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For: Guo XG, Wang ZH, Dong W, He XD, Liu FC, Liu H. Specific CYP450 Genotypes in the Chinese Population Affect Sorafenib Toxicity in HBV/HCV-associated Hepatocellular Carcinoma Patients. Biomed Environ Sci 2018;31:586-595. [PMID: 30231963 DOI: 10.3967/bes2018.080] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [What about the content of this article? (0)] [Subscribe] [Scholar Register] [Received: 12/14/2017] [Accepted: 08/04/2018] [Indexed: 06/08/2023]

For:	Guo XG, Wang ZH, Dong W, He XD, Liu FC, Liu H. Specific CYP450 Genotypes in the Chinese Population Affect Sorafenib Toxicity in HBV/HCV-associated Hepatocellular Carcinoma Patients. Biomed Environ Sci 2018;31:586-595. [PMID: 30231963 DOI: 10.3967/bes2018.080] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [What about the content of this article? (0)] [Subscribe] [Scholar Register] [Received: 12/14/2017] [Accepted: 08/04/2018] [Indexed: 06/08/2023]

Number

Cited by Other Article(s)

Zhang Y, Wang Z, Wang Y, Jin W, Zhang Z, Jin L, Qian J, Zheng L. CYP3A4 and CYP3A5: the crucial roles in clinical drug metabolism and the significant implications of genetic polymorphisms. PeerJ 2024;12:e18636. [PMID: 39650550 PMCID: PMC11625447 DOI: 10.7717/peerj.18636] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2024] [Accepted: 11/12/2024] [Indexed: 12/11/2024] Open

Choudhary HB, Mandlik SK, Mandlik DS. Role of p53 suppression in the pathogenesis of hepatocellular carcinoma. World J Gastrointest Pathophysiol 2023;14:46-70. [PMID: 37304923 PMCID: PMC10251250 DOI: 10.4291/wjgp.v14.i3.46] [Citation(s) in RCA: 4] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/27/2023] [Revised: 05/19/2023] [Accepted: 05/31/2023] [Indexed: 06/01/2023] Open

Ding L, Ning S, Hu W, Xue Y, Yu S. Distinctive Metabolism-Associated Gene Clusters That Are Also Prognostic in Intrahepatic Cholangiocarcinoma and Hepatocellular Carcinoma. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY 2022;2022:6595989. [PMID: 36199423 PMCID: PMC9527115 DOI: 10.1155/2022/6595989] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 08/02/2022] [Revised: 08/22/2022] [Accepted: 08/29/2022] [Indexed: 11/29/2022]

Abstract

Objective

To offer new prognostic evaluations by exploring potentially distinctive genetic features of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC).

Methods

There were 12 samples for gene expression profiling processes in this study. These included three HCC lesion samples and their matched adjacent nontumor liver tissues obtained from patients with HCC, as well as three ICC samples and their controls collected similarly. In addition to the expression matrix generated on our own, profiles of other cohorts from The Cancer Genome Atlas (TCGA) program and the Gene Expression Omnibus (GEO) were also employed in later bioinformatical analyses. Differential analyses, functional analyses, protein interaction network analyses, and gene set variation analyses were used to identify key genes. To establish the prognostic models, univariate/multivariate Cox analyses and subsequent stepwise regression were applied, with the Akaike information criterion evaluating the goodness of fitness.

Results

The top three pathways enriched in HCC were all metabolism-related; they were fatty acid degradation, retinol metabolism, and arachidonic acid metabolism. In ICC, on the other hand, additional pathways related to fat digestion and absorption and cholesterol metabolism were identified. Consistent characteristics of such a metabolic landscape were observed across different cohorts. A prognostic risk score model for calculating HCC risk was constructed, consisting of ADH4, ADH6, CYP2C9, CYP4F2, and RDH16. This signature predicts the 3-year survival with an AUC area of 0.708 (95%CI = 0.644 to 0.772). For calculating the risk of ICC, a prognostic risk score model was built upon the expression levels of CYP26A1, NAT2, and UGT2B10. This signature predicts the 3-year survival with an AUC area of 0.806 (95% CI = 0.664 to 0.947).

Conclusion

HCC and ICC share commonly abrupted pathways associated with the metabolism of fatty acids, retinol, arachidonic acids, and drugs, indicating similarities in their pathogenesis as primary liver cancers. On the flip side, these two types of cancer possess distinctive promising biomarkers for predicting overall survival or potential targeted therapies.

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Tan T, Han G, Cheng Z, Jiang J, Zhang L, Xia Z, Wang X, Xia Q. Genetic Polymorphisms in CYP2C19 Cause Changes in Plasma Levels and Adverse Reactions to Anlotinib in Chinese Patients With Lung Cancer. Front Pharmacol 2022;13:918219. [PMID: 35814206 PMCID: PMC9257029 DOI: 10.3389/fphar.2022.918219] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/12/2022] [Accepted: 05/31/2022] [Indexed: 11/13/2022] Open

Abstract Background: Anlotinib is a small molecular multi-targeting tyrosine kinase inhibitor. Growing evidence indicates that treatment efficacy, and toxicity varies considerably between individuals. Therefore, this study aimed to investigate the relationship between cytochrome P450 (CYP450) gene polymorphisms, drug concentrations, and their adverse reactions in anlotinib-treated patients with lung cancer.Methods: We enrolled 139 patients with lung cancer, treated with anlotinib. Twenty loci in the following five genes of the CYP450 family were genotyped: CYP450 family 3 subfamily A member 5 (CYP3A5), 3 subfamily A member 4 (CYP3A4), 2 subfamily C member 9 (CYP2C9), 2 subfamily C member 19 (CYP2C19), and 1 subfamily A member 2 (CYP1A2). Data on adverse reactions were collected from patients, and plasma anlotinib concentrations were measured.Results: There were significant variances in plasma trough concentration (3.95–52.88 ng/ml) and peak plasma concentration (11.53–42.8 ng/ml) following administration of 8 mg anlotinib. Additionally, there were significant differences in the plasma trough concentration (5.65–81.89 ng/ml) and peak plasma concentration (18.01–107.18 ng/ml) following administration of 12 mg anlotinib. Furthermore, for CYP2C19-rs3814637, the peak plasma concentrations of mutant allele T carriers (TT+CT) were significantly higher than those of wildtypes (CC). For CYP2C19-rs11568732, the peak plasma concentrations of the mutant allele G carriers (GT+GG) were significantly higher than those of the wild-type (TT). More importantly, the incidence rates of hypertension and hemoptysis (peripheral lung cancer) with TT+CT in rs3814637 and GT+GG in rs11568732 were significantly higher than those with CC and TT.Conclusions: The plasma trough and peak concentrations varied significantly for both 8 and 12 mg of anlotinib. Single-nucleotide polymorphisms in CYP2C19 are significantly associated with hypertension, hemoptysis, and anlotinib peak concentrations. Polymorphisms in CYP450 may explain inter-individual differences in anlotinib-related adverse reactions. Collapse

Marin JJ, Macias RI, Monte MJ, Romero MR, Asensio M, Sanchez-Martin A, Cives-Losada C, Temprano AG, Espinosa-Escudero R, Reviejo M, Bohorquez LH, Briz O. Molecular Bases of Drug Resistance in Hepatocellular Carcinoma. Cancers (Basel) 2020;12:cancers12061663. [PMID: 32585893 PMCID: PMC7352164 DOI: 10.3390/cancers12061663] [Citation(s) in RCA: 104] [Impact Index Per Article: 20.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/04/2020] [Revised: 06/19/2020] [Accepted: 06/20/2020] [Indexed: 12/11/2022] Open

Affiliation(s)

Jose J.G. Marin Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.) Center for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, 28029 Madrid, Spain Correspondence: (J.J.G.M.); (O.B.); Tel.: +34-663182872 (J.J.G.M.); +34-923294674 (O.B.)
Rocio I.R. Macias Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.) Center for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, 28029 Madrid, Spain
Maria J. Monte Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.) Center for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, 28029 Madrid, Spain
Marta R. Romero Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.) Center for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, 28029 Madrid, Spain
Maitane Asensio Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.)
Anabel Sanchez-Martin Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.)
Candela Cives-Losada Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.)
Alvaro G. Temprano Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.)
Ricardo Espinosa-Escudero Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.)
Maria Reviejo Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.)
Laura H. Bohorquez Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.)
Oscar Briz Experimental Hepatology and Drug Targeting (HEVEFARM) Group, University of Salamanca, IBSAL, 37007 Salamanca, Spain; (R.I.R.M.); (M.J.M.); (M.R.R.); (M.A.); (A.S.-M.); (C.C.-L.); (A.G.T.); (R.E.-E.); (M.R.); (L.H.B.) Center for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, 28029 Madrid, Spain Correspondence: (J.J.G.M.); (O.B.); Tel.: +34-663182872 (J.J.G.M.); +34-923294674 (O.B.)

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Cabral LKD, Tiribelli C, Sukowati CHC. Sorafenib Resistance in Hepatocellular Carcinoma: The Relevance of Genetic Heterogeneity. Cancers (Basel) 2020;12:1576. [PMID: 32549224 PMCID: PMC7352671 DOI: 10.3390/cancers12061576] [Citation(s) in RCA: 95] [Impact Index Per Article: 19.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/26/2020] [Revised: 06/08/2020] [Accepted: 06/10/2020] [Indexed: 02/06/2023] Open

De Mattia E, Cecchin E, Guardascione M, Foltran L, Di Raimo T, Angelini F, D’Andrea M, Toffoli G. Pharmacogenetics of the systemic treatment in advanced hepatocellular carcinoma. World J Gastroenterol 2019;25:3870-3896. [PMID: 31413525 PMCID: PMC6689804 DOI: 10.3748/wjg.v25.i29.3870] [Citation(s) in RCA: 57] [Impact Index Per Article: 9.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/15/2019] [Revised: 05/23/2019] [Accepted: 07/03/2019] [Indexed: 02/06/2023] Open

Abstract

Hepatocellular carcinoma (HCC) accounts for the majority of primary liver cancers. To date, most patients with HCC are diagnosed at an advanced tumor stage, excluding them from potentially curative therapies (i.e., resection, liver transplantation, percutaneous ablation). Treatments with palliative intent include chemoembolization and systemic therapy. Among systemic treatments, the small-molecule multikinase inhibitor sorafenib has been the only systemic treatment available for advanced HCC over 10 years. More recently, other small-molecule multikinase inhibitors (e.g., regorafenib, lenvatinib, cabozantinib) have been approved for HCC treatment. The promising immune checkpoint inhibitors (e.g., nivolumab, pembrolizumab) are still under investigation in Europe while in the US nivolumab has already been approved by FDA in sorafenib refractory or resistant patients. Other molecules, such as the selective CDK4/6inhibitors (e.g., palbociclib, ribociclib), are in earlier stages of clinical development, and the c-MET inhibitor tivantinib did not show positive results in a phase III study. However, even if the introduction of targeted agents has led to great advances in patient response and survival with an acceptable toxicity profile, a remarkable inter-individual heterogeneity in therapy outcome persists and constitutes a significant problem in disease management. Thus, the identification of biomarkers that predict which patients will benefit from a specific intervention could significantly affect decision-making and therapy planning. Germ-line variants have been suggested to play an important role in determining outcomes of HCC systemic therapy in terms of both toxicity and treatment efficacy. Particularly, a number of studies have focused on the role of genetic polymorphisms impacting the drug metabolic pathway and membrane translocation as well as the drug mechanism of action as predictive/prognostic markers of HCC treatment. The aim of this review is to summarize and critically discuss the pharmacogenetic literature evidences, with particular attention to sorafenib and regorafenib, which have been used longer than the others in HCC treatment.

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