ArticleCell2012
Mutational processes molding the genomes of 21 breast cancers.
Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04873427 (In Situ Clonal Heterogeneity in Prostatic Diagnostic Biopsies), which is not on this map. Cited by 1,211 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.
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.
In Situ Clonal Heterogeneity in Prostatic Diagnostic Biopsies: Impact on Prostate Cancer Evolution and Clinical Outcome. A Retrospective, Proof of Concept Study
Who cites it
1,211 citing papers in PubMed, 1,984 citations in OpenAlex.
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- The BRCA1-A complex restricts replication fork reversal-dependent DNA repair in ATM deficient cells.Nature communications · 2026Article
- NeoCircle: pre- and post-operative circulating tumor DNA dynamics predicts survival in neoadjuvant-treated early breast cancer.EMBO molecular medicine · 2026Article
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- Unsupervised Deep Representation Learning and Probabilistic Clustering for the Systems-Level Discovery of Germline Mutation Signatures in Pediatric Cancers.Biomedicines · 2026Article
- Effects of ethanol and acetaldehyde on multi-organ genomic mutation landscapes.Cell biology and toxicology · 2026Article
- Clonal evolution and mutational trajectories of metastatic colorectal cancer shaped by anticancer therapies.Nature communications · 2026Article
- Single-cell whole-genome sequencing reveals convergent evolution in Burkitt lymphoma.Nature communications · 2026Article
- Mapping DNA glycosylase binding across lesion sequence contexts reveals extended sequence and structural recognition logic.Nature communications · 2026Article
- Robust discovery of mutational signatures using power posteriors.PLoS computational biology · 2026Article
1,151 more citing papers are in PubMed but not listed here.
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Authors and funding
54 authors at 13 institutions in 8 countries.
Funding
Abstract
All cancers carry somatic mutations. The patterns of mutation in cancer genomes reflect the DNA damage and repair processes to which cancer cells and their precursors have been exposed. To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes. Multiple distinct single- and double-nucleotide substitution signatures were discernible. Cancers with BRCA1 or BRCA2 mutations exhibited a characteristic combination of substitution mutation signatures and a distinctive profile of deletions. Complex relationships between somatic mutation prevalence and transcription were detected. A remarkable phenomenon of localized hypermutation, termed "kataegis," was observed. Regions of kataegis differed between cancers but usually colocalized with somatic rearrangements. Base substitutions in these regions were almost exclusively of cytosine at TpC dinucleotides. The mechanisms underlying most of these mutational signatures are unknown. However, a role for the APOBEC family of cytidine deaminases is proposed.
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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.