ArticleNature structural & molecular biology2011
DNA secondary structures and epigenetic determinants of cancer genome evolution.
Article in Nature structural & molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
136 citing papers in PubMed, 246 citations in OpenAlex.
- CGGBP1-Regulated Heterogeneous C-T Transition Rates Correlate with G-quadruplex Potential of Terrestrial Vertebrate Genomes.Journal of molecular evolution · 2026Article
- CTCF directly binds G-quadruplex structures to regulate genome topology and gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Non-B DNA structures and their contributions to genetic diversity, aging, and disease.Nucleic acids research · 2026Review
- BLM and FANCJ role in the response to G-quadruplex-dependent telomeric replicative stress.Communications biology · 2026Article
- Article
- CIP2A mediates mitotic recruitment of SLX4/MUS81/XPF to resolve replication stress-induced DNA lesions.Nature communications · 2025Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- G-quadruplexes as a source of vulnerability in BRCA2Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- DNA methylation dysregulation patterns in the 1p36 region instability.Journal of applied genetics · 2025Article
- Landscape and mutational dynamics of G-quadruplexes in the complete human genome and in haplotypes of diverse ancestry.bioRxiv : the preprint server for biology · 2025Article
- DNA replication initiation drives focal mutagenesis and rearrangements in human cancers.Nature communications · 2024Article
- Potential protein kinase inhibitors that target G-quadruplex DNA structures in the human telomeric regions.Molecular diversity · 2024Article
- Centromeres in cancer: Unraveling the link between chromosomal instability and tumorigenesis.Medical oncology (Northwood, London, England) · 2024Review
- The DNA methylome of pediatric brain tumors appears shaped by structural variation and predicts survival.Nature communications · 2024Article
- Genetic and epigenetic instability as an underlying driver of progression and aggressive behavior in IDH-mutant astrocytoma.Acta neuropathologica · 2024Review
- A global transcriptional activator involved in the iron homeostasis in cyanobacteria.Science advances · 2024Article
- Unveiling Alterations of Epigenetic Modifications and Chromatin Architecture Leading to Lipid Metabolic Reprogramming during the Evolutionary Trastuzumab Adaptation of HER2-Positive Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- G-quadruplex-mediated genomic instability drives SNVs in cancer.Nucleic acids research · 2024Article
- Multifaceted Role of PARP1 in Maintaining Genome Stability Through Its Binding to Alternative DNA Structures.Journal of molecular biology · 2024Review
- Alternative DNA structures in hematopoiesis and adaptive immunity.Advances in immunology · 2024Review
76 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
2 authors at 1 institution in 1 country.
Funding
Abstract
An unstable genome is a hallmark of many cancers. It is unclear, however, whether some mutagenic features driving somatic alterations in cancer are encoded in the genome sequence and whether they can operate in a tissue-specific manner. We performed a genome-wide analysis of 663,446 DNA breakpoints associated with somatic copy-number alterations (SCNAs) from 2,792 cancer samples classified into 26 cancer types. Many SCNA breakpoints are spatially clustered in cancer genomes. We observed a significant enrichment for G-quadruplex sequences (G4s) in the vicinity of SCNA breakpoints and established that SCNAs show a strand bias consistent with G4-mediated structural alterations. Notably, abnormal hypomethylation near G4s-rich regions is a common signature for many SCNA breakpoint hotspots. We propose a mechanistic hypothesis that abnormal hypomethylation in genomic regions enriched for G4s acts as a mutagenic factor driving tissue-specific mutational landscapes in cancer.
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What OpenQuestion holds
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.