Literature DB >> 34951993

Molecular Signature Predictive of Long-Term Liver Fibrosis Progression to Inform Antifibrotic Drug Development.

Tongqi Qian1, Naoto Fujiwara2, Bhuvaneswari Koneru1, Atsushi Ono3, Naoto Kubota1, Arun K Jajoriya1, Matthew G Tung4, Emilie Crouchet5, Won-Min Song6, Cesia Ammi Marquez1, Gayatri Panda1, Ayaka Hoshida1, Indu Raman7, Quan-Zhen Li7, Cheryl Lewis8, Adam Yopp9, Nicole E Rich1, Amit G Singal1, Shigeki Nakagawa10, Nicolas Goossens11, Takaaki Higashi10, Anna P Koh1, C Billie Bian1, Hiroki Hoshida1, Parissa Tabrizian12, Ganesh Gunasekaran12, Sander Florman12, Myron E Schwarz12, Spiros P Hiotis12, Takashi Nakahara3, Hiroshi Aikata3, Eisuke Murakami3, Toru Beppu9, Hideo Baba9, Sangeeta Bhatia13, Masahiro Kobayashi14, Hiromitsu Kumada14, Austin J Fobar15, Neehar D Parikh15, Jorge A Marrero16, Steve Hategekimana Rwema4, Venugopalan Nair17, Manishkumar Patel17, Seunghee Kim-Schulze17, Kathleen Corey4, Jacqueline G O'Leary18, Goran B Klintmalm19, David L Thomas20, Mohammed Dibas21, Gerardo Rodriguez21, Bin Zhang6, Scott L Friedman17, Thomas F Baumert22, Bryan C Fuchs23, Kazuaki Chayama24, Shijia Zhu25, Raymond T Chung26, Yujin Hoshida27.   

Abstract

BACKGROUND & AIMS: There is a major unmet need to assess the prognostic impact of antifibrotics in clinical trials because of the slow rate of liver fibrosis progression. We aimed to develop a surrogate biomarker to predict future fibrosis progression.
METHODS: A fibrosis progression signature (FPS) was defined to predict fibrosis progression within 5 years in patients with hepatitis C virus and nonalcoholic fatty liver disease (NAFLD) with no to minimal fibrosis at baseline (n = 421) and was validated in an independent NAFLD cohort (n = 78). The FPS was used to assess response to 13 candidate antifibrotics in organotypic ex vivo cultures of clinical fibrotic liver tissues (n = 78) and cenicriviroc in patients with nonalcoholic steatohepatitis enrolled in a clinical trial (n = 19, NCT02217475). A serum protein-based surrogate FPS was developed and tested in a cohort of compensated cirrhosis patients (n = 122).
RESULTS: A 20-gene FPS was defined and validated in an independent NAFLD cohort (adjusted odds ratio, 10.93; area under the receiver operating characteristic curve, 0.86). Among computationally inferred fibrosis-driving FPS genes, BCL2 was confirmed as a potential pharmacologic target using clinical liver tissues. Systematic ex vivo evaluation of 13 candidate antifibrotics identified rational combination therapies based on epigallocatechin gallate, which were validated for enhanced antifibrotic effect in ex vivo culture of clinical liver tissues. In patients with nonalcoholic steatohepatitis treated with cenicriviroc, FPS modulation was associated with 1-year fibrosis improvement accompanied by suppression of the E2F pathway. Induction of the PPARα pathway was absent in patients without fibrosis improvement, suggesting a benefit of combining PPARα agonism to improve the antifibrotic efficacy of cenicriviroc. A 7-protein serum protein-based surrogate FPS was associated with the development of decompensation in cirrhosis patients.
CONCLUSION: The FPS predicts long-term fibrosis progression in an etiology-agnostic manner, which can inform antifibrotic drug development.
Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Companion Biomarker; Drug Development; Liver Fibrosis; Prognostic Prediction

Mesh:

Substances:

Year:  2021        PMID: 34951993      PMCID: PMC8934284          DOI: 10.1053/j.gastro.2021.12.250

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   33.883


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