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)

Involvement of inferior vena cava (IVC) by tumor thrombus occurs in up to 10% of patients with nephroblastoma. Right atrial involvement by tumor thrombus is much less frequent. Four patients presenting with advanced nephroblastoma were diagnosed as having IVC involvement with tumor thrombus. Two of these patients had in addition thrombus extending up to the right atrium. All 4 patients were treated with preoperative chemotherapy (vincristine, actinomycin D, 4-epi-Adriamycin). Nephrectomy was subsequently performed without undue difficulty on all 4 patients. The intravascular tumor thrombus had completely cleared in all 4 patients and most of the primary renal tumor was necrotic. The results obtained with preoperative chemotherapy as given to these patients mediates strongly against difficult surgery being undertaken as primary treatment for such patients.
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PMID:Successful management of inferior vena cava and right atrial nephroblastoma tumor thrombus with preoperative chemotherapy. 130 7

Dibutyryl cyclic AMP was administered to 7 cases with hepatocellular carcinoma and its tumor thrombosis in portal vein, combined with intraarterial infusion of Mitomycin C or Adriamycin with implanted reservoir. Among these cases, tumor regressed in 5 cases, and therapeutic effect on tumor thrombosis was observed in 4 cases. The median survival time after initial treatment was about 5 months in 5 cases of Vp3, and more than 18 months in 2 cases of Vp2. Reduction of liver dysfunction by cholinesterase and hepaplastin test was found in most cases, and no severe side effects were observed. It is suggested that dibutyryl cyclic AMP has an antitumor effect on hepatocellular carcinoma, especially on its tumor thrombosis in portal vein, and also may assist in recovery from liver dysfunction.
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PMID:[Effect of dibutyryl cyclic AMP in the treatment of hepatocellular carcinoma--intraarterial infusion therapy combined with anticancer agent for hepatocellular carcinoma with portal vein thrombosis]. 130 35

A carcinogen-transformed rat hepatoma cell line (Reuber H-35) was utilized as a model system for investigation of the biochemical factors which may limit the effectiveness of chemotherapy in intrinsically resistant tumors such as hepatocellular carcinoma. Northern blotting demonstrated expression of mRNA coding for the P-170 membrane-glycoprotein associated with the multi-drug resistance phenotype, while Western blotting identified the P-170 glycoprotein in the hepatoma cell membrane. Consistent with these observations, tumor cell sensitivity to the vinca alkaloids, vincristine and vinblastine, to the anthracycline antibiotics, Adriamycin and daunorubicin, and to the demethylepipodophyllotoxin derivative, VM-26, was enhanced by continuous incubation in the presence of the calcium channel antagonist, verapamil. Verapamil produced a minimal change in cell sensitivity to the demethylepipodophyllotoxin derivative, VP-16, and to the aminoacridine, m-AMSA. Relatively high detoxification potential via the glutathione metabolic pathway was also observed in the hepatoma cell. The capacity of topoisomerase II in nuclear extracts from the hepatoma cell to mediate cleavable complex formation stimulated by VM-26, VP-16 and m-AMSA appeared to be at least comparable to, if not greater than that from drug-sensitive HL-60 cells, suggesting that drug resistance may not occur at the level of this enzyme. Consistent with findings in a number of tumor cell lines resistant to antineoplastic drugs, the antiproliferative activity of the topoisomerase II inhibitors VM-26, VP-16 and m-AMSA appeared to be dissociable from the induction of DNA strand breaks, suggesting that such lesions in DNA may fail to fully account for the antiproliferative activity of these agents in the hepatoma cell.
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PMID:Components of intrinsic drug resistance in the rat hepatoma. 131 Aug 53

Adriamycin-Lipiodol suspension was administered to 44 patients with metastatic liver tumor using the transcatheter arterial infusion method. The result revealed 23% in the over all effect (partial response or more) of the therapy which was evaluated by comparing the CT images of the tumor, 47% in the 25% or more of the decrease of the tumor, and 65%, very effective in the decrease of the smaller tumor (less than 50 cm2). Except for a case of hepatic subcapsular hematoma after the infusion of Adriamycin-Lipiodol suspension, minor complications were experienced such as abdominal pain, slight fever, and so on. No serious exacerbation in liver function test and white blood cell count was noted.
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PMID:[Transcatheter arterial infusion of adriamycin-lipiodol suspension to patients with metastatic liver tumor]. 131 13

Clinically, human testicular nonseminomatous germ cell tumors exhibit remarkable sensitivity to platinum-based chemotherapy. To define better the mechanistic basis for this unusual sensitivity, the biochemical determinants of platinum-induced cytotoxicity have been investigated in a human testicular tumor cell line (GCT27) established from a previously untreated patient and in an in vitro derived 5.6-fold cisplatin-resistant stable variant (GCT27cisR). Compared to 12 ovarian and 5 cervical human tumor cell lines, the parent GCT27 line was among the most sensitive to the cytotoxic effects of both cisplatin (dosage producing 50% inhibition, 0.2 microM) and carboplatin (dosage producing 50% inhibition, 2.9 microM), thus reflecting clinical data. A 4-day exposure sulforhodamine B-staining assay was used to determine that GCT27cisR was cross-resistant to carboplatin and iproplatin and the classical bifunctional alkylating agents melphalan and chlorambucil. Partial cross-resistance was observed to tetraplatin, methotrexate, and mitomycin C. No cross-resistance was observed to Adriamycin, etoposide, vinblastine, bleomycin, 1-beta-D-arabinofuranosylcytosine, and 5-fluorouracil. Intracellular cisplatin accumulation across the dose range 2.5-100 microM (for 2 h) was 1.6 +/- 0.39-fold (mean +/- SD) greater for the parent line. There was no significant difference in glutathione levels between the two lines. The acquired resistance line was 1.9-fold more resistant than the parent line to the cytotoxic effects of cadmium chloride. There was no significant difference between the two lines, however, in the total amounts of platinum bound to DNA after cisplatin exposure (25, 50, or 100 microM for 2 h). The removal of total platinum adducts from DNA was significantly faster for GCT27cisR compared to the parent line (half-times of removal, 32 and 67 h, respectively). These data suggest that the abnormal sensitivity of the parent testicular tumor cell line to platinum-containing anticancer drugs may be due predominantly to an inherent defect in the ability of these cells to remove platinum from their DNA. This defect is apparently lost in the acquired resistance counterpart. Reduced intracellular accumulation and increased cytoplasmic concentrations of metallothionein may also contribute, in part, to the acquisition of cisplatin resistance in this model.
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PMID:Establishment and characterization of an in vitro model of acquired resistance to cisplatin in a human testicular nonseminomatous germ cell line. 131 97

Centrifugal elutriation was used to obtain synchronized cell populations in various cell cycle phases without prior growth-perturbing manipulation. Treatment of these subpopulations with novobiocin (NOVO), a putative inhibitor of the mammalian topoisomerase II enzyme, revealed a unique cell cycle phase-dependent cytotoxicity for this agent. At a concentration of 0.3 mM, NOVO was cytotoxic only to a specific cell subpopulation in the G1-S phase boundary. Cells in other cell cycle phases were completely unaffected. Additionally, S and G2M phase cells progressed through the cell cycle relatively unaffected by NOVO but were blocked at the G1-S boundary. NOVO treatment protected tumor cells from Adriamycin (ADR)-induced lethality but sensitized them to the toxic action of 4-hydroperoxycyclophosphamide, and alkylating agent. These opposing effects of NOVO were demonstrated in all of the four tumor cell lines investigated: A431 and HEp3 (derived from human squamous cell carcinomas); MLS, a human ovarian cancer cell line; and a Chinese hamster ovary cell line. The degree of protection against ADR was the greatest for S-phase cells, intermediate for cells in early G1 and M phases, and the least for late G1 cells. This cell cycle-dependent protection by NOVO, which is identical to the cell cycle-dependent cytotoxicity of ADR, was consistent with the idea that NOVO interfered directly with the cell-killing mechanism of ADR. In contrast, even though the cytotoxic activity of 4-hydroperoxycyclophosphamide exhibited significant cell cycle dependency, NOVO enhanced 4-hydroperoxycyclophosphamide lethality equally for all cell cycle phases.
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PMID:Modulation of the cell cycle-dependent cytotoxicity of adriamycin and 4-hydroperoxycyclophosphamide by novobiocin, an inhibitor of mammalian topoisomerase II. 131 22

Adriamycin (ADM) was linked covalently to the murine monoclonal antibody (McAb) HAb18 against human hepatocellular carcinoma via a dextran T-40 bridge. The molar ratio of HAb18: DEX: ADM was 1:2.4:56 in the conjugate. It was confirmed by immunochemical staining and ELISA that the antigen binding capacity of HAb18 in the conjugate was well preserved. In vitro study indicated that the conjugate cytotoxicity to tumor target cell lines was selective. The radio-immunoimaging and distribution of the conjugate labelled with 125I in the nude mice bearing human hepatocellular carcinoma showed that 125I-HAb 18-DEX-ADM conjugate was localized in the tumor site. The HAb18-DEX-ADM targeting therapy in nude mice bearing human hepatocellular carcinoma showed the following results: decreased tumor size and partly necrosed cancer tissue in contrast to the rapidly growing tumor in the control group (P < 0.05). Our study suggested that targeting therapy with HAb18-DEX-ADM conjugate may be useful in the treatment of patients with hepatocellular carcinoma.
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PMID:[Targeting therapy with adriamycin-monoclonal antibody (HAb18) conjugate in nude mice with human hepatocellular carcinoma xenografts]. 133 Feb 27

A number of human tumor cell lines of various histological origin were examined for their sensitivity and resistance to tumor necrosis factor-alpha (TNF) and Adriamycin (ADR). Six ovarian lines, and one each of a renal, lung, and B-cell line, were tested for putative mechanisms of resistance to these agents. Cytotoxicity resulting from TNF or ADR showed no overall correlation in these lines. The combination of TNF and ADR produced enhanced cytotoxicity against these tumor lines and furthermore resulted in overcoming the resistance of TNF or ADR alone or in combination. A proposed mechanism of TNF resistance in tumor cells is the endogenous production of TNF mRNA and protein. There was a positive correlation between resistance to TNF and the constitutive production of TNF mRNA and protein. The TNF-resistant lines that did not constitutively produce TNF mRNA and protein and the three TNF-sensitive tumor lines exhibited up-regulation of their TNF mRNA in the presence of TNF or phorbol myristate acetate/ionophore, but did not secrete any detectable protein. Due to the enhanced cytotoxicity seen with the combination of TNF and ADR, the effect of this combination on the level of TNF mRNA was examined. ADR alone reduced the constitutive level of TNF mRNA and in combination with TNF reduced the level of induction produced by TNF. This down-regulation of TNF mRNA by ADR may play a role in the enhanced cytotoxicity seen with the combination of these 2 agents.
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PMID:Sensitivity of resistant human tumor cell lines to tumor necrosis factor and adriamycin used in combination: correlation between down-regulation of tumor necrosis factor-messenger RNA induction and overcoming resistance. 133 Feb 98

Woodfruticosin (woodfordin C) (WFC), a new inhibitor of DNA topoisomerase II (topo-II), was isolated from methanol extract of Woodfordia fruticosa Kurz (Lythraceae) and studied for in vitro and in vivo antitumor activities in comparison with Adriamycin (ADR) and etoposide (ETP), well known inhibitors of topo-II. The inhibitory activity against DNA topo-II shown by WFC was much stronger than that shown by ETP or ADR. WFC inhibited strongly intracellular DNA synthesis but not RNA and protein synthesis. On the other hand, WFC had a weaker growth inhibitory activity against various human tumor cells than ETP or ADR, but it showed remarkable activity against PC-1 cells and moderate activity against MKN45 and KB cells. Furthermore, WFC had in vivo growth inhibitory activity against s.c. inoculated colon38. These results indicate that the mechanism by which WFC exhibits antitumor activity may be through inhibition of topo-II.
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PMID:Woodfruticosin (woodfordin C), a new inhibitor of DNA topoisomerase II. Experimental antitumor activity. 133 1

A randomized clinical trial comparing L-TAE with Farmorubicin (FARM) and L-TAE with Adriamycin (ADR) in the treatment of hepatocellular carcinoma was conducted from October 1989 through December 1990. In all, 192 hospitals participated in this study and 117 patients were entered. The patients were randomly allocated to group A (L-TAE+FARM) or group B (L-TAE+ADR). There was no significant intergroup difference in background factors. Additional treatment consisting of repeated TAE or surgery was given to 66 patients. Four factors were analyzed in this study: the percentage of reduction in tumor size, the change in the AFP level, lipiodol accumulation, and survival. None of these factors differed significantly between the two groups. The final evaluation of this study will be based on differences in survival after a long-term follow-up. Toxic effects manifested less frequently in group A than in group B, and the decrease in the platelet count in the peripheral blood was significantly lower in group A than in group B. These results suggest that FARM exerts a more favorable effect than does ADR in the treatment of hepatocellular carcinoma.
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PMID:Prospective and randomized clinical trial for the treatment of hepatocellular carcinoma--a comparison of L-TAE with Farmorubicin and L-TAE with adriamycin (second cooperative study). The Cooperative Study Group for Liver Cancer Treatment of Japan. 133 3


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