Investigation of Possible Telomerase Reverse Transcriptase Promoter Mutation in Human Chemically Induced Liver Progenitors.
1/5 보강
[AIM] This study aimed to investigate the presence of telomerase reverse transcriptase (TERT) promoter mutations in human chemically induced liver progenitors (hCLiPs) and to evaluate their potential
APA
Askeyev B, Soyama A, et al. (2025). Investigation of Possible Telomerase Reverse Transcriptase Promoter Mutation in Human Chemically Induced Liver Progenitors.. Hepatology research : the official journal of the Japan Society of Hepatology, 55(10), 1398-1403. https://doi.org/10.1111/hepr.14240
MLA
Askeyev B, et al.. "Investigation of Possible Telomerase Reverse Transcriptase Promoter Mutation in Human Chemically Induced Liver Progenitors.." Hepatology research : the official journal of the Japan Society of Hepatology, vol. 55, no. 10, 2025, pp. 1398-1403.
PMID
40590767
Abstract
[AIM] This study aimed to investigate the presence of telomerase reverse transcriptase (TERT) promoter mutations in human chemically induced liver progenitors (hCLiPs) and to evaluate their potential association with carcinogenesis.
[METHODS] TERT promoter mutations were analyzed in 20 formalin-fixed, paraffin-embedded HCC samples, 19 liver cirrhosis (LC) samples, and five hCLiPs derived from cirrhotic liver tissue. Genomic DNA was extracted, and droplet digital PCR was performed to detect TERT promoter mutations (C228T and C250T).
[RESULTS] No TERT promoter mutations were detected in hCLiPs or LC samples. In contrast, 11 of 20 (55%) HCC samples carried the C228T mutation, with mutant allele frequencies ranging from 2.7% to 28.0% (mean ± SD: 21.6 ± 11.05%). The C250T mutation was not identified in any sample.
[CONCLUSION] These findings show that hCLiPs reprogrammed using small molecules do not harbor TERT promoter mutations, supporting their genomic stability and potential safety for clinical applications.
[METHODS] TERT promoter mutations were analyzed in 20 formalin-fixed, paraffin-embedded HCC samples, 19 liver cirrhosis (LC) samples, and five hCLiPs derived from cirrhotic liver tissue. Genomic DNA was extracted, and droplet digital PCR was performed to detect TERT promoter mutations (C228T and C250T).
[RESULTS] No TERT promoter mutations were detected in hCLiPs or LC samples. In contrast, 11 of 20 (55%) HCC samples carried the C228T mutation, with mutant allele frequencies ranging from 2.7% to 28.0% (mean ± SD: 21.6 ± 11.05%). The C250T mutation was not identified in any sample.
[CONCLUSION] These findings show that hCLiPs reprogrammed using small molecules do not harbor TERT promoter mutations, supporting their genomic stability and potential safety for clinical applications.