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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective analysis of 35 stage IV HCC (26 IV-A case and 9 IV-B cases) which underwent reduction surgery from 1983 suggested a possibility to extend their survival period by decrease in their tumor-mass and subsequent immunochemotherapy for improvement of their depressed immunity. Their operability depended on the clinical stage of accompanying liver cirrhosis and extent of distant organ metastasis. It is of first importance for reduction surgery to select intrahepatic multiple tumors, slow-growing and not rapidly to induce distant organ metastases, among them. Intrahepatic tumors arising from multicentric origins were found in 42% in IV-A cases but 0% in IV-B. DNA ploidy analysis of the multicentric tumors in 8 cases did not show any clear indication of resectable tumors according to DNA index. The present immunochemotherapy is composed of a continuous infusion of IL2 and intermittent one-shot injections of 10mg ADR to the remnant liver by using subcutaneously implanted pump. In patients who could enhance peripheral NK and LAK activities by the immunotherapy, decreases in intra- and extra- hepatic tumors were observed. The 2 year-survival rate was 49% in IV-A, but only one case who is receiving the immunotherapy is surviving over 2 years in IV-B.
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PMID:[Significance of reduction surgery for stage IV hepatocellular carcinoma (HCC) and postoperative immunochemotherapy for extension of survival period]. 165 92

Fifteen to 20 years ago, the natural history of HCC demonstrated approximately 1.5 months median survival after diagnosis with rare cases of one-year survival. Ten to 15 years ago, one shot intraarterial (IA) injection of mitomycin C (MMC) or doxorubicin (ADR) became the prevailing treatment and prolonged median survival to 3-5 months. Ten years ago, transcatheter arterial embolization was introduced and improved the survival rate dramatically. In the earlier period, TAE was performed with gelatin sponge (GS) plus ADR or MMC and showed shrinkage of HCC in the well-capsulated case. Combined use of Lipiodol (LPD) with anticancer drug and GS in later period showed further progress in antitumor response and survival. The one year survival rate obtained from our 100 cases was 53.8%, and the 2 year one was 36.5%. We speculate that the effective response of LPD plus drug to intrahepatic daughter nodules contributed to this improvement because we clarified the efflux of LPD to peripheral portal vein clinically and experimentally. Since the metastatic liver tumor originating from colon or gastric cancer is usually hypovascular and shows limited response to intra-arterial chemotherapy, a special device is needed for improvement. We introduced an S.C. implanted port for injection route and long-term intermittent IA combination therapy with ADR or MMC and degradable starch microspheres (DSM), which embolise arteries temporarily for 20-30 minutes. These new methods achieved a favorable response rate with better quality of life, and would be expected to prolong the life span of patients with metastatic liver tumor.
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PMID:[Recent progress in multidisciplinary treatment of hepatic cancer]. 254 1

When a large amount of iodized oil (LPD) is selectively administered to targeted segments of the liver, the tumor vessels and sinusoids around the tumor are filled with LPD, subsequently regurgitating excessive LPD via the hepatic arterioportal communication into the portal branches surrounding the tumor. Segmental arterioportal chemoembolization in HCC with Doxorubicin-in-oil emulsion (DOE), which we named cement therapy, was performed in 18 patients with HCC. DOE was administered selectively into one segment division of Couinaud in ten patients, two segments in seven and three segments in one. Computed tomography and ultrasonography following the cement therapy revealed an overall response rate of 39%. The one-year cumulative survival rate was 80%, and that for three-years was 33%. Three cases underwent segmental hepatectomy and these specimens revealed total necrosis of the main tumor and whole daughter nodules, followed by various degrees of hepatic parenchymal infarction. This cement therapy realizes the simultaneous chemoembolization via the artery and portal vein, and was considered an effective treatment for extra-capsular infiltration and daughter nodules of HCC nourished by the portal vein blood flow. Limited administration of DOE to the targeted segments enables transarterial oily chemoembolization (TOCE) without any serious side effects.
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PMID:[Segmental arterio-portal chemo-embolization in hepatocellular carcinoma (cement therapy)]. 255 Dec 28

Since 1987, 14 patients (10 colorectal, 3 gastric and 1 lung cancer) with unresectable liver metastases received intra-arterial infusion chemo-embolization therapy using implantable infusion port. All patients had more than one lesion in bilateral lobe (H2 and H3). Infusion catheters were placed in the proper hepatic artery through the gastroduodenal artery on laparotomy. Infusion ports were implanted in the subcutaneous tissue of the abdominal wall. Various kinds of chemotherapeutic agents such as MMC, ADR, THP-ADR, CDDP and 5-FU were injected with embolization material (DSM or Lipiodol), every 1 to 4 weeks at the outpatient clinic. Among 10 cases of H2 grade metastases, 1 CR and 3 PR (40% clinical response) were obtained. However, all 4 cases of H3 grade were judged PD. All patients except one with H2 grade metastases are still alive, but 3 out of 4 with H3 grade died within 7 to 11 months. Catheter occlusion was observed in 4 cases for 3 to 7 months. Infection around the port occurred in 1 patient. A patient with metastatic liver cancer was treated by intermittent bolus injection with MMC and DSM. Partial response was confirmed by CT and tumor markers. Histological response was demonstrated in the specimen obtained at partial hepatectomy. It is concluded that this treatment is variable to prolong the survival of patients with H2 grade metastatic liver cancer, together with maintenance of the quality of life.
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PMID:[Chemo-embolization therapy of unresectable liver metastases using implantable infusion port]. 255 Dec 30

Degradable starch microspheres (DSM) have a mean diameter of 45 micron and temporarily obstruct blood flow at the arteriolar (micro-circulatory) level. A new approach was attempted to improve the anticancer effect on non-resectable liver cancer with simultaneous administration of DSM and MMC (mitomycin C) or ADR (adriamycin) into hepatic artery. Three patients with primary liver cancer were treated with DSM (600-1200 mg) and ADR (20-60 mg), and five with metastatic liver cancer were treated with DSM and MMC (10-20 mg). The treatment was repeated two to ten times. Partial or minor responses were observed in 1 out of 3 cases of primary liver cancer and 3 out of 5 metastatic cases. Side effects of DSM were temporary and mild epigastric or chest pain, vomiting, fever, slight dyspnea, etc. A temporary change in the liver functional data (GOT, GPT) was noted in 3 patients. Selective intra-hepatic arterial chemo-embolization therapy with DSM would appear to be beneficial for the treatment of liver cancers with appropriate indications. Cases in which DSM and anticancer drugs were effected were presented in detail.
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PMID:[Hepatic arterial infusion of degradable starch microspheres (DSM) with adriamycin or mitomycin C in liver cancer]. 313 87

Documented is hemopoietic toxicity encountered in patients with primary liver cancer (PLC), metastatic breast cancer, and colorectal cancer treated with various anthracyclines (doxorubicin [adriamycin, ADR], 4-'epidoxorubicin [4-'epiADR], and esorubicin) or anthracenes (mitoxantrone and bisantrene, as single agents as well as different combinations). Mitoxantrone, 14 mg/m2 three times weekly, was significantly more toxic than ADR, 60 mg/m2 three times weekly, for patients with PLC (P less than 0.01). In patients with colon cancer the toxicity of esorubicin did not differ significantly from that of 4-'epiADR. There was a tendency toward cumulative leukopenia with mitoxantrone and esorubicin, and cumulative thrombocytopenia with mitoxantrone and ADR. Although nadir counts for cycles 1 and 3 were similar, the percentage of patients receiving the full planned dose by the third cycle differed with the different drugs and in the different disease categories. Doxorubicin can be effectively combined with other cytostatics (e.g., cyclophosphamide + ADR + fluorouracil) to give improved results without undue hemopoietic toxicity in patients with breast cancer.
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PMID:Hematological toxicity: experience with anthracyclines and anthracenes. 385 85

In this paper we report the results we obtained after chemoembolization in 46 patients with HCC in cirrhosis. Chemoembolization is performed by introducing, through an angiographic catheter placed after the origin of the gastroduodenal artery, 20 mg of Doxorubicin Chlorhydrate mixed with 20 ml of Lipiodol and with 10 ml of contrast agent followed by embolization with Spongostan. Chemoembolization results were assessed comparing site, size and local spread of the tumor, hepatic compromission (according to Child's classification) and number of chemoembolization maneuvers with survival in each patient. Overall survival rates are 95.7% at 6 months, 88.5% at 12 months, 60% at 18 months, 36.4% at 24 and 31.8% at 30 months. The best responses were obtained with lesions smaller than 5 cm (100% survival at 6 months, 91.7% at 12 months, 71.4% at 18 and 42.8% at 24 months). Other factors favoring good treatment response were a single lesion (92.9% at 6 months, 91.7% at 12 months, 71.4% at 18 and 42.8% at 24 months), at least 3 cycles of chemoembolization (100% at 6 months, 90% at 12 months, 85.7% at 18 and 42.8% at 24 months) and a low degree of hepatic compromission (Child A and B rather than Child C; in the latter group the survival rates were 75% a 6 months and 0% at 12 months). In conclusion, chemoembolization proves to be the treatment of choice in the HCC patients who cannot undergo surgery.
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PMID:[Survival in 46 patients with hepatocarcinoma treated by chemoembolization]. 793 27

Tamoxifen (TAM) is a non-steroidal anti-estrogen used to treat patients with estrogen receptor-positive breast cancer and as a chemopreventive agent against breast cancer in high risk pre- and post-menopausal women. However, recent studies have shown that tamoxifen causes endometrial and hepatic cancer. In this study, we examined the effects of tamoxifen (5, 10, 25 and 50 microM) on the growth and proliferation of nine tumoral cell lines (UACC62, MCF-7, NCI-460, K-562, OVCAR-03, PC-03, HT-29, 786-0, NCI-ADR) and non-tumoral cell lines (3T3, V79, MDCK, VERO). Chinese hamster lung fibroblasts (V79) were the most sensitive lineage to tamoxifen, with 21.6% of the cells showing apoptosis at 50 microM TAM. Microscopic analysis showed that, the cellular transformation caused by TAM in V79 cells was similar to that seen with 7,12-dimethylbenz(a)anthracene, thus indicating the carcinogenicity of TAM.
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PMID:Cytotoxicity of tamoxifen in normal and tumoral cell lines and its ability to induce cellular transformation in vitro. 1526 Nov 61

The effects of tocotrienols on murine liver cell viability and their apoptotic events were studied over a dose range of 0-32 microg mL(-1). Normal murine liver cells (BNL CL.2) and murine liver cancer cells (BNL 1ME A.7R.1) were treated with tocotrienols (T(3)), alpha tocopherol (alpha-T) and the chemo drug, Doxorubicin (Doxo, as a positive control). Cell viability assay showed that T(3) significantly (P < or = 0.05) lowered the percentage of BNL 1ME A.7R.1 cell viability in a dose-responsive manner (8-16 microg mL(-1)), whereas T did not show any significant (P>0.05) inhibition in cell viability with increasing treatment doses of 0-16 microg mL(-1). The IC(50) for tocotrienols were 9.8, 8.9, 8.1, 9.7, 8.1 and 9.3 microg mL(-1) at 12, 24, 36, 48, 60 and 72 hours respectively. Early apoptosis was detected 6 hours following T(3) treatment of BNL 1ME A.7R.1 liver cancer cells, using Annexin V-FITC fluorescence microscopy assay for apoptosis, but none were observed for the non-treated liver cancer cells at the average IC(50) of 8.98 microg mL(-1) tocotrienols for liver cancer cells. Several apoptotic bodies were detected in BNL 1ME A.7R.1 liver cancer cells at 6 hours post-treatment with tocotrienols (8.98 microg mL(-1)) using Acridine Orange/Propidium Iodide fluorescence assay. However, only a couple of apoptotic bodies were seen in the non-treated liver cancer cells and the BNL CL.2 normal liver cells. Some mitotic bodies were also observed in the T(3)-treated BNL 1ME A.7R.1 liver cancer cells but were not seen in the untreated BNL 1ME A.7R.1 cells and the BNL CL.2 liver cells. Following T(3)-treatment (8.98 microg mL(-1)) of the BNL 1ME A.7R.1 liver cancer cells, 24.62%, 25.53% and 44.90% of the cells showed elevated active caspase 3 activity at 9, 12 and 24 hours treatment period, respectively. DNA laddering studies indicated DNA fragmentation occurred in the T(3)-treated liver cancer cells, BNL 1ME A.7R.1 but not in non-treated liver cancer cells and the T(3)-treated and non-treated normal liver cells. These results suggest that tocotrienols were able to reduce the cell viability in the murine liver cancer cells at a dose of 8-32 microg mL(-1) and that this decrease in percentage cell viability may be due to apoptosis.
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PMID:Effects of tocotrienols on cell viability and apoptosis in normal murine liver cells (BNL CL.2) and liver cancer cells (BNL 1ME A.7R.1), in vitro. 1632 44

Cancer has been the leading cause of death in Taiwan over the past two decades and liver cancer is the leading cause of all cancer deaths in Taiwan with a trend of increase in incidence. Therapeutic options and efficacy for liver cancer have been limited and the 5-year survival rate is less than 7% in the Unite States. The study was conducted to establish a histoculture system of human hepatocellular carcinomas (HCC) for biological and pharmacological studies and to determine the efficacy of anticancer drugs with the established HCC histocultures. Patient HCC tissues freshly obtained after surgeries were prepared and histocultured. The histocultured HCC were treated with doxorubicin and paclitaxel of various concentrations for 96-h. Upon drug treatments, the activity of tumor cell proliferation and extent of cell death induction were measured and changes of the alpha-fetoprotein levels in the culture medium were determined. We demonstrated that human HCC can be successfully cultured in a 3-dimensional histoculture system and used for pharmacological studies. Doxorubicin and paclitaxel showed concentration-dependent activities in anti-proliferation and cell death induction against the human HCC. Inhibitory effects of both drugs on alpha-fetoprotein production of the cultured HCC were in agreement with their anti-proliferative effects. Exposure time-dependent antitumoral effects of paclitaxel treatments at 3-, 24-, and 96-h against the histocultured HCC PLC/PRF/5 xenograft tumors were also observed. In conclusion, we have demonstrated a histoculture system for patient HCC and it can be utilized in selection of active drugs prior to treatments in patients and in evaluation of new agents against HCC, for which therapeutic agents are in desperate needs worldwide.
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PMID:Effects of paclitaxel and doxorubicin in histocultures of hepatocelular carcinomas. 1720 90


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