Skip to main content
. Author manuscript; available in PMC: 2014 Mar 27.
Published in final edited form as: Nat Med. 2013 Aug 6;19(8):998–1004. doi: 10.1038/nm.3267

Table 2.

Oncogenic Risks for Methods of Pluripotency Induction in Somatic Cells

Method of Induction Strengths Weaknesses
Lentiviral vector Robust reprogramming efficiency Genomic integration, Reactivation of integrated transgenes
Adenoviral vector Low risk for genomic integration Low transduction efficiency, Limited transgene expression
Cre recombinase Little genomic disruption Low transduction efficiency, Integration of LoxP sites into host genome
PiggyBac transposition Minimal risk for genomic disruption Low transduction efficiency, Risk for uncontrolled rounds of excision-integration
Plasmid transduction Minimal risk for genomic disruption Very low transduction efficiency, Typically require use of oncogenes such as SV40LT antigen for successful induction of pluripotency
Minicircle Minimal risk for genomic disruption Low transduction efficiency
Sendai Virus Minimal risk for genomic integration, relatively high transduction efficiency Risk for continuous replication of viral vector in cytoplasm leading to improper silencing of pluripotency transgenes
Synthetic mRNA No risk for genomic integration, ability to control transgene expression Variable transduction efficiencies, High technical expertise required
Protein transduction No risk for genomic integration, ability to control transgene expression Very low transduction efficiency, Labor intensive
Small molecules No risk for genomic integration Variable off-target effects