Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic arterial infusion of low-dose CDDP (10 mg/day), 5-FU (250 mg/day) was performed in 5 unresectable hepatocellular carcinoma (HCC) patients with tumor thrombi in the trunk and/or the first branch of the portal vein. Infusion chemotherapy was continued for five days, then discontinued for the subsequent two days. This procedure was performed repeatedly for at least three weeks. Decrease in the serum levels of the alpha-fetoprotein after the treatment was found in 3 of 4 patients. In one patient, the size of the primary tumor decreased 92%. In two of five patients, the tumor thrombi in the portal vein disappeared, or decreased in size. Side effects of the chemotherapy included liver functional disorder (Grade 3; 1 case), thrombocytopenia (Grade 3; 1 case, Grade 2; 1 case), and leukopenia (Grade 2; 1 case). The present protocol proved to be effective and applicable for patients with advanced HCC associated with severe cirrhosis.
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PMID:[Hepatic arterial infusion of low-dose cisplatin, 5-fluorouracil for hepatocellular carcinoma with tumor thrombi in the portal vein]. 1056 Apr 6

Hepatocellular carcinoma (HCC) with vascular invasion and/or intrahepatic metastasis (IM) has a poor prognosis, so advanced HCC may be considered as a contraindication for hepatectomy. We experienced a case of HCC with hepatic venous and portal venous tumor thrombus and multiple IM who survived over 1 year after the operation with combined locoregional chemotherapy. (Case): A 67-year-old male patient was diagnosed with HCC with extracapsular invasion after transarterial embolization (TAE). CT scan revealed the HCC had a right portal venous tumor thrombus and multiple IM. Posterior lobectomy and thrombectomy of hepatic venous and portal venous tumor thrombus and placement of portal venous catheter ware performed. From the first day after operation the patient received continuous intravenous and intraportal 5-FU for 3 weeks. At the first month after operation, TAE and PEIT were given against residual IM. After discharge the patient received hepatic arterial infusion chemotherapy (MTX/CDDP/5-FU/Leucovorin). Fourteen months after operation, the patient is surviving in good physical condition.
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PMID:[A case report of hepatocellular carcinoma with hepatic and portal venous tumor thrombus and multiple intrahepatic metastasis who survived over 1 year after the operation with combined locoregional chemotherapy]. 1056 Apr 20

A 69-year-old man with unresectable hepatocellular carcinoma and portal vein tumor thrombus was treated by chemotherapy with 5-fluorouracil. A dose of 500 mg/day of 5-fluorouracil was continuously administered via a central venous catheter. After 4 months, the alpha-fetoprotein level was decreased from 50,000 ng/mL to 4,760 ng/mL. Computed tomography revealed disappearance of the low-density area in the liver parenchyma, but the portal vein tumor thrombus was not changed. After 6 months, pancytopenia appeared and continuous infusion of 5-fluorouracil was stopped. After 8 months, the patient died of pneumonia, at which time the alpha-fetoprotein level was 12,000 ng/mL. Continuous intravenous infusion of 5-Fluorouracil was effective against unresectable primary hepatocellular carcinoma, but had little influence on portal vein tumor thrombus.
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PMID:Hepatocellular carcinoma responding to chemotherapy with 5-FU. 1102 Aug 93

Primary and secondary liver tumors have a reputation for being resistant to chemotherapy and, in the absence of surgical resection, rapidly fatal. Until recently, such a reputation was well justified: response rates above 20% were not seen, and complete responses were distinctly rare. Over the past 5 years, the mood of those in the field has become rather more optimistic and a pattern of effective therapy is emerging. This involves combination therapy in patients with unresectable disease to increase the operative rates, and postoperative adjuvant therapy to decrease the high relapse rate which is so characteristic of both primary and secondary liver tumors. In the case of hepatocellular carcinoma, the combination therapy involves cytotoxic drugs and interferon. With secondary colorectal cancer (CRC), the combination of 5-fluorouracil (FU) and leucovorin, together with one of the new cytotoxic agents such as oxaliplatin or irenotecan, is producing much higher response rates and prolonged survival, and permitting a higher resection rate. Postoperative treatment is also showing promise in decreasing the relapse rate. With CRC metastatic to the liver, this involves hepatic artery infusion (HAI), systemic 5-FU, and leucovorin. Adjuvant systemic therapy of HCC has not yet been widely tested, but success with locoregional lipiodol iodine131 is proof of principle. The coming decade should see a significant improvement in the outlook of patients with malignant liver tumors as multimodality treatment becomes more widely investigated and practiced.
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PMID:Systemic chemotherapy of liver tumors. 1112 76

Chemotherapy is not effective for hepatocellular carcinoma (HCC). HMG-CoA redutase inhibitors have cytostatic activity for cancer cells, but their clinical usefulness is unknown. To investigate whether pravastatin, a potent HMG-CoA reductase inhibitor, prolongs survival in patients with advanced HCC, this randomized controlled trial was conducted between February 1990 and February 1998 at Osaka University Hospital. 91 consecutive patients <71 years old (mean age 62) with unresectable HCC were enroled in this study. 8 patients were withdrawn because of progressive liver dysfunction; 83 patients were randomized to standard treatment with or without pravastatin. All patients underwent transcatheter arterial embolization (TAE) followed by oral 5-FU 200 mg(-1)d for 2 months. Patients were then randomly assigned to control (n = 42) and pravastatin (n = 41) groups. Pravastatin was administered at a daily dose of 40 mg. The effect of pravastatin on tumour growth was assessed by ultrasonography. Primary endpoint was death due to progression of HCC. The duration of pravastatin administration was 16.5 +/- 9.8 months (mean +/- SD). No patients in either group were lost to follow-up. Median survival was 18 months in the pravastatin group versus 9 months in controls (P = 0.006). The Cox proportional hazards model showed that pravastatin was a significant factor contributing to survival. Pravastatin prolonged the survival of patients with advanced HCC, suggesting its value for adjuvant treatment.
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PMID:Effect of pravastatin on survival in patients with advanced hepatocellular carcinoma. A randomized controlled trial. 1128 66

Hepatocellular carcinoma and gastric cancer are the most prevalent tumors worldwide. Hep3B hepatocellular carcinoma and HS746T gastric cancer were used as models for these diseases in culture and in vivo. The PKC beta inhibitor 317615.2HCl was not very cytotoxic toward HS746T or Hep3B cells in culture and was, in the main, additive in cytotoxicity with cisplatin, 5-fluorouracil and gemcitabine when cell in monolayer were exposed to these agents in combination with 317615.2HCl. Treatment of nude mice bearing HS746T or Hep3B xenografts with 317615.2HCl orally twice daily resulted in a small decreased in CD31-stainable intratumoral vessels in the HS746T tumors and 60% decrease in CD31-stainable vessels in the Hep3B tumors. Somewhat larger decreases were observed in the vessel stained with CD105. As a single agent 317615.2HCl produced tumor growth delays between 6.5 and 15 days in the HS746T xenograft and between 5 and 25 days in the Hep3B xenograft over the dosage range (3 to 30 mg/kg). Sequential and simultaneous combinations with 317615.2HCl and 5-fluorouracil and gemcitabine resulted in increases in tumor growth delay on both schedules. Gemcitabine produced a 15-day tumor growth delay of the HS746T gastric carcinoma that was increased to 40 days when combined simultaneously with 317615.2HCl and to 30 days with the sequential treatment regimen. 5-Fluorouracil produced a 9-day tumor growth delay of the Hep3B hepatocellular carcinoma that increased to 31 days by simultaneous treatment with 317615.2HCl and to 43 days with the sequential treatment regimen. Treatment with the protein kinase C beta inhibitor 317615.2HCl decreased HS746T and Hep3B angiogenesis and improved treatment outcome with 5-fluorouracil and gemcitabine.
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PMID:Antiangiogenic and antitumor effects of a protein kinase C beta inhibitor in human hepatocellular and gastric cancer xenografts. 1149 Oct 13

We reported a case of hepatocellular carcinoma (HCC) with multiple lymph node metastases. The patient was a 67-year-old male with C type liver cirrhosis. He underwent microwave coagulation therapy (MCT) for HCC (5 cm and 1.5 cm) 1.5 years before admission. Abdominal CT scan revealed a well-enhanced tumor (2 cm) in caudate lobe of the liver and excessive lymph node metastases, locating in the inferior phrenic, periportal and para-aortic area. The preoperative serum AFP and AFP-L3 levels were 41.9 ng/ml and 93.1%, respectively. At laparotomy, systematic dissection of the enlarged lymph nodes and MCT of the hepatic tumor was performed. After operation, residual inferior phrenic lymph node was treated with irradiation therapy (total 50.4 Gy). The lymph node showed complete response (CR) for about a year and the AFP-L3 level returned to the normal range. After 9 months, a supra-clavicular lymph node was detected on abdominal CT scan. Irradiation therapy (total 45 Gy) in combination with CDDP (100 mg) and 5-FU (4,000 mg) was applied. The lymph node had been assessed as partial response for 6 months. The patient lived quite well after these therapies, but died of hepatic failure 32 months after the initial operation. In conclusion, we recommend this therapeutic strategy using operative excision and chemo-radiation therapy for HCC with multiple lymph node metastases.
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PMID:[Lymph node excision with laparotomy and chemo-radiation therapy for a hepatocellular carcinoma patient with multiple lymph node metastases]. 1170 13

A 56-year-old male patient with chronic C type hepatitis had HCC which invaded right portal vein trunk (Vp3). In August 2000, we performed intrahepatic artery infusion chemotherapy with CDDP and 5-FU under subcutaneous interferon alpha treatment. In addition, we used chemoradiation therapy for portal tumor thrombus in HCC. As the result of such therapy, the size of HCC and portal tumor thrombus reduced and the level of PIVKA-II decreased. There were no side effects except fever due to interferon alpha treatment. In February 2001, we performed devascularization and RFA therapy for HCC in S7 of liver under laparoscope. The level of PIVKA-II was within the normal range. It is important to perform interdisciplinary therapy appropriate for the HCC status.
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PMID:[Good response in case of hepatocellular carcinoma with portal tumor thrombs--a case report of interdisciplinary local therapy]. 1170 14

We report herein a case of spindle cell type hepatocellular carcinoma responding to hepatic intra-arterial infusion chemotherapy. A 50-year-old woman was hospitalized for right epigastralgia. A computed tomography scan demonstrated cloudy liver tumor with a diameter of 12 cm in S5 and S8. Surgery was performed based on the diagnosis of liver tumor. However, because the tumor was also present in the left lobe, we did only a biopsy for a part of tumor. From the pathological findings, this was diagnosed as a spindle cell type hepatocellular carcinoma. After the operation, hepatic intra-arterial injection therapy of continuous infusion with 5-FU was conducted for two weeks. A small reduction in the tumor was seen with computed tomography after the completion of two courses.
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PMID:[A case of spindle cell type hepatocellular carcinoma responding to hepatic intra-arterial infusion chemotherapy]. 1181 71

Chronic hepatitis C infection (HCV) accounts for approximately 50% of the cases of hepatocellular carcinoma (HCC) in the United States. Cirrhosis or an advanced stage of fibrosis is the major risk factor of HCC; patients with cirrhosis are recommended to undergo surveillance with alpha-fetoprotein and ultrasound. Alpha interferon (IFN-alpha) is associated with a reduced risk of HCC in patients with chronic infection but insufficient data exist to recommend treatment of patients with cirrhosis and HCV for this reason alone. Resection and liver transplantation are the only "curative" therapies available. Advanced fibrosis or cirrhosis in patients with HCC limits the number of patients for whom resection is applicable. Moreover, the remaining liver is at high risk of developing a second primary tumor. Partial hepatic resection for hepatocellular carcinoma should be restricted to patients with well-compensated cirrhosis (Child's A class). Acceptable parameters include a single lesion not exceeding 5 cm, normal levels of bilirubin, and absence of portal hypertension. Liver transplantation is the best definitive treatment for HCV-infected patients who have small, localized HCC (solitary lesion not greater than 5 cm, or no more than 3 lesions, none of which are greater than 3 cm). Limitations of liver transplantation as a therapy for HCC are the scarcity of donor organs and the prolonged waiting time during which continued tumor growth occurs. Living donors can reduce waiting time and increase the number of patients treatable by transplantation. Chemoembolization and local ablation therapies have not been shown to confer survival benefits as primary treatments for HCC. The potential benefit of these procedures in controlling tumor growth to "bridge" patients to liver transplantation must be further investigated. Similarly, systemic chemotherapy and hormonal therapy do not generally produce a survival advantage. However, recent studies that used octreotide and combination doxorubicin/cisplatin/5-FU/interferon appear to be promising.
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PMID:Hepatitis C and hepatocellular carcinoma. 1205 93


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