ArticleActa biochimica et biophysica Sinica2022
The origin of unwanted editing byproducts in gene editing.
Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Harnessing the potential of gene editing technology for CAR-T cell therapy of solid tumors.Inflammation and regeneration · 2025Review
- Cas9-Rep fusion tethers donor DNA in vivo and boosts the efficiency of HDR-mediated genome editing.Plant biotechnology journal · 2025Article
- Transfer of mitochondrial DNA into the nuclear genome during induced DNA breaks.Nature communications · 2024Article
- Assessing and advancing the safety of CRISPR-Cas tools: from DNA to RNA editing.Nature communications · 2023Review
- Safeguarding genome integrity during gene-editing therapy in a mouse model of age-related macular degeneration.Nature communications · 2022Article
- CRISPR/Cas9-induced structural variations expand in T lymphocytes in vivo.Nucleic acids research · 2022Article
- Triple kill: DDR inhibitors, radiotherapy and immunotherapy leave cancer cells with no escape.Acta biochimica et biophysica Sinica · 2022Review
- Install, repair and outcomes: a special issue on physiological and programmed DNA lesions.Acta biochimica et biophysica Sinica · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The rapid development of CRISPR-Cas genome editing tools has greatly changed the way to conduct research and holds tremendous promise for clinical applications. During genome editing, CRISPR-Cas enzymes induce DNA breaks at the target sites and subsequently the DNA repair pathways are recruited to generate diverse editing outcomes. Besides off-target cleavage, unwanted editing outcomes including chromosomal structural variations and exogenous DNA integrations have recently raised concerns for clinical safety. To eliminate these unwanted editing byproducts, we need to explore the underlying mechanisms for the formation of diverse editing outcomes from the perspective of DNA repair. Here, we describe the involved DNA repair pathways in sealing Cas enzyme-induced DNA double-stranded breaks and discuss the origins and effects of unwanted editing byproducts on genome stability. Furthermore, we propose the potential risk of inhibiting DNA repair pathways to enhance gene editing. The recent combined studies of DNA repair and CRISPR-Cas editing provide a framework for further optimizing genome editing to enhance editing safety.
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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.