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

Daily food intake and corresponding feeding activity (measured as duration) and feeding efficiency (amount of food ingested per unit of feeding activity) were measured both in normal Sprague-Dawley and Buffalo rats and during growth of Walker 256 and 4M mammary carcinomas in Sprague-Dawley rats and of Morris 5123 hepatoma in Buffalo rats. Estimates of meal size and frequency were also obtained. Growth of the carcinomas produced a decline in feeding activity accompanied, early in tumor growth, by a compensatory increase in feeding efficiency with no resultant effect on food intake. This compensated decline in feeding activity was due to reduction in average meal duration. Later, meal frequency was also reduced, with further reduction in feeding activity and reduction in food intake. There was little change in average meal size. The hepatoma produced a different detailed pattern of effect on feeding behavior. These effects are not nonspecific reactions to foreign tissue. The effects imply behavioral compensation for the breakdown of a rapidly responding physiological control of food intake and can be interpreted in terms of successive impairment of feeding control mechanisms that have different response rates and different behavioral modes.
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PMID:Generation and compensation of the cancer cachectic process by spontaneous modification of feeding behavior. 17 8

Line 10, a transplantable hepatocellular carcinoma, was obtained originally from an NIH strain-2 male guinea pig fed diethylnitrosamine. The antitumor activity of BCG and BCG extracts was evaluated in strain-2 guinea pigs obtained both from NIH and the National Jewish Hospital and Research Center (NJH). Animals were immunized with these materials and then tested for their capacity to resist the growth of intradermally injected line-10 tumor cells. Tumor growth was not prevented in 18 NIH animals immunized with living BCG. No tumor growth occurred in 1 of 22 NIH animals immunized with a residue that remained after exhaustive methanol extraction of BCG and in 1 of 44 NIH guinea pigs immunized with BCG extracts. In contrast, tumor growth was prevented in 13 of 22 similarly immunized NJH guinea pigs.
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PMID:Prevention of tumor growth after intradermal injection of BCG extracts: a comparison of results in strain-2 guinea pigs from the National Institutes of Health and from the National Jewish Hospital and Research Center. 17 90

Young BUF rats of similar ages were inoculated with the transplantable Morris hepatoma No. 7777. At 4 weeks after inoculation, 1 group was given total iv (parenteral) feeding at high caloric and nutritional levels for 2 weeks. Such total iv feeding (hyperalimentation) of rats stimulated a more rapid tumor growth in the host. In addition, the tumors from rats fed parenterally for 2 weeks had higher mitotic activity and larger areas of necrosis, which indicate that iv feeding caused the tumor to undergo faster cell turnover with greater cell production and cell loss. Analysis of organ weights showed that parenteral feeding caused atrophy of the intestines, whereas spleen weights of the hepatoma-bearing rats fed iv were greater than those of the orally fed hepatoma-bearing rats.
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PMID:Stimulation of growth of a transplantable hepatoma in rats by parenteral nutrition. 17 98

In tissue culture experiments, cells derived from glioma 26, a transplantable tumor of C57B1/6 mice, were sensitive to both floxuridine (5-fluorodeoxyuridine) and 5-fluorodeoxyuridine-5'-(5-iodo-3-indolyl)phosphate, an enzyme-mediated drug activated by 5'-nucleotide phosphodiesterase. When these compounds were tested on the tumor in animals at a level of 5 mg/kg for 5 days, tumor growth was inhibited approximately 20% by both compounds. When higher levels of 5-fluorodeoxyuridine, 100 mg/kg four times weekly throughout the lifespan of the mouse, were given, the tumor, although inhibited at first, developed resistance and continued to grow until it killed the animal. Phosphodiesterase levels in the tumor rose as the tumor grew. On the other hand, thymidine kinase levels dropped as anticipated from the known 5-fluorodeoxyuridine-resistant hepatoma tissue culture data. This enzyme pattern was maintained in transplantable mouse glioma lines established from the resistant tumors. One of these lines, tested at a level of 5 mg/kg for 5 days, showed no response to 5-fluorodeoxyuridine but was still sensitive to 5-fluorodeoxyuridine-5'-(5-iodo-3-indolyl) phosphate. These experiments, therefore, offer a model system and a rationale for the design and study of more compounds that could be activated by the enzyme phosphodiesterase. Such compounds might be used alternatively when resistance to 5-fluorodeoxyuridine develops, a common clinical experience in the use of this anticancer drug.
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PMID:5'-nucleotide phosphodiesterase activity of floxuridine-resistant mouse glioma. 17 49

In inbred guinea pigs, administration of Mycobacterium bovis strain BCG by scarification at a site distant from an excised skin tumor, but in the regional lymph node drainage, was evaluated for its immunotherapeutic effect on the development of lymph node metastases. Scarification was performed after surgical excision of intradermally transplanted syngeneic (line-10) hepatocarcinoma at a time when microscopic foci of tumor cells were present in regional lymph nodes. Various strains of BCG were evaluated for their immunotherapeutic potential: fresh-frozen Phipps, Pasteur, and Tice; and lyophilized Pasteur, Tice, and Connaught. Scarification commenced 3 days after surgical removal of the tumor and continued once a week for 5 weeks. Only lymph nodes from fresh-frozen Phipps- and Pasteur-scarified animals were significantly smaller than those in the control groups. Differences in lymph node weight correlated histologically with less detectable metastases. This cytostatic effect was short lived; eventually, the metastatic tumor growth was not significantly different from that of control animals. No significant differences were observed in mean survival time: All animals died as a result of metastases 3 months after tumor inoculation. These results demonstrated that limited scarification with BCG of certain strains temporarily inhibits the growth and proliferation of metastases in regional lymph nodes after removal of the primary tumor.
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PMID:Evaluation of BCG administered by scarification for immunotherapy of metastatic hepatocarcinoma in the guinea pig. 18 11

Considerable thymidine kinase and pyrroline-5-carboxylate reductase activities were found in the plasma of rats bearing a transplanted lymphoma; neither activity was detected in plasma of hosts carrying hepatic, renal, mammary, or submaxillary gland tumors. All host livers exhibited signs of biochemical immaturity as indicated by the appropriate increases or decreases in the concentrations of the nine enzymes measured. The extent and time schedule of the changes in host liver varied with the enzyme and with the tumor that caused them. The hepatic concentrations of ornithine aminotransferase, arginase, pyrroline-5-carboxylate reductase, and glucokinase (all diminished), and of peptidyl proline hydroxylase and hexokinase (increased) were sensitive indicators of tumor growth in general. The concentration of ornithine aminotransferase decreased before the tumors became palpable. At more advanced stages, the high hepatic thymidine kinase activity distinguished the presence of hepatoma and lymphoma from those of all other equally fast-growing tumors. However, only in lymphoma-bearing rats did a fivefold elevation of hepatic thymidine kinase occur as early as 4 days after implantation. Additional observations on the lymphoma itself, on blood cells, and on the involuting thymus of normal rats indicate that the striking systemic effects of this tumor cannot be explained by a release of enzymes from the thymus or by the increased number of lymphoma cells present in blood or liver.
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PMID:The effect of lymphoma and other neoplasms on hepatic and plasma enzymes of the host rat. 18 34

Tumor growth and survival time were followed in rats transplanted with Morris hepatoma 5123 and previously injected with a crude homogenate of the same tumor by the intradermic or intralymphatic route. Female rats treated by the intralymphatic route showed a longer survival time and impaired tumor growth. Male rats did not show any difference.
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PMID:Administration of antigen by intralymphatic route in the rat. II. Results in tumor active immunotherapy (delta). Preliminary report. 18 86

The rates of urea synthesis in rat liver and in a series of rat liver neoplasms with widely different growth rates and degree of differentiation were investigated using tissue slices incubated in a Krebs-Ringer bicarbonate buffer. Urea synthesis did not occur in fast-growing, poorly differentiated Novikoff and Morris 3924A hepatomas, but it did occur in slow-growing, well- and highly differentiated hepatomas; however, there was no correlation with growth rate or degree of differentiation. Urea synthesis was comparable with normal liver, at about 32 mumoles/hr/g tissue, in the slow-growing Morris hepatomas 21, 28A, 47C, and 44; but it was very low in two other slow-growing, highly differentiated hepatomas, 9618A and 20. The well-differentiated Morris hepatoma 5123C had intermediate levels of urea synthesis. This pattern of urea synthesis closely paralleled the previously reported activity of carbamyl phosphate synthetase in these tumors. The rate of urea synthesis was normal in livers of Buffalo rats bearing fast- or slow-growing hepatomas in low urea synthesis rates, but it was markedly lowered in the livers of rats bearing large, slow-growing tumors with high urea synthesis rates. Urea synthesis in liver declined as the tumors increased in size. The total rate of urea synthesis in liver and tumor, as well as the concentrations of urea in the serum and urine of tumor-bearing animals, remained remarkably constant throughout the period of tumor growth, suggesting the existence of a homeostatic mechanism that controls the urea cycle activity in accordance with the synthetic activity of the tumor. In parabiotic animals, carbamyl phosphate synthetase activity and urea synthesis were lowered in the host livers of partners bearing tumors with high carbamyl phosphate synthetase- and urea-synthetic activity, but there was no significant effect on urea cycle activity in the normal partners. This result discounts the likelihood of a circulating humoral factor that controls hepatic urea cycle activity.
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PMID:Urea synthesis in Novikoff and Morris hepatomas. 18 16

The effect of depletion of immunocompetence of metastasis of a mouse hepatoma MH-134 was studied in syngeneic C3H/He mice. (2) Development of metastasis in the lung and lymph nodes was remarkably enhanced in the mice which were thymectomized, irradiated, bone marrow-reconstituted (Tx-X-BM), and grafted intramuscularly with tumor cells. (2) Number of tumor cells detected in the blood stream was within the same range in the control mice and the Tx-X-BM mice after intramuscular tumor-grafting. (3) Metastatic foci were not detected in the stomach and intestines, not only in control mice but also in the Tx-X-BM mice after intramuscular tumor-grafting. However, tumors grew progressively in the subserosal tissues of these organs of the Tx-X-BM mice, but not of the control mice, when a small number of tumor cells were directly inoculated into such tissues. (4) On 9th day after an intravenous injection of a large number of tumor cells, tumor growth was detected to almost the same extent in the lungs of the control mice and the Tx-X-BM mice. Tumors grew progressively in the Tx-X-BM mice thereafter, whereas the tumors regressed in the control mice. These results suggest that inhibition of metastasis by immune response depends primarily upon suppression of proliferation of the tumor cells lodged in individual organs.
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PMID:Enhanced development of metastatic foci in thymectomized, irradiated, and bone marrow-reconstituted mice. 19 77

The activity of estrogen 16alpha-hydroxylase was measured for nine Morris hepatomas of different growth rates and host livers. Activity was measured in the microsomal fraction of the cell (100,000 X g). In the spectrum of hepatomas studied, 16alpha-hydroxylase activity was significantly decreased in parallel with the increase in hepatoma growth rate. The decrease in enzymic activity ranged from 16 to 19% for the slow-growing tumors (Hepatomas 44, 28A, and 9633), 2 to 9% for the intermediate-growing tumors (Hepatomas 38B, 7795, and 5123A), and 0% for the fast-growing tumors (Hepatomas 7288C, 7777, and 42A). Estrogen 16alpha-hydroxylase activity of the liver of tumor-bearing rats differed from that of liver of healthy animals. There was a decrease in enzymic activity ranging from 66% to 90% of normal control rats. The activity level of the host liver did not correlate with tumor growth rate. Stimulation of 16alpha-hydroxylase with phenobarbital showed a 4-fold increase in activity in normal liver and only a 2- to 3-fold increase in host livers. The slow- and intermediate-growing hepatomas showed a 1.2-to 1.4-fold increase in enzyme activity, and no activity or stimulation in the fast-growing hepatomas was observed.
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PMID:Metabolism of estrogens in hepatomas of different growth rates. 19 Nov 75


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