ArticleNature communications2015
Whole-genome sequencing reveals activation-induced cytidine deaminase signatures during indolent chronic lymphocytic leukaemia evolution.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 1 of them a synthesis that pooled it.
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Who cites it
181 citing papers in PubMed, 1 synthesis or guideline pooled it, 273 citations in OpenAlex.
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- Single-agent ibrutinib in relapsed or refractory follicular lymphoma: a phase 2 consortium trial.Blood · 2018Trial
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- A phenome-wide association study of CNVs genotyped from genome sequencing read depth in the UK Biobank.American journal of human genetics · 2026Article
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- Detection of heterogeneous resistance mechanisms to tyrosine kinase inhibitors from cell-free DNA.Cell genomics · 2025Article
- Evaluation of the Role of AID-Induced Mutagenesis in Resistance to B-Cell Receptor Pathway Inhibitors in Chronic Lymphocytic Leukemia.Current issues in molecular biology · 2025Article
- StarSignDNA: mutation-to-signature attribution for accurate representation of mutational processes in low-mutation contexts.NAR genomics and bioinformatics · 2025Article
- Whole-genome sequencing reveals rare and structural variants contributing to psoriasis and identifies CERCAM as a risk gene.Cell genomics · 2025Article
- Long-read sequencing of single cell-derived melanoma subclones reveals divergent and parallel genomic and epigenomic evolutionary trajectories.bioRxiv : the preprint server for biology · 2025Article
- Transcriptomic and miRNA Signatures of ChAdOx1 nCoV-19 Vaccine Response Using Machine Learning.Life (Basel, Switzerland) · 2025Article
- Genomic landscape of multiple myeloma and its precursor conditions.Nature genetics · 2025Article
- Evaluating topography of mutational signatures with SigProfilerTopography.Genome biology · 2025Article
121 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Patients with chromosome 13q deletion or normal cytogenetics represent the majority of chronic lymphocytic leukaemia (CLL) cases, yet have relatively few driver mutations. To better understand their genomic landscape, here we perform whole-genome sequencing on a cohort of patients enriched with these cytogenetic characteristics. Mutations in known CLL drivers are seen in only 33% of this cohort, and associated with normal cytogenetics and unmutated IGHV. The most commonly mutated gene in our cohort, IGLL5, shows a mutational pattern suggestive of activation-induced cytidine deaminase (AID) activity. Unsupervised analysis of mutational signatures demonstrates the activities of canonical AID (c-AID), leading to clustered mutations near active transcriptional start sites; non-canonical AID (nc-AID), leading to genome-wide non-clustered mutations, and an ageing signature responsible for most mutations. Using mutation clonality to infer time of onset, we find that while ageing and c-AID activities are ongoing, nc-AID-associated mutations likely occur earlier in tumour evolution.
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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.