ArticleCancer reports (Hoboken, N.J.)2025
APOBEC3B Does Not Promote Tumor Progression in Tp53 Hemizygous Mice.
Article in Cancer reports (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Collapsing retroviruses for efficient delivery of viro-toxic cargoes.bioRxiv : the preprint server for biology · 2026Article
- TMEM158-mediated TGF-β signaling pathway modulates the sensitivity of TP53-deficient osteosarcoma to USP14 inhibitors.Molecular and cellular biochemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundDNA cytosine deaminase APOBEC3B (A3B) is one of the endogenous sources of somatic mutations in many types of human cancers and is associated with tumor progression rather than tumorigenesis. However, it remains uncertain whether APOBEC3B-induced mutations accelerate tumor progression or not. In this paper, we established a mouse model with A3B overexpression and investigated whether the introduction of A3B overexpression accelerates tumor development in Tp53 hemizygous mice.
methodsWe established A3B transgenic mouse by microinjection and selected the mouse which has only one A3B transgene by genomic qPCR and southern blotting using the probe against the transgene. A3B expression was validated by qPCR, immunoblotting, immunohistochemistry and in vitro CDA assays using lysates of this transgenic mouse liver, spleen and bone marrow. We interbreed this transgenic mouse model with CAG-Cre and Tp53 knockout mice and observed differences in tumor progression and survival between Tp53 hemizygous mice and Tp53 homozygous mice irrespective of A3B expression. Finally, comprehensive genomic mutation analysis was done using the developed tumors.
resultsWe established A3B transgenic mouse which has only one transgene. A3B expression and its CDA activity were confirmed in liver cells and tumor tissues of mice overexpressing A3B. Tp53 hemizygous mice developed osteosarcomas, spindle and pleomorphic sarcomas, and squamous cell carcinomas, however we did not observe any difference in tumor development between the mice with or without A3B expression. The tumor with A3B expression has more high-VAF mutations than the one without A3B, but these mutations are not APOBEC signature.
conclusionWe developed a Cre inducible A3B transgenic mouse model bearing single copy of A3B gene. Although the introduction of A3B overexpression did not accelerate tumor development in Tp53 hemizygous mice, our mouse model with A3B overexpression is well-validated and useful for further research.
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.