Background: The efficacy of tivantinib for MET-high hepatocellular carcinoma remains controversial. We conduct this meta-analysis to explore the efficacy of tivantinib versus placebo for MET-high hepatocellular carcinoma.
Methods: We have searched PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases through November 2022 and included randomized controlled trials (RCTs) assessing the efficacy and safety of tivantinib versus placebo for MET-high hepatocellular carcinoma.
Results: Three RCTs were included in the meta-analysis. Overall, compared with control group for MET-high hepatocellular carcinoma, tivantinib showed no obvious impact on overall survival (hazard ratio [HR] = 0.77; 95% confidence interval [CI] = 0.52-1.13; P = .18) or progression-free survival (HR = 0.78; 95% CI = 0.56-1.08; P = .14). In addition, tivantinib was associated with the increase in grade ≥3 neutropenia (odd ratio [OR] = 11.76; 95% CI = 2.77-49.89; P = .0008) and leukopenia (OR = 14; 95% CI = 1.68-116.82; P = .01), but demonstrated no impact on the incidence of grade ≥ 3 anemia (OR = 2.74; 95% CI = 0.14-53.43; P = .51).
Conclusions: Tivantinib may not benefit to the treatment of MET-high hepatocellular carcinoma.
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http://dx.doi.org/10.1097/MD.0000000000032591 | DOI Listing |
Drug Deliv Transl Res
November 2024
Department of Pharmaceutics, Faculty of Pharmacy, Alexandria University, Alexandria, 21521, Egypt.
Despite its established anti-diabetic activity, Metformin hydrochloride (MET) has been repurposed for the management of hepatocellular carcinoma (HCC). Owing to MET high aqueous solubility and poor oral permeability, a novel nanoplatform is sought to overcome the current challenges of traditional formulations. In this study, we developed MET-bridged nanocochleates (MET-CO) using a direct bridging method followed by optimization and assessment using various in-vitro and in-vivo pharmacokinetic methods.
View Article and Find Full Text PDFMedicine (Baltimore)
April 2023
Department of Hepatology, Chongqing Traditional Chinese Medicine Hospital, Chongqing, China.
Cell Death Dis
November 2022
Aix-Marseille Univ, CNRS, Developmental Biology Institute of Marseille (IBDM), Turing Center for Living Systems, Parc Scientifique de Luminy, Marseille, France.
Enhanced activation of the transcription factor MYC and of the receptor tyrosine kinase MET are among the events frequently occurring in hepatocellular carcinoma (HCC). Both genes individually act as drivers of liver cancer initiation and progression. However, their concomitant alteration in HCC has not been explored, nor functionally documented.
View Article and Find Full Text PDFEvid Based Complement Alternat Med
June 2022
Key Laboratory for Biorheological Science and Technology of Ministry of Education (Chongqing University), Chongqing University Cancer Hospital, Chongqing 400044, China.
J Biomed Res
December 2021
National Health Commission Key Laboratory of Antibody Techniques, Nanjing Medical University, Nanjing, Jiangsu 211166, China.
c-Met is a hepatocyte growth factor receptor overexpressed in many tumors such as hepatocellular carcinoma (HCC). Therefore, c-Met may serve as a promising target for HCC immunotherapy. Modifying T cells to express c-Met-specific chimeric antigen receptor (CAR) is an attractive strategy in treating c-Met-positive HCC.
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