ArticleCarcinogenesis2018
APOBEC3A/B deletion polymorphism and cancer risk.
Article in Carcinogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 48 citations in OpenAlex.
- Genome-wide association study of inhaled corticosteroid response in admixed children with asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Trial
- Motif-centered analyses reveal universal and tissue-specific mutagenic mechanisms operating in the human body.NAR cancer · 2026Article
- Motif-Centered Analyses Reveal Universal and Tissue-Specific Mutagenic Mechanisms Operating in the Human Body.bioRxiv : the preprint server for biology · 2026Article
- APOBEC3 Proteins: From Antiviral Immunity to Oncogenic Drivers in HPV-Positive Cancers.Viruses · 2025Review
- Recent Advance in Single-Molecule Fluorescent Biosensors for Tumor Biomarker Detection.Biosensors · 2024Review
- Article
- Viral infection, APOBEC3 dysregulation, and cancer.Frontiers in genetics · 2024Review
- Seven chromatin regulators as immune cell infiltration characteristics, potential diagnostic biomarkers and drugs prediction in hepatocellular carcinoma.Scientific reports · 2023Article
- Does Human Papillomavirus Play a Causative Role in Prostate Cancer? A Systematic Review Using Bradford Hill's Criteria.Cancers · 2023Review
- APOBEC3A/B Polymorphism Is Not Associated with Human Papillomavirus Infection and Cervical Carcinogenesis.Pathogens (Basel, Switzerland) · 2023Article
- Involvement of APOBEC3A/B Deletion in Mouse Mammary Tumor Virus (MMTV)-like Positive Human Breast Cancer.Diagnostics (Basel, Switzerland) · 2023Article
- Addressing the benefits of inhibiting APOBEC3-dependent mutagenesis in cancer.Nature genetics · 2022Review
- APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?Annual review of virology · 2022Review
- APOBEC mediated mutagenesis drives genomic heterogeneity in endometriosis.Journal of human genetics · 2022Article
- Mouse Mammary Tumour Virus (MMTV) in Human Breast Cancer-The Value of Bradford Hill Criteria.Viruses · 2022Review
- Revisiting the MMTV Zoonotic Hypothesis to Account for Geographic Variation in Breast Cancer Incidence.Viruses · 2022Article
- Prostate cancer and the human papilloma virus: causative association, role of vaccines, and the impact of the COVID-19 pandemic.Prostate cancer and prostatic diseases · 2022Review
- Impact of the APOBEC3A/B deletion polymorphism on risk of ovarian cancer.Scientific reports · 2021Article
- APOBEC3B deletion polymorphism and lung cancer risk in the southern Chinese population.Annals of translational medicine · 2021Article
- CancerFrontiers in immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Activity of the apolipoprotein B mRNA editing enzyme, catalytic-polypeptide-like (APOBEC) enzymes has been linked to specific mutational processes in human cancer genomes. A germline APOBEC3A/B deletion polymorphism is associated with APOBEC-dependent mutational signatures, and the deletion allele has been reported to confer an elevated risk of some cancers in Asian populations, while the results in European populations, so far, have been conflicting. We genotyped the APOBEC3A/B deletion polymorphism in a large population-based sample consisting of 11 106 Caucasian (Norwegian) individuals, including 7279 incident cancer cases (1769 breast, 1360 lung, 1585 colon, and 2565 prostate cancer) and a control group of 3827 matched individuals without cancer (1918 females and 1909 males) from the same population. Overall, the APOBEC3A/B deletion polymorphism was not associated with risk of any of the four cancer types. However, in subgroup analyses stratified by age, we found that the deletion allele was associated with increased risk for lung cancer among individuals <50 years of age (OR 2.17, CI 1.19-3.97), and that the association was gradually reduced with increasing age (P = 0.01). A similar but weaker pattern was observed for prostate cancer. In support of these findings, the APOBEC3A/B deletion was associated with young age at diagnosis among the cancer cases for both cancer forms (lung cancer: P = 0.02; dominant model and prostate cancer: P = 0.03; recessive model). No such associations were observed for breast or colon cancer.
Indexed as
Identifiers
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.