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)

The contribution of both non-inherited (stochastic, random, environmental, and other non-inherited influences) and inherited factors (genetic and inherited epigenetic factors) to the variability of spontaneous lung metastasis formation in over 100 metastatic lines from each of three murine tumors was measured. The contribution of inherited and genetic sources of variability to metastasis formation was significantly greater than 0 in all cases, but only in the lines of sarcoma SANH was it the major influence on metastatic variability. In the sarcoma SA4020 and hepatocarcinoma HCA-1 lines, non-inherited factors accounted for the majority of the variation in spontaneous lung metastasis formation. A similar situation was also observed in the variability of the tumors with respect to the diameter doubling time. In conclusion, both non-inherited and genetic/inherited factors significantly influenced the formation of spontaneous metastases in the tumors examined. The significance of this finding for the cloning of metastatic genes is discussed.
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PMID:The use of quantitative genetics for estimating the non-inherited and inherited contributions to metastasis formation. 158 85

The connective tissue content of four different human liver tumors (Fibrolamellar carcinoma, FLC; hepatocellular carcinoma, HCC; focal nodular hyerplasia, FNH and hepatocellular adenoma, HCA) was investigated by computer aided morphometry. A significantly higher connective tissue content was found in FNH and FLC as compared to HCA and HCC. The distribution of the connective tissue was homogeneous in the cases of FNH, HCA and HCC, while a highly unhomogeneous distribution was observed in FLC cases.
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PMID:Connective tissue content of fibrolamellar carcinoma and other human liver tumors. 166

The connective tissue content of four different human liver tumors (Fibrolamellar carcinoma, FLC; hepatocellular carcinoma, HCC; focal nodular hyperplasia, FNH and hepatocellular adenoma, HCA) was investigated by computer aided morphometry. A significantly higher connective tissue content was found in FNH and FLC as compared to HCA and HCC. The distribution of the connective tissue was homogeneous in the cases of FNH, HCA and HCC, while a highly unhomogeneous distribution was observed in FLC cases.
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PMID:Connective tissue content of fibrolamellar carcinoma and other human liver tumors. 166 1

This study was performed to determine whether the growth rate and metastatic potential of tumors generated by spontaneous lung metastases is influenced by transplantation methods. Three different tumors syngeneic to C3Hf/Kam mice were studied: the SA-NH and SA-4020 sarcomas and the hepatocarcinoma HCA-I. Solitary tumors in the legs of mice were generated by a single metastatic nodule taken at random from lung metastases, by a single metastatic nodule taken from each mouse with the highest number of metastases, by a mixture of cells from lung metastases taken randomly, or by a mixture of cells from primary leg tumors. These transplantation procedures were repeated for two to four isotransplant generations. Repeated isotransplants of primary tumors showed little if any change in the growth rate and metastatic spread. In contrast, primary tumors derived from spontaneous metastases frequently exhibited a decrease in their growth rate and an increase in metastatic potential. This was particularly frequent when tumors were established from single metastatic nodules taken randomly from the lung, or taken from lungs that contained the largest number of metastatic nodules. The magnitude of this change varied greatly among the three tumors studied. Increased metastatic formation in the lung was also frequently associated with slower growth of the primary tumors. Thus, transplantation methods used for establishing primary tumors have an important influence on the metastatic potential of tumor transplants.
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PMID:Influence of tumor transplantation methods on tumor growth rate and metastatic potential of solitary tumors derived from metastases. 235 Sep 21

The diagnostic findings of hepatocellular adenoma and focal nodular hyperplasia became more frequent in the last years in our as in western experience. The improvement in diagnostic technique, a correct pathological identification and the diffusion of oral contraceptives explain this increase of incidence. In our series were present 11 hepatocellular adenomas and 19 focal nodular hyperplasias: all the HCA cases were radically resected, while only 15 FNH were resected, only two biopsied and two submitted to periodical follow-up. The tendency to spontaneous bleeding and the presence of diagnostic uncertainty versus well-differentiated hepatocellular carcinoma are mandatory indications for radical resections in all the HCA cases. FNH resection is reserved to symptomatic cases and wide wedge biopsy is at least required in presence of diagnostic doubts: the asymptomatic FNH ("hot spot" on Tc99m-HIDA scintigraphy) may be followed-up only.
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PMID:[Hepatocellular adenoma and focal nodular hyperplasia]. 256 31

The differentiation-inducing agent N-methylformamide (NMF) enhances the sensitivity of some cell lines to ionizing radiation. To elucidate the mechanism of NMF-mediated radiosensitization, we examined the effects of this agent on gamma-ray-induced DNA double-strand breaks and micronuclei in two cell lines, clone A (human colon carcinoma) and HCA-1 (murine hepatocarcinoma). Both cell lines form a better differentiated phenotype upon exposure to NMF, yet only clone A is radiosensitized. The neutral (pH 9.6) elution assay was used to evaluate the effects of this maturational agent on radiation-induced double-strand breaks in these cell lines. Exposure of HCA-1 cells to NMF had no effect on the level of DNA double-strand breaks induced by gamma rays. In clone A cells, however, exposure to NMF enhanced the initial formation of gamma-ray-induced double-strand breaks at each dose tested. The repair of double-strand breaks in both cell lines was not influenced by NMF. As a measure of chromosome fragmentation after irradiation, we evaluated micronuclei using the cytokinesis block method. Exposure to NMF had no effect on radiation-induced micronuclei formation in HCA-1 cells yet significantly enhanced the frequency of micronuclei induced by radiation in clone A cells. In clone A cells, the increases in radiation-induced double-strand breaks and micronuclei as a function of NMF exposure time reached maximums by approximately 72 h. These data suggest that NMF-mediated radiosensitization is the result of an increase in the initial level of radiation-induced DNA double-strand breaks.
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PMID:Enhancement of radiation-induced DNA double-strand breaks and micronuclei in human colon carcinoma cells by N-methylformamide. 275 7

The effect of treatment with the hypoxic cell radiosensitizer misonidazole (MISO) and the radioprotector diethyldithiocarbamate (DDC) on the formation of spontaneous lung metastases of four different spontaneously metastasizing murine tumors was investigated. The tumors were mammary carcinoma MCA-K, hepatocarcinoma HCA-1, and sarcomas SA-4020 and SA-NH. Multiple daily treatments with MISO significantly enhanced the incidence of metastases only in MCA-K. Because only MCA-K, but not the three remaining tumors, is immunogenic, the treatment with MISO may be associated with the promotion of metastasis primarily in the immunogenic tumors. Treatment of mice with DDC had no influence on metastatic spread. However, when given prior to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), DDC reduced BCNU-induced enhancement of HCA-1 metastases.
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PMID:Effect of the radiosensitizer misonidazole and the radioprotector diethyldithiocarbamate on spontaneous metastasis formation of murine tumors. 301 3

The effects of the differentiation-inducing polar solvent N-methylformamide (NMF) on artificially induced and spontaneous metastases from a murine hepatocarcinoma (HCA-1) in C3Hf/Kam mice were investigated. Exposure of HCA-1 cells in vitro for 6 days to 1.0% or 1.25% NMF resulted in an increase in the number of lung nodules formed in mice when these cells were injected into their tail veins. This in vitro NMF exposure increased cell volume and induced only a slight amount of cytotoxicity. Administration of NMF to mice 1 day before i.v. tumour cell inoculation resulted in a dose-dependent increase in the number of lung nodules formed, beginning at an NMF dose of 600 mg kg-1. NMF caused a similar magnitude of metastasis enhancement in immunosuppressed mice. However, when the maximum dose tested (1,800 mg kg-1) was administered as 6 daily fractions of 300 mg kg-1 each, no increase in artificial metastases was detected. Administration of NMF to mice one day after i.v. tumour cell injection resulted in a dose-dependent decrease in the number of lung nodules. In mice bearing 5-6 mm HCA-1 leg tumours, treatment with 6 daily fractions of NMF (300 mg kg-1 each) significantly reduced the number of spontaneous pulmonary metastases, yet had very little effect on the growth of the primary tumour. These data suggest that, in a clinically relevant treatment setting, NMF can reduce metastasis formation.
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PMID:The effects of N-methylformamide on artificial and spontaneous metastases from a murine hepatocarcinoma. 356 58

The effects of the differentiating agent N-methylformamide (NMF) on radiation-induced DNA damage and repair in vitro were investigated using the alkaline elution assay. Two tumor cell lines were examined: Clone A, a human colon adenocarcinoma, and HCA-1, a murine hepatocarcinoma. Both cell lines showed changes suggestive of a better differentiated phenotype when exposed to NMF. Treatment with NMF enhanced the radiation sensitivity of Clone A cells but had no effect on the radiation response of HCA-1 cells. Irradiation of NMF-treated cells, both Clone A and HCA-1, induced the formation of DNA-protein crosslinks (DPCs). The level of DPCs induced increased linearly as a function of increasing gamma-ray dose. The DPCs did not seem to be the result of NMF exposure alone, but rather an NMF-mediated modification of the spectrum of gamma-ray-induced DNA lesions. When the DPCs were removed by proteolytic digestion, no NMF effect was observed on either strand-break formation or repair.
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PMID:Enhancement of radiation-induced DNA-protein crosslinking by N-methylformamide. 357 57

N-Methylformamide (NMF), a cell-differentiating agent, was assessed for its antitumor activity against a fibrosarcoma (FSA), a hepatocarcinoma (HCA-I) and a mammary carcinoma (MCA-K), syngeneic to C3Hf/Kam mice. Tumors were grown as solitary tumors in the leg or as artificial or spontaneous micrometastases in the lung. NMF, at a dose of 300 mg/kg, was administered i.p. daily for 6 to 18 days. NMF slowed the growth of FSA and HCA-I tumors and totally inhibited the growth of the MCA-K tumor. However, the effect was transient; tumors resumed their pretreatment growth rate upon cessation of the treatment. Histologically, MCA-K tumors treated with NMF (300 mg/kg daily for six days) underwent considerable cell depopulation and reduction in mitotic activity. The number of artificial metastases, as well as the incidence and the number of spontaneous metastases, were markedly reduced by NMF. This resulted in a prolongation of the survival of mice that had artificial metastases of MCA-K tumor. The in vitro clonogenicity of MCA-K, but not of FSA or HCA-I cells, was reduced. However, in vivo reduction of MCA-K cell clonogenicity was minimal, if any. Thus, NMF is effective in restricting the growth of both solitary tumors and metastases, but the degree of response is highly dependent on tumor type.
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PMID:Antitumor and antimetastatic activity of the differentiating agent N-methylformamide in murine tumor systems. 366 21


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