ArticleJNCI cancer spectrum2018
Mutation Signatures Including APOBEC in Cancer Cell Lines.
Article in JNCI cancer spectrum, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- APOBEC3 activity and DNA polymerase-ε deficiency are associated with distinct IDH1 R132 hotspot mutations.Molecular oncology · 2026Article
- Squamous-state excursions activate APOBEC3A in cancer.bioRxiv : the preprint server for biology · 2026Article
- APOBEC3 mutagenesis drives therapy resistance in breast cancer.Nature genetics · 2025Article
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- Article
- Mutational impact of APOBEC3A and APOBEC3B in a human cell line and comparisons to breast cancer.PLoS genetics · 2023Article
- Structural basis of sequence-specific cytosine deamination by double-stranded DNA deaminase toxin DddA.Nature structural & molecular biology · 2023Article
- Molecular correlates of invasion pattern in HPV-associated endocervical adenocarcinoma: emergence of two distinct risk-stratified tiers.Histopathology · 2023Article
- Lactobacillus for ribosome peptide editing cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Aberrant APOBEC3B Expression in Breast Cancer Is Linked to Proliferation and Cell Cycle Phase.Cells · 2023Article
- Primary mucosal melanomas of the head and neck are characterised by overexpression of the DNA mutating enzyme APOBEC3B.Histopathology · 2023Article
- Review
- APOBEC3A suppresses cervical cancer via apoptosis.Journal of Cancer · 2023Article
- Article
- KMT2C-deficient tumors have elevated APOBEC mutagenesis and genomic instability in multiple cancers.NAR cancer · 2022Article
- Mutational signatures are markers of drug sensitivity of cancer cells.Nature communications · 2022Article
- The von Hippel-Lindau Cullin-RING E3 ubiquitin ligase regulates APOBEC3 cytidine deaminases.Translational research : the journal of laboratory and clinical medicine · 2021Article
- Distinct genetic landscape and a low response to doxorubicin in a luminal-A breast cancer cell line of Pakistani origin.Molecular biology reports · 2021Article
- Loss of the abasic site sensor HMCES is synthetic lethal with the activity of the APOBEC3A cytosine deaminase in cancer cells.PLoS biology · 2021Article
- Comprehensive integrative profiling of upper tract urothelial carcinomas.Genome biology · 2021Article
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Authors and funding
4 authors.
Funding
Abstract
backgroundMultiple endogenous and exogenous sources of DNA damage contribute to the overall mutation burden in cancer, with distinct and overlapping combinations contributing to each cancer type. Many mutation sources result in characteristic mutation signatures, which can be deduced from tumor genomic DNA sequences. Examples include spontaneous hydrolytic deamination of methyl-cytosine bases in CG motifs (AGEING signature) and C-to-T and C-to-G mutations in 5'-TC(A/T) motifs (APOBEC signature).
methodsThe deconstructSigs R package was used to analyze single base substitution mutation signatures in over 1000 cancer cell lines. Two additional approaches were used to analyze the APOBEC mutation signature.
resultsMost cell lines show evidence for multiple mutation signatures. For instance, the AGEING signature, which is the largest source of mutation in most primary tumors, predominates in the majority of cancer cell lines. The APOBEC mutation signature is enriched in cancer cell lines from breast, lung, head/neck, bladder, and cervical cancers, where this signature also comprises a large fraction of all mutations.
conclusionsThe single base substitution mutation signatures of cancer cell lines often reflect those of the original tumors from which they are derived. Cancer cell lines with enrichments for distinct mutation signatures such as APOBEC have the potential to become model systems for fundamental research on the underlying mechanisms and for advancing clinical strategies to exploit these processes.
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