mutation changes the coding region in the DNA and RNA but not the protein sequence. Importantly, oncogenes such as TERT or miR-21 as well as tumor suppressor genes such as TP53/p53, APC, BRCA1, or RB1 can be affected by these alterations. In summary, coding-independent mutations can affect gene regulation from transcription, splicing, mRNA stability to translation, and hence, this largely neglected area needs functional studies to elucidate the mechanisms underlying tumorigenesis. This review will focus on the important role and novel mechanisms of these non-coding or allegedly silent mutations in tumorigenesis.
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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.