Improvement in the Current Therapies for Hepatocellular Carcinoma Using a Systems Medicine Approach.
genome scale metabolic models
hepatocellular carcinoma
molecular-targeted therapies
network-driven stratification
systemic therapies
Journal
Advanced biosystems
ISSN: 2366-7478
Titre abrégé: Adv Biosyst
Pays: Germany
ID NLM: 101711718
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
received:
24
01
2020
revised:
02
03
2020
accepted:
09
03
2020
entrez:
13
6
2020
pubmed:
13
6
2020
medline:
12
8
2021
Statut:
ppublish
Résumé
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death primarily due to the lack of effective targeted therapies. Despite the distinct morphological and phenotypic patterns of HCC, treatment strategies are restricted to relatively homogeneous therapies, including multitargeted tyrosine kinase inhibitors and immune checkpoint inhibitors. Therefore, more effective therapy options are needed to target dysregulated metabolic and molecular pathways in HCC. Integrative genomic profiling of HCC patients provides insight into the most frequently mutated genes and molecular targets, including telomerase reverse transcriptase, the TP53 gene, and the Wnt/β-catenin signaling pathway oncogene (CTNNB1). Moreover, emerging techniques, such as genome-scale metabolic models may elucidate the underlying cancer-specific metabolism, which allows for the discovery of potential drug targets and identification of biomarkers. De novo lipogenesis has been revealed as consistently upregulated since it is required for cell proliferation in all HCC patients. The metabolic network-driven stratification of HCC patients in terms of redox responses, utilization of metabolites, and subtype-specific pathways may have clinical implications to drive the development of personalized medicine. In this review, the current and emerging therapeutic targets in light of molecular approaches and metabolic network-based strategies are summarized, prompting effective treatment of HCC patients.
Identifiants
pubmed: 32529800
doi: 10.1002/adbi.202000030
doi:
Substances chimiques
CTNNB1 protein, human
0
TP53 protein, human
0
Tumor Suppressor Protein p53
0
beta Catenin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2000030Informations de copyright
© 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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