Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, we compared the survival of patients with multi tumor hepatocellular carcinoma (HCC) following their treatment with liver resection versus TAE. A total of 336 HCC patients were treated at Osaka University Hospital between 1980 and 1989. Of these, 140 patients underwent liver resection in the presence or absence of TAE and 173 subjects were treated with TAE alone. Our TAE protocol consisted of 50 mg Adriamycin, 3-5 ml lipiodol, and Gelfoam. The 1-, 3-, and 5-year survival values found for the liver resection group were 87.4%, 66.0%, and 47.4%, respectively, whereas the values calculated for the TAE group were 64.6%, 29.9%, and 15.8%, respectively. The survival of patients in the resection group was clearly better than that of subjects in the TAE group. Of the 140 patients who underwent resection, 36 cases were proven to have multiple lesions by histopathological examination. The 1- and 3-year survival values determined for this special group were 67.9% and 33.3%, respectively. Of the TAE cases, 113 were diagnosed as having multiple lesions by imaging examination, and their 1- and 3-year survival values were 59.7% and 24.9%, respectively. No significant differences in survival was found between these two different treatment modalities for these multiple-lesion cases. The results of this study indicate that it is unlikely that surgical resection is superior to TAE alone for the treatment of HCC patients with multiple lesions.
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PMID:Selection of therapeutic modalities for hepatocellular carcinoma in patients with multiple hepatic lesions. 133 7

We formulated a new lipiodol-Adriamycin suspension (ADM/lipiodol, 50 mg/10 ml) that remained stable for 48 h (half-life, 25 +/- 3 days). In five cases of hepatocellular carcinoma (HCC) resected after intra-arterial infusion of this agent, the ADM concentration in the tumor was quite high and the tumor necrosis rate was more than 80% on histological examination. Over a 5-year period, 180 patients with unresectable HCC underwent transcatheter arterial embolization therapy (TAE) in the presence or absence of this agent. The regimens consisted of suspension injection alone (A, n = 54), suspension injection + TAE using gelatin sponge (B, n = 29), TAE followed by suspension injection (C, n = 34), and TAE alone (D, n = 63). The estimated 1-year survival values determined for patients treated with these regimens were 70%, 73%, 43%, and 39% respectively, and the corresponding 3-year survival values were 27%, 31%, 15%, and 10%. The survival achieved using suspension injection was thus superior to that obtained using conventional TAE, and combined therapy with suspension injection followed by TAE seemed to enhance survival, although there were some biases in tumor size and in the stage of tumor progression. For patients with tumors measuring 5 cm or more in diameter, the survival obtained using regimen A was lower than that achieved using regimen D, but the combination of TAE and suspension injection improved the 1-year survival value obtained using regimen D from 34% to 52%. For patients with tumors measuring less than 5 cm in diameter, the survival achieved using regimen A was markedly better than that obtained using regimen D, although no difference was found between the survival value achieved using regimen A and that obtained using regimens B and C. On the basis of these results, our newly formulated ADM-lipiodol suspension was surmised to be effective by itself against relatively small HCC tumors, whereas it enhanced the efficacy of conventional TAE in large lesions.
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PMID:Assessment of chemoembolization therapy for primary liver cancer using a stabilized adriamycin-lipiodol suspension. 133 9

A total of 135 patients with hepatocellular carcinoma (HCC) were treated by intra-arterial injection of an Adriamycin/mitomycin C oil (lipiodol) suspension (ADMOS) alone or of ADMOS plus cis-diammine-dichloroplatinum (CDDP). In all, 59 patients were treated with ADMOS alone and 76 were treated with ADMOS plus CDDP. A reduction of more than 25% in the tumor size was obtained in 13 of 38 (34%) evaluable patients in the former group and in 39 of 76 (51%) evaluable patients in the latter group. Serum alpha-fetoprotein (AFP) levels decreased by more than 50% in 10 of 17 (59%) and 23 of 33 (70%) patients in the respective groups whose pretreatment AFP level was estimated to be over 200 ng/ml. Overall, the 1-year survival value was 68% and the 2-year value was 41% as determined by the Kaplan-Meier method. No statistically significant difference in survival was observed between the two groups. The initial tumor response correlated with the survival value. No severe complication was encountered except for one case of liver abscess formation. No serious change in the laboratory data was observed following treatment with these regimens. Although the tumor response was significantly better in patients treated with ADMOS combined with CDDP injection than in those treated with ADMOS alone (P < 0.05), no significant difference in survival was found between the two groups.
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PMID:Comparison of the anticancer effect of ADMOS alone and ADMOS with CDDP in the treatment of hepatocellular carcinoma by intra-arterial injection. 133 10

Arterial infusion chemotherapy of EPF (etoposide, cisplatin, and 5-fluorouracil) or EAP (etoposide, Adriamycin, and cisplatin) was carried out in 28 cases of advanced hepatocellular carcinoma (HCC) between January 1988 and December 1990, and assessment was made of the anticancer efficacy of each treatment method. In all, 13 patients were treated with EPF therapy and 15 received EAP therapy. The anticancer agents were infused through a catheter inserted into the proper or common hepatic artery. The catheter was inserted via the axillary artery or common femoral artery using Seldinger's method or the cut-down method. The results of each therapy were analyzed in relation to the tumor regression rate and the side effects encountered. The tumor regression rate was determined on the basis of two-dimensional evidence obtained by computed tomography performed before and after treatment. The treatment results were also compared with the results of chemoembolization therapy using a mixture of cisplatin (CDDP), Adriamycin (ADM) and lipiodol. Of the 28 patients treated with arterial infusion chemotherapy, 14 (50%) attained a regression rate of 50% (PR). In all, 46% of the EPF group and 53% of the EAP group achieved a PR. These results were superior to those obtained using chemoembolization therapy. In general, the side effects were relatively mild and transient.
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PMID:Arterial infusion chemotherapy for advanced hepatocellular carcinoma using EPF and EAP therapies. 133 15

PANC02 is a ductal adenocarcinoma of the pancreas that is resistant to every known class of clinically active antitumor agent. To study the mechanism(s) underlying the intrinsic drug resistance of this tumor, a mammary adenocarcinoma (CA-755) that also grows in C57/BL mice and is known to be drug sensitive was used for comparison. PANC02 resistance and CA-755 sensitivity to several antitumor agents and to X-ray therapy was confirmed in mice, and PANC02 also demonstrated relative resistance in tissue culture. Relative to Chinese hamster ovary (CHO) and CA-755 cells, PANC02 did not appear to show a higher rate of mutation to drug resistance in culture as based on the 6-thioguanine resistance marker. Although P-glycoprotein characteristic of the multidrug resistance (MDR) phenomenon could be demonstrated at the mRNA level using a sensitive RNAse protection assay, the level of expression found was several orders of magnitude lower than that observed in phenotypic MDR cell lines. Furthermore, quinidine failed to increase the sensitivity of PANC02 cells to Adriamycin under conditions that clearly potentiated the toxicity of the drug to a CHO cell line exhibiting classic MDR traits. The heterogeneity in the distribution of drugs was inferred as being significantly greater in PANC02 versus CA-755 cells in vivo as based on measurements of within-animal, within-tumor variance in the distribution of the marker compounds inulin and antipyrine. Although it may not be the only mechanism involved, this greater intratumor heterogeneity in drug distribution could theoretically play a major role in the intrinsic drug resistance of PANC02 in vivo.
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PMID:Intrinsic resistance to anticancer agents in the murine pancreatic adenocarcinoma PANC02. 134 74

To investigate the possible role of the multidrug resistance phenotype to chemoresistance in human ovarian carcinoma, we have analyzed human multidrug resistance gene (mdr 1) expression in 8 human ovarian adenocarcinoma cell lines. An increase in P-glycoprotein level specific to multidrug-resistant tumor cells was not apparently associated with the increase in resistance to vincristine (VCR) or doxorubicin (Adriamycin). Mdr 1 transcripts (4.5 kilobases) were observed in the RNA preparation obtained from only one cell line (SHIN-3) that showed the highest resistance to both drugs in vitro and in vivo. No cell lines showed mdr 1 DNA amplification. These results suggest that the insensitivity of human ovarian carcinoma to chemotherapy could be partly explained by the expression of mdr 1.
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PMID:Expression of a human multidrug resistance gene in human ovarian carcinoma cell lines. 134 3

We succeeded in establishing a cell line (KEN-3) for subculture from a fibrosarcoma which originated in the ovary in a girl aged 17 years. Its characteristics and sensitivity to anticancer agents are reported in this paper. 1. Characteristics of established cell line. Lined cells consist of multinucleated giant cells mixed among many spindle-shaped cells. They grow in small colonies and have none of the pavement-like arrangement characteristic of epithelial tumor cells. The number of chromosomes ranged from 45 to 128 (mode: pseudo-triploidy region, 65). The doubling time, cellular density and plating efficiency were 76.9 hours, 5.4 x 10(5)/cm2 and 30.2%, respectively. Concerning tumor markers, CEA and sialyl SSEA-1 were only produced in small quantities. Subculture was possible subcutaneously in the nude mouse with no capacity for the production of ascites. 2. Susceptibility to anticancer agents and GP170 expression. The in vitro susceptibility to about 12 types of anticancer agents was investigated with the MTT assay. IC50/PPC was shown to be less than 1 for Adriamycin only. The sensitivity to CDDP (IC50/PPC: 4.8) was low, and no sensitivity was observed at all to DTIC, which is used frequently for mesenchymal tumors. GP170 (mdr-1 products) was positive in established cells in immunohistochemical stain.
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PMID:[Establishment and characterization of human ovarian fibrosarcoma cell line and its sensitivity to anticancer agents]. 135 14

FK-506, a novel immunosuppressive agent, was examined for its reversing effect on multidrug-resistant tumor cells. FK-506 at 3 microM completely reversed the resistance against vincristine (VCR) in vitro in VCR-resistant mouse leukemia P388 cells (P388/VCR). FK-506 also enhanced the cytotoxicity of VCR in Adriamycin(ADM)-resistant human ovarian cancer A2780 cells (AD10) and ADM-resistant human myelogenous leukemia K562 cells (K562/ADM) in vitro. FK-506 was also effective in modulating sensitivity to ADM in AD10 cells in vitro. FK-506 enhanced the chemotherapeutic effect of VCR in P388/VCR-bearing mice. When 20 mg/kg FK-506 was combined with 200 micrograms/kg VCR, a T/C value of 151% was obtained. Under the protocol used in this study, FK-506 was more potent than cyclosporin A (CsA) and verapamil. FK-506 inhibited [3H]azidopine binding to P-glycoprotein efficiently. The binding of VCR to K562/ADM plasma membrane was inhibited by FK-506 as effectively as by CsA. Moreover, the accumulation of VCR in AD10 cells was increased by FK-506 as efficiently as that of CsA and verapamil. These results indicate that FK-506 directly interacts with P-glycoprotein like CsA and verapamil, inhibits the active efflux of vincristine from resistant cells, increases the vincristine accumulation in resistant cells, and thus overcomes multidrug resistance in vitro and in vivo.
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PMID:Reversal of multidrug resistance by an immunosuppressive agent FK-506. 137 Jul 65

Antineoplastic agents are currently being administered through catheters placed intraperitoneally to treat cancer localized to the peritoneum. This route allows for high local concentrations of antineoplastic drug at the tumor site with low levels of the drug systemically, thereby reducing the systemic toxicity. However, there are complications with this mode of delivery, including a decrease in catheter patency and induction of adhesion formation, which leads to decreased drug dispersion and limits continuing drug administration. A model was developed in rats to mimic this method of antineoplastic drug administration that produced fibrin deposition around the catheter and adhesion formation involving bowel, intestines and liver. All antineoplastic agents tested, including Adriamycin, methotrexate, bleomycin, mitoxantrone and cisplatin, induced moderate to severe adhesion formation with varying effects on catheter patency. When an intraperitoneal bolus of tometin encapsulated in liposomes was tested with Adriamycin delivered via an osmotic minipump, a reduction in adhesion formation was observed. However, highly significant adhesion reduction was found when tolmetin was coadministered with the antitumor agents.
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PMID:Effect of tolmetin sodium dihydrate on adhesion formation by intraperitoneal administration of antineoplastic agents. 137 Jul 66

The antitumor effect of a synthetic lipid A analogue, DT-5461, was investigated using syngeneic tumor models in mice. Intravenous injection of DT-5461 into mice transplanted with solid tumors of MethA fibrosarcoma, MH134 hepatoma, MM46 mammary carcinoma, Lewis lung carcinoma (3LL), and colon adenocarcinomas 26 and 38 resulted in significant reductions in the weight of all tumors except Colon 26, with marked hemorrhagic necrosis of tumor tissues. Efficacy was almost equal to that of an Escherichia coli-type synthetic lipid A (compound 506), and also to those of some chemotherapeutics including Adriamycin, mitomycin C, fluorouracil and cisplatin. Furthermore, DT-5461 was more effective than other immunotherapeutics, including picibanil (OK-432) and lentinan. However, its antitumor effects were inferior to those of Adriamycin or OK-432 against the malignant ascites caused by intraperitoneal inoculation with MethA or with MH134 cells; life span was not prolonged by either intraperitoneal or intravenous administration. In addition, although DT-5461 showed direct inhibitory effects on the in vitro growth of MethA or MH134, these were much weaker than those of Adriamycin. These findings clearly indicated that DT-5461 with systemic administration is a highly effective antitumor agent on solid tumors, and suggest that the antitumor effect of DT-5461 with potent necrotizing activity might derive from indirect mechanisms related to the activation of host immune systems and not to the weak direct cytotoxicity.
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PMID:Significant antitumor effect of a synthetic lipid A analogue, DT-5461, on murine syngeneic tumor models. 139 35


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