Treatment of hepatocellular carcinoma (HCC) with systemic chemotherapy combining epirubicin, cisplatinum and infusional 5-fluorouracil (ECF regimen)

Boucher, Éveline; Corbinais, Stéphane; Brissot, Pierre; Boudjéma, Karim; Raoul, Jean‐Luc

doi:10.1007/s00280-002-0503-x

Cited by 65 publications

(44 citation statements)

References 17 publications

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“…Generally, 5-FU was given at 60-66 mg kg À1 daily in treatment of either human HCC or gastric tumors in animals. 36,37 Moreover, the application of 5-FU was often associated with some side effects including myelosuppression, gastrointestinal and skin toxicity. 38 However, because of the low dose of 5-FU used, these toxic effects were not found in our mouse model.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effect of α-fetoprotein promoter-mediated tBid and chemotherapeutic agents on orthotopic liver tumor in mice

Chen

Yip

et al. 2010

Gene Ther

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Previous studies have shown that the application of Ad/AFPtBid significantly and specifically killed hepatocellular carcinoma (HCC) cells in culture and subcutaneously implanted in mice. This study was to test the therapeutic efficacy of Ad/AFPtBid in an orthotopic hepatic tumor model. Four weeks after implantation of tumor cells into the liver, nude mice were treated with Ad/ AFPtBid alone or in combination with 5-fluorouracil (5-FU). Serum a-fetoprotein (AFP) was measured as a marker for tumor progression. The results showed that Ad/AFPtBid significantly inhibited Hep3B tumor growth. Ad/AFPtBid and 5-FU in combination was more effective than either agent alone. Tumor tissues of Ad/AFPtBid alone or combination treatment groups showed a decrease in cells positive for proliferation cell nuclear antigen, but an increase in apoptosis. Ad/AFPtBid did not suppress the hepatic tumor formed by non-AFP-producing hepatoma SK-HEP-1 cells or colorectal adenocarcinoma DLD-1 cells. The survival rate was higher in mice treated with Ad/AFPtBid plus 5-FU than those treated with either agent alone. No acute toxic effect was observed in mice receiving Ad/AFPtBid. Collectively, Ad/AFPtBid can specifically target and effectively suppress the AFP-producing orthotopic liver tumor in mice without obvious toxicity, indicating that it is a promising tool in combination with chemotherapeutic agents for treatment of AFP-producing HCC.

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Section: Discussionmentioning

confidence: 99%

Therapeutic effect of α-fetoprotein promoter-mediated tBid and chemotherapeutic agents on orthotopic liver tumor in mice

Chen

Yip

et al. 2010

Gene Ther

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“…Other combination such as epirubicin, cisplatin and 5-FU (ECF) regimen or capecitabine and cisplatin have been evaluated as well. The combinations tend to have higher response rate but no definite conclusion can be drawn from these studies due to small number of patients (37).…”

Section: -Fu Based Combination Chemotherapymentioning

confidence: 94%

Hepatocellular carcinoma (HCC): beyond sorafenib—chemotherapy

Kim

Talati

Kim

2017

J. Gastrointest. Oncol.

255

168

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Hepatocellular carcinoma (HCC) is the most common primary liver cancer with poor prognosis.The incidence of HCC and HCC-related deaths have increased over the last several decades. However, the treatment options for advanced HCC are very limited. Sorafenib remains the only drug approved for systemic treatment for advanced HCC. However, prior to sorafenib era conventional cytotoxic chemotherapies have been studied in advanced HCC. In this review, clinical studies of systemic chemotherapy for advanced HCC will be summarized and discussed.

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“…Even though locoregional therapies such as hepatic artery ligation Tables I and II (samples were collected or embolization have been developed in the past decades, they have failed to significantly prolong the overall survival of liver cancer patients (22)(23)(24). Despite decades of efforts made by researchers worldwide, the investigation of anti-liver cancer drugs is stagnant (25)(26)(27)(28). Conventionally, the commonly used drugs for liver cancer chemotherapy are 5-fluorouracil, mitomycin C, cisplatin, doxorubicin and their derivatives.…”

Section: Discussionmentioning

confidence: 99%

A novel cell cycle blocker extracted from Stellera chamaejasme L. inhibits the proliferation of hepatocarcinoma cells

Kan

Chen

et al. 2016

Oncology Reports

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Abstract. Currently, liver cancer is the sixth most prevalent cancer and the third most common cause of cancer-related death. However, effective chemotherapeutic drugs with low drug resistance and few side-effects for the clinical treatment of liver cancer are lacking. Therefore, the search for novel drugs to compensate for the defects of existing drugs is urgently needed. Herein, we successfully screened an extract named from Stellera chamaejasme L. (SCL), a historically confimed antitumor plant, through a novel extraction platform. In the present study, we firstly screened the anticancer effect of ESC by the sulforhodamine B (SRB) cell proliferation assay in a wide range of malignant cell lines, including A549, NCI-H157, NCI-H460, SK-HEP-1 and HepG2. With the highest inhibitory rate in hepatocarcinoma cells, we further identified the tumor-suppressive efficacy and the safety of ESC in an H22 hepatocarcinoma xenograft model in vivo. In a mechanistic study, flow cytometry and western blot analysis were performed to evaluate the effects of ESC on the induction of cell apoptosis, intervention of cell cycle distribution and its influence on key G2/M-phase regulators. The results showed that ESC significantly inhibited the cell growth of liver cancer cell lines. Accordingly, the tumor inhibition rate was also increased following ESC administration with little systemic toxicity in H22-transplanted mice. Mechanistically, ESC caused obvious G2/M-phase arrest in both the SK-HEP-1 and HepG2 cell lines without cell apoptosis. Furthermore, cyclin B1 was downregulated, while the phosphorylation level of CDK1 was increased in response to ESC treatment. All these data confirmed that ESC possesses potent anti-proliferative efficacy for hepatocarcinoma through the induction of cyclinmediated cell cycle arrest. Thus, ESC is a promising candidate for hepatocarcinoma treatment in the future. IntroductionAs one of the major global public health issues, cancer greatly threatens human survival and has become the leading cause of mortality of humankind in this century (1). Clinically, during the rapid development of anticancer strategies, chemotherapy has consistently played an important role in cancer treatment. To date, classical botanical agents, as represented by paclitaxel or vincristine, are still first-line drugs and are widely applied as the primary choice against multiple malignancies (2). Benefitting from these agents, treatment effectiveness and the survival rate of cancer patients have greatly improved in recent years. However, in spite of the satisfactory tumor-suppressive activities, with their extensive application worldwide, growing evidence reveals that side-effects and drug resistance are still the leading obstacles largely limiting the clinical use of classic tumor-toxic agents (3).In recent years, liver cancer has become one of the most prevalent types of cancer and is the third most common cause of cancer-related mortality (4,5). Notably, its incidence and mortality rank second among Chinese cancer patients (6) an...

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Treatment of hepatocellular carcinoma (HCC) with systemic chemotherapy combining epirubicin, cisplatinum and infusional 5-fluorouracil (ECF regimen)

Abstract: Systemic chemotherapy using the ECF regimen gave a poor response and low survival rates. It would appear reasonable to pursue the search for potentially efficacious chemotherapy protocols using other drug combinations.

Cited by 65 publications

References 17 publications

Therapeutic effect of α-fetoprotein promoter-mediated tBid and chemotherapeutic agents on orthotopic liver tumor in mice

Therapeutic effect of α-fetoprotein promoter-mediated tBid and chemotherapeutic agents on orthotopic liver tumor in mice

Hepatocellular carcinoma (HCC): beyond sorafenib—chemotherapy

A novel cell cycle blocker extracted from Stellera chamaejasme L. inhibits the proliferation of hepatocarcinoma cells

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