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Genetics Variants and Serum Levels of MHC Class I Chain-related A in Predicting Hepatocellular Carcinoma Development in Chronic Hepatitis C Patients Post Antiviral Treatment

Authors :
Chung-Feng Huang
Cing-Yi Huang
Ming-Lun Yeh
Shu-Chi Wang
Kuan-Yu Chen
Yu-Min Ko
Ching-Chih Lin
Yi-Shan Tsai
Pei-Chien Tsai
Zu-Yau Lin
Shinn-Cherng Chen
Chia-Yen Dai
Jee-Fu Huang
Wan-Long Chuang
Ming-Lung Yu
Source :
EBioMedicine, Vol 15, Iss C, Pp 81-89 (2017)
Publication Year :
2017
Publisher :
Elsevier, 2017.

Abstract

Background/aims: The genome-wide association study has shown that MHC class I chain-related A (MICA) genetic variants were associated with hepatitis C virus (HCC) related hepatocellular carcinoma. The impact of the genetic variants and its serum levels on post-treatment cohort is elusive. Methods: MICA rs2596542 genotype and serum MICA (sMICA) levels were evaluated in 705 patients receiving antiviral therapy. Results: Fifty-eight (8·2%) patients developed HCC, with a median follow-up period of 48·2 months (range: 6–129 months). The MICA A allele was associated with a significantly increased risk of HCC development in cirrhotic non-SVR patients but not in patients of non-cirrhotic and/or with SVR. For cirrhotic non-SVR patients, high sMICA levels (HR/CI: 5·93/1·86–26.38·61, P = 0·002) and the MICA rs2596542 A allele (HR/CI: 4·37/1·52–12·07, P = 0·002) were independently associated with HCC development. The risk A allele or GG genotype with sMICA > 175 ng/mL provided the best accuracy (79%) and a negative predictive value of 100% in predicting HCC. Conclusions: Cirrhotic patients who carry MICA risk alleles and those without risk alleles but with high sMICA levels possessed the highest risk of HCC development once they failed antiviral therapy.

Details

Language :
English
ISSN :
23523964
Volume :
15
Issue :
C
Database :
Directory of Open Access Journals
Journal :
EBioMedicine
Publication Type :
Academic Journal
Accession number :
edsdoj.3ce3c35d2637413987947d14e3fe1ddd
Document Type :
article
Full Text :
https://doi.org/10.1016/j.ebiom.2016.11.031