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Effects of an oral iron chelator, deferasirox, on advanced hepatocellular carcinoma

World Journal of Gastroenterology 2016年第40期22卷 8967-8977页

作者： Issei Saeki Naoki Yamamoto Takahiro Yamasaki Taro Takami Masaki Maeda Koichi Fujisawa Takuya Iwamoto Toshihiko Matsumoto Isao Hidaka Tsuyoshi Ishikawa Koichi Uchida Kenji Tani Isao Sakaida Department of Gastroenterology and Hepatology Yamaguchi University Graduate School of Medicine Yamaguchi 755-8505 Japan Yamaguchi University Health Administration Center Yamaguchi 755-8511 Japan Department of Oncology and Laboratory Medicine Yamaguchi University Graduate School of Medicine Yamaguchi 755-8505 Japan Department of Human Nutrition Faculty of Nursing and Human Nutrition Yamaguchi 755-8502 Japan Center of Research and Education for Regenerative Medicine Yamaguchi University Graduate School of Medicine Yamaguchi Prefectural University Yamaguchi 755-8505 Japan Department of Veterinary Surgery Joint Faculty of Veterinary Medicine Yamaguchi University Yamaguchi 755-8511 Japan

AIM To evaluate the inhibitory effects of deferasirox(DFX) against hepatocellular carcinoma(HCC) through basic and clinical *** In the basic study, the effect of DFX was investigated in three hepatoma cell lines(Hep G2, Hep3 B, and Huh7), as well as in an N-nitrosodiethylamine-induced murine HCC model. In the clinical study, six advanced HCC patients refractory to chemotherapy were enrolled. The initial dose of DFX was 10 mg/kg per day and was increased by 10 mg/kg per day every week, until the maximum dose of 30 mg/kg per day. The duration of a single course of DFX therapy was 28 consecutive days. In the event of dose-limiting toxicity(according to the Common Terminology Criteria for Adverse Events v.4.0), DFX dose was *** Administration of DFX inhibited the proliferation of hepatoma cell lines and induced the activation of caspase-3 in a dose-dependent manner in vitro. In the murine model, DFX treatment significantly suppressed the development of liver tumors(P < 0.01), and significantly upregulated the mR NA expression levels of hepcidin(P < 0.05), transferrin receptor 1(P < 0.05), and hypoxia inducible factor-1α(P < 0.05) in both tumor and non-tumor tissues, compared with control mice. In the clinical study, anorexia and elevated serum creatinine were observed in four and all six patients, respectively. However, reduction in DFX dose led to decrease in serum creatinine levels in all patients. After the first course of DFX, one patient discontinued the therapy. We assessed the tumor response in the remaining five patients; one patient exhibited stable disease, while four patients exhibited progressive disease. The one-year survival rate of the six patients was 17%.CONCLUSION We demonstrated that DFX inhibited HCC in the basic study, but not in the clinical study due to dose-limiting toxicities.

关键词： Liver tumor Hepatocellular carcinoma Advanced stage iron-chelator Deferasirox

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