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)

A 73-year-old male was admitted with suspected Grawitz tumor. Aspiration cytology from the tumor was diagnosed as Class V with suspected sarcoma. He died 17 days after admission. Autopsy revealed this to be a massive hepatic tumor occupying over half of the right lobe. It showed protrusion into the right retroperitoneum. Histology of the tumor evidenced widespread proliferation of sarcoma-like neoplastic cells besides a minute area of definite liver cell carcinoma in the center of the tumor mass. Definite transitional features between liver cell carcinoma and a sarcomatous pattern, the latter involving a major part of this tumor, were noted. Thus, we diagnosed this tumor to be liver cell carcinoma with a sarcoma-like histological pattern. The possibility of collision tumor or carcinosarcoma could be ruled out.
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PMID:[Liver cell carcinoma with extensive proliferation of sarcoma-like neoplastic cells--an autopsy case]. 631 85

The 1H NMR spin-lattice relaxation time (T1), spin-spin relaxation time (T2), and spin-lattice relaxation time in the rotating frame (T1rho) were determined for Novikoff hepatoma, Walker-256 Carcinosarcoma, Sarcoma-180 and Ehrlich Ascites tumor as well as for 7 normal tissues in the rat at 2.18 MHz. T1 values yielded improved discrimination of normal and malignant tissue compared to previous results at higher frequencies.
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PMID:Improved discrimination of normal and malignant tissue using 1H NMR relaxation time measurements at 2.18 MHz. 654 47

The metabolism of deoxycytidine (dCyd) and dCyd nucleotides in Yoshida ascites sarcoma (YS) cells and the host rat liver was investigated with reference to the increased excretion of urinary dCyd. Incorporation of [14C]orotic acid into the livers of rats at the fifth day after the transplantation of YS cells, the time when the amount of excretion of dCyd in urine was near maximal, was 2 times higher than that into the normal rat livers. After the injection of [14C]orotic acid, the ratio of the specific radioactivity of cytidylate to uridylate moieties of the host liver RNA was measured and found to be higher than that of normal rat liver RNA and to be similar to that of YS cell RNA. When [14C]orotic acid was injected into rats followed by the transplantation of YS cells, the radioactivities present in the livers disappeared more rapidly than those in the control rat livers. The activities of pyrimidine de novo synthesis enzymes, such as cytidine triphosphate synthetase (EC 6.3.4.2) and cytidine diphosphate reductase (EC 1.17.4.1), in YS were higher than those in both rat ascites hepatoma AH 7974 and Walker 256 carcinosarcoma, the transplantations of which did not induce increased excretion of dCyd into urine of the hosts. The activities of dCyd kinase (EC 2.7.1.10) and dCyd deaminase (EC 3.5.4.5) in YS cells were lower than those in the other two tumors investigated. The activities of cytidine triphosphate synthetase and cytidine diphosphate reductase in the livers of YS-bearing rats were elevated compared with those in the livers of rat ascites hepatoma AH 7974- or Walker 256 carcinosarcoma-bearing rats and normal rats, while the activities of dCyd kinase, 5'-nucleotidase (EC 3.1.3.5), and dCyd deaminase were similar between normal rat livers and tumor-bearing rat livers. These results suggest that the increased excretion of urinary dCyd in YS-bearing rats could be caused by both the stimulation of the synthesis of dCyd nucleotides and the low activity of dCyd deaminase in YS cells as well as in the host liver.
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PMID:Origin of increased deoxycytidine excretion into urine of rats bearing Yoshida ascites sarcoma. 672 78

The metabolism, antitumor activity, and acute toxicity of 5-fluoro-1,3-bis-(tetrahydro-2-furanyl)-2,4-pyrimidinedione (FD-1) were investigated in animals, compared with 5-fluoro-1-(tetrahydro-2-furanyl)-2,4-pyrimidinedione (FT). It was found that after oral administration of FD-1, the level of 5-fluorouracil (5-FU) was maintained higher and longer than after administration of FT, and that a large amount of 5-FU was released from FD-1 by liver microsomal drug-metabolizing enzymes or spontaneous hydrolysis via 5-fluoro-3-(tetrahydro-2-furanyl)-2,4-pyrimidinedione (3-FT) and FT. FD-1 had a significant activity against the solid form of Ehrlich carcinoma, sarcoma-180, hepatoma AH130, Yoshida sarcoma, Walker carcinosarcoma-256, and leukemia L1210 and P388, but not the ascitic forms, and it produced greater inhibition of tumor growth than FT. The acute toxicity of FD-1 was less than that of FT.
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PMID:Metabolism, antitumor activity, and acute toxicity of 5-fluoro-1,3-bis(tetrahydro-2-furanyl)-2,4-pyrimidinedione by oral administration to animals. 676 37

Succinylacetone (SA, 4,6-dioxoheptanoic acid) inhibits d-aminolevulinic acid dehydrase, the second enzyme of the heme biosynthetic pathway and thereby inhibits heme biosynthesis. In the present study SA is shown to inhibit the growth of the Walker carcinosarcoma (W256) in vitro and in vivo, the Novikoff hepatoma in vivo, and L1210 leukemia in vitro, but only slightly in vivo. Rats can tolerate significantly larger doses of SA for at least twice as long as were administered in the present study without gross evidence of toxicity. In contrast to findings in previously published studies with murine erythroleukemia cells, the inhibition of growth of L1210 and W256 cells by SA in vitro is not accompanied by a decrease in cellular heme and is not reversed by addition of hematin to the medium. This suggests a second mechanism of growth inhibition of tumor cells unrelated to heme biosynthesis. Although the growth of both W256 and L1210 cells was markedly inhibited by the same concentration of SA in culture, there was a great difference in responsiveness in vivo, in that much greater inhibition of the growth of the Walker tumor was produced by SA.
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PMID:Growth inhibitory activity of succinylacetone: studies with Walker 256 carcinosarcoma, Novikoff hepatoma and L1210 leukemia. 682 92

The Walker 256 carcinosarcoma growing in Sprague-Dawley rats and the Morris 5123 hepatoma growing in Buffalo rats both produce cachexia but have widely differing patterns of host metabolism and tumor growth. Both organisms respond to exogenous insulin with increased food intake and rate of weight gain of host. The insulin treatment response of food intake was 1.5 to 2 times and of body weight gain was 2 to 3 times that of tumor-free controls. Insulin does not accelerate tumor growth. On withdrawal of insulin, the reactive hypophagia seen in tumor-free rats does not occur in tumor bearers, and the host weight does not return to the expected untreated value as it does in tumor-free rats. Most of the weight gained during insulin treatment of tumor bearers above that gained by tumor-free rats is retained after withdrawal of insulin. A computer model based on the inference from these results, that the tumor-bearing host is blind to body weight error, indicates that this abnormality of feeding control could account for only about one-third of the observed depression of host weight and food intake.
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PMID:Feeding response of tumor-bearing rats to insulin and insulin withdrawal and the contribution of autonomous tumor drain to cachectic depletion. 704 59

This study investigates the specificity of two antigenic proteins with molecular weights of 39,000 and 49,000, respectively (p39 and p49), present in Novikoff ascites hepatoma. Chromatins and cytosol fractions were assayed from a number of tumorigenic cell lines by identifying antigenic species immunologically on nitrocellulose transfers containing proteins separated electrophoretically. Immunoreactivity was confirmed with complement-fixation. Although the p49 antigen was present only in Novikoff ascites hepatoma and a tissue culture line derived from these ascites cells, the p39 antigen was found in every carcinoma cell line examined. In contrast, neither antigen was present in a representative sarcoma, fibrosarcoma, or Walker 256 carcinosarcoma. These results suggest that the p39 antigen is a protein specific for malignant cells derived from the epithelium. The overall expression of the p39 antigen by the various cell lines examined did not appear to be influenced by in vivo or in vitro growth of homologous cell lines. This latter feature suggests that the p39 antigen is a stable, possibly structural component of neoplastic cells.
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PMID:Distribution of Novikoff ascites hepatoma antigens p39 and p49 in various tumorigenic cell lines. 706 17

A new anthramycin-group antitumor antibiotic, neothramycin, isolated from a Streptomyces culture, showed activity against experimental tumors such as lymphocytic leukemia P388 ascites sarcoma-180, hepatoma AH130, Walker carcinosarcoma-256 and mouse mammary adenocarcinoma (CCMT). In particular, the tumor growth inhibition ratio was as high as 96% when neothramycin was injected intraperitoneally at a daily dose of 2 mg/kg into Wistar strain rats previously inoculated with Walker carcinosarcoma-256 by the subcutaneous route. Successive intraperitoneal injections of the compound were more effective than a single injection with the P388 system.
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PMID:Antitumor effect of a new antibiotic, neothramycin. 741 76

Previous studies have shown that human IgG1 contains a 'reactive' disulfide bridge (SS*), detectable by a 24-hour disulfide exchange reaction, and that the serum level of this IgG subclass is selectively diminished in patients with various malignant diseases. Here we present evidence that in rats IgG2b is the only subclass that carries one SS* per molecule. Furthermore, it is shown that rats inoculated with experimental tumor lines, i.e., the Yoshida hepatoma ascites tumor and the Walker 256 carcinosarcoma growing in ascites or as solid tumor, exhibit significantly decreased SS* per mole IgG which corresponds to a selective diminution of IgG2b. Although at later stages there is a quantitative correlation with the tumor burden, with the Walker tumor this effect becomes significant as early as 24 h after inoculation, i.e., well before exponential tumor growth and an absolute reduction of total IgG. Control animals injected intraperitoneally with either viable spleen cells or irradiated Walker 256 cells did not show comparable alterations in their IgG subclass profile. Thus, the selective defect of IgG2b requires the presence of viable and proliferating tumor cells. Possible mechanism(s) of tumor-associated shifts in IgG subclasses are discussed.
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PMID:A decrease in reactive disulfide bonds of serum IgG signals a characteristic change in the IgG subclass patterns of rats bearing experimental tumors. 824 96

Carcinosarcoma of the liver with mesenchymal differentiation are very rare in adult patients. A case is reported with an exhaustive pathologic examination and review of the literature. A 61-year old man presented with general fatigue and dull abdominal pain. Two liver masses were diagnosed and resected by a right hepatectomy. Specimen pathology revealed that the tumor and lymph node consisted of two cancerous components. One carcinomatous component corresponding to a hepatocellular carcinoma and a sarcomatous component characterized by a diffuse proliferation of spindle shaped cells with chondrosarcomatous and osteosarcomatous changes. Patient died 9 months later of a diffusion of the tumor. For the first time, to our knowledge, a mesenchymal differentiation is demonstrated in liver carcinosarcoma.
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PMID:Carcinosarcoma of the liver with mesenchymal differentiation: a case report. 868 74


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