Transient transcription factor (OSKM) expression is key towards clinical translation of in vivo cell reprogramming.
Level 5 - mechanism / opinion, no new human data
Commentary and expert opinion discussing animal studies with no new clinical data.
PubMed 28455313 · doi:10.15252/emmm.201707650
What was done
This commentary discusses preclinical evidence on in vivo cellular reprogramming using Oct3/4, Sox2, Klf4, and c-Myc (OSKM) transcription factor overexpression, focusing specifically on a cyclic, short-term induction protocol developed by the Izpisúa-Belmonte laboratory.
What was found
The abstract reports no primary quantitative data. It describes that sustained in vivo OSKM expression induces teratomas, whereas a short-term, cyclic expression protocol prevents complete reprogramming to pluripotency and avoids tumorigenesis while enhancing tissue regeneration.
Why it matters
Short-term OSKM induction provides a potential strategy to utilize in vivo cellular reprogramming for regenerative medicine while mitigating the severe risk of teratoma development.
Limits
This article is a commentary rather than primary research and presents no original measurements or sample sizes. The cited findings are derived from preclinical animal models, and human safety, dosing parameters, and long-term consequences are unestablished.
Cited by
- supports In vivo expression of all four original Yamanaka factors (OSKM) leads to tissue dysfunction, teratoma/cancer formation, or death in animals.