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)

PSK is a protein-bound polysaccharide prepared from cultured mycelium of the Basidiomycete Coriolus versicolor. Effects of PSK on the immunologic responsiveness in tumor-bearing animals were investigated using syngeneic or allogeneic tumors in mice (Lewis lung carcinoma, B16 melanoma, Meth A fibrosarcoma, adenocarcinoma 755, X5563 plasmacytoma, colon 26, MOPC 31C myeloma, sarcoma 180 and Ehrlich carcinoma), rats (BC47 bladder carcinoma, Walker 256 sarcoma and AH7974 hepatoma), hamsters (HA-1T tumor and RPMI 1846 melanoma), guinea pigs (line-10 hepatoma) and rabbit (VX2 and VX7 tumor). Oral or intraperitoneal administration of PSK restored the depressed delayed hypersensitivity against sheep erythrocytes to a normal level in these tumor-host systems. Also, oral administration of PSK lowered the activity of immunosuppressive substances in the serum of tumor-bearing animals. These results suggest that PSK exhibits antitumor effects by restoring the depressed immunologic responsiveness in tumor-bearing animals.
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PMID:[Restoration of immunologic responsiveness by PSK in tumor-bearing animals]. 378 58

To assess the antineoplastic potential of vitamin K compounds, the effects of vitamin K3 (menadione), vitamin K1 (phylloquinone), and warfarin on L1210 murine leukemia cell growth were studied in a flask culture system. When the cytotoxic potential of vitamin K3 was recognized, the effects of vitamin K3 on human tumor colony formation were studied in 34 tumor explants using a soft agar (clonogenic) assay system. Complete inhibition of L1210 growth in flask culture was achieved at concentrations of 200 micrograms/ml of warfarin, 75 micrograms/ml of vitamin K1, and 4 micrograms/ml of vitamin K3. Combined use of vitamin K and warfarin enhanced cytotoxicity because a concentration of 1 micrograms/ml of vitamin K3 together with 70 micrograms/ml of warfarin resulted in nearly complete inhibition of L1210 growth. Comparable inhibition of growth was seen against malignant murine cell lines in the soft agar assay system, where greater than 70% decrease in colony formation was seen with vitamin K3 at concentrations of 6.4 micrograms/ml for L1210 leukemia and 1 microgram/ml for HII4E hepatoma lines. Vitamin K3 was also cytotoxic in the same dosage range when tested in vitro against the 34 human tumor explants in the soft agar assay system. Tumor types evaluated included adenocarcinoma of the breast (16 patients), ovary (five), colon (two), stomach (two), kidney (two), and unknown primary (two); squamous cell carcinoma of the lung (two); melanoma (one), transitional cell carcinoma of the bladder (one); and hepatocellular carcinoma (one).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamin K3 inhibition of malignant murine cell growth and human tumor colony formation. 400 75

The factor(s) present in extracts prepared from the brains of newborn A/J or C57B1/6 mice, which inhibits S20Y neuroblastoma cell growth in vitro, was partially characterized. Twice as much inhibitory activity was extracted per gram wet weight of brain than torso, and inhibitor recovery was greatest in extracts prepared from brains of mice 1 week or less in age. The inhibitory factor(s) was water-soluble and was stable to heating at 100 degrees C, to freezing, and to lyophilization. It was susceptible to the action of pronase. The factor(s) behaved like a molecule of molecular weight approximately 700 upon passage through ultrafiltration membranes. Growth of rat hepatoma (H4), murine melanoma (B16), and transformed murine fibroblasts (WT19 and B6-HCMV) was not significantly inhibited by brain extract. Growth of rat glioma cells (C6) was significantly reduced but to a lesser degree than that of murine neuroblastoma cells (S20Y and N115) and glioma cells (G26-20). These results suggest that the inhibitor expresses a cell specificity.
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PMID:Partial characterization of a brain extract factor(s) inhibitory to transformed neural cells. 405 87

Forty-eight patients with ;cold areas' on (99m)Tc sulphur colloid liver scintiscans were scanned again using (75)Se-selenomethionine. In 11 patients with primary hepatocellular carcinoma considerable uptake of (75)Se-selenomethionine could be demonstrated in the area of the tumour and uptake of (75)Se-selenomethionine was also observed over extrahepatic metastases in two of these cases. In contrast uptake was low in cholangiocellular carcinoma, Kupffer cell sarcoma, and secondary hepatic deposits (excepting melanoma metastases). No cause for the ;cold area' on the (99m)Tc scan could be discovered in 16 of 25 patients with cirrhosis and in these patients the uptake of the two isotopes in the area of the ;false positive' filling defect was almost equal. Positive identification of primary hepatocellular tumours using this dual scanning technique can be of value in determining and assessing treatment by surgery or cytotoxic therapy.
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PMID:75se-selenomethionine in the scintiscan diignosis of primary hepatocellular carcinoma. 432 48

Influences of different incubation temperatures within the physiological range on three different biological activities of human leukocyte-derived alpha interferon (IFN) (the antiviral effect, the antiproliferative activity, and the augmentation of natural killer cell (NK) activity) were investigated in vitro. Using the plaque-reduction assay (U cells challenged with VSV), the antiviral activity by IFN was found to be lower at 35 degrees C and higher at 38 degrees C and 39 degrees C than at 37 degrees C. Using the CPE (cytopathogenic effect) inhibition technique (Vero cells challenged with VSV), the antiviral activity was slightly enhanced at 38 degrees C, 39 degrees C, and 40 degrees C, respectively, when compared with 37 degrees C. The antiproliferative activity on Daudi cells and G-361 melanoma cells was enhanced at elevated temperatures. On the other hand, the antiproliferative activity on PLC/PRF/5 hepatoma cells was lower at 38 degrees C and 39 degrees C than at 37 degrees C, but higher at 40 degrees C. NK activity of PBL after 2 h incubation at 41 degrees C was remarkably lower than that at 37 degrees C, while it was not affected by 2 h incubation at 35 degrees C and 39 degrees C, respectively. When PBL was treated with IFN for 2 h at the temperatures described above, NK activity was equally augmented at all temperatures tested. Our results suggest that elevated incubation temperature potentiates the antiviral and the antiproliferative activities, but does not affect the NK augmenting activity of HuIFN-alpha (Le).
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PMID:Temperature influences on different human alpha interferon activities. 609 82

We tested the ability of the in vitro clonogenic assay (CLAS) to predict clinical response for patients with solid tumors. Patients had objectively measurable disease and received at least one course of chemotherapy. The correlation between clinical responses and in vitro sensitivity was evaluated retrospectively. Tumor types included melanoma (19), sarcoma (five), hepatoma (one), and carcinoma of the stomach (two), colon (three), lung (one), and breast (one). Five patients received two separate courses of chemotherapy with different drugs or drug regimens. In nine of 11 (82%) instances, tumors were sensitive to a particular drug, and the patient had at least 50% regression of tumor following treatment with the tested drug. Two patients whose tumors were sensitive in vitro had no evidence of clinical response. In 25 of 26 assays, the CLAS accurately predicted tumor resistance, and only one patient had evidence of clinical response (96%). Associations of in vitro results with clinical responses were highly significant. The CLAS can accurately predict the chemosensitivity of a variety of solid tumors.
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PMID:Clinical correlations with drug sensitivities in the clonogenic assay: a retrospective study. 617 23

The paper reports on the experiments carried out for the evaluation of the effect of two antiproteinases, aprotinin, and epsilon-amino caproic acid (EACA), on several transplantable tumors and cells in culture. It was demonstrated that aprotinin has a preferential therapeutic effect on the solid form of L1210, in comparison with its ascitic form. Treatment with aprotinin of Lewis lung carcinoma, Melanoma B16, and Hepatoma 22, in a limited chronic time schedule 1-9, and 1-11 brought no significant increase in survival; positive therapeutic effects had been shown for the first and the last of the tumors mentioned with life-time injections of the drug. Moreover, aprotinin treatment increased the number of lung nodules for the Lewis lung carcinoma inoculated either subcutaneously or intravenously. EACA applied same schedule had no effect on the survival of tumor-bearing animals. These data are discussed in terms of their relevance to antiproteinase therapy in human cancer. No selective inhibition of proliferation for more tumorigenic cell culture lines of spontaneous and viral origin was demonstrated after treatment with both compounds.
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PMID:Effect of two antiproteinases on the growth of transplantable tumors and the proliferation of untransformed and transformed cells in culture. 618 75

The ultrastructural features on interaction of tumor cells and blood vessels in the process of hematogenous metastasis formation by Yoshida sarcoma, 5 strains of Yoshida rat ascites hepatoma, murine B16 melanoma variant sublines, and others have been described and illustrated. Intravasation and extravasation of tumor cells appeared to be similar cell biological phenomenon, in which two different ways were involved: 1) tumor cells migrated through the pores in the vascular walls which were produced by direct actions of tumor cells, and 2) endothelial cell cytoplasms enclosed the tumor cells neighboring to the vascular walls and as a result intravascular or extravascular tumor cell movement occurred. Tumor cells arrested in a target organ were in close contact with vascular endothelial cells and further with basement membrane when the endothelial linings were removed. In some regions we found junction-like structures between these cells. This appeared to be corresponding to the lodgement of tumor cells in the target organ. Extravasated tumor cells produced three different features of metastatic lesions in the combination of tumor strain and the organ affected; formation of tumor nodules accompanying neovasculature, spreading of tumor cells along the perivascular tissue of an organ, and diffuse infiltration of tumor cells in an organ. It has been discussed that these features in every process mentioned above are determined by specific interaction of tumor cells and host cellular components, especially blood vessels including tumor neovasculature.
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PMID:[Cancer metastasis and blood vessels]. 619 86

Murine tumors contain low molecular weight factors that inhibit macrophage accumulation at inflammatory foci. Certain oncogenic murine leukemia viruses contain similar inhibitory activity and the active component of the retroviruses was shown to be the envelope protein P15E. A number of murine malignant and nonmalignant cell lines, as well as primary tumors, have now been examined to determine whether production of retroviral P15E or a related protein is characteristic of neoplastic cells. Tumor lines examined included the Hep 129 hepatocarcinoma, BP8 fibrosarcoma, RL1 lymphoma, and three variants of the B16 melanoma. Tumor lines were virus negative by electron microscopy. Nonmalignant cells examined included ST0, 3T3/BALB, and 3T3/L1 fibroblasts and unstimulated, as well as mitogen-stimulated murine splenocytes. Cells were pulse-labeled with [35S]methionine, proteins immunoprecipitated with two monoclonal antibodies to P15E and analyzed by SDS-PAGE and gel fluorography. All tumor lines synthesized a approximately 19,000-dalton protein that co-migrated with retroviral P15E on SDS-PAGE. None of the nonmalignant cells synthesized this protein. Two-dimensional gel electrophoresis of the proteins precipitated from two B16 melanoma lines by monoclonal anti-P15E showed them to be physicochemically similar to P15E from Rauscher leukemia virus. A competition ELISA assay for P15E was developed and confirmed the results obtained by metabolic labeling and demonstrated P15E-related antigens in the tumor cell lines and also in the ascites fluid of mice injected with Hep 129 cells. More importantly, P15E antigens were expressed in both a spontaneous mammary adenocarcinoma and in a primary methylcholanthrene-induced fibrosarcoma. Nonmalignant tissues from animals bearing these tumors contained no detectable P15E antigen. Extracts from the primary fibrosarcomas, when injected into the thighs of mice, inhibited the intraperitoneal accumulation of inflammatory macrophages. The inhibitory activity was specifically removed by absorption with monoclonal antibody to P15E. These results suggest that synthesis of the immunosuppressive retroviral protein P15E, or a very similar protein, routinely occurs during the growth of murine neoplastic cells. This P15E-related protein is present in spontaneous murine primary tumors as well as in all murine tumor cell lines tested. The expression of such proteins by transformed cells in vivo could confer a selective advantage for their sustained growth since they would be more likely to escape immune surveillance.
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PMID:Murine malignant cells synthesize a 19,000-dalton protein that is physicochemically and antigenically related to the immunosuppressive retroviral protein, P15E. 619 38

Protamine sulfate reversibly inhibits serum-induced mitogenic stimulation of several nontransformed and neoplastic cell types in vitro. Fifty percent inhibition was induced by approximately 120-150 micrograms protamine sulfate/ml. Cells were affected directly, and inhibition depended on the duration of cell exposure. Heparin, chondroitin sulfate, heparan sulfate, and dextran sulfate neutralized protamine sulfate effects during the early stages of treatment. Nontransformed cells [bovine aortic endothelial cells, adult human gingival fibroblasts (strains 423 and 1101), fetal rat skin (strain 921-K) and muscle fibroblasts] required longer exposure to induce inhibition than did neoplastic cells [rat 3-methylcholanthrene-induced fibrosarcoma cell lines (MCA-6 and MCA-9), a macrophage-like cell line (NCTC-3749), Walker 256 rat carcinoma cells (ATCC-CCL-38), rat Morris hepatoma cells (ATCC-CCL-144), murine melanoma cells (B16), and rat bladder squamous cell carcinoma cells (804-G)]. Other polycationic compounds, including histone type VIII-S, poly-L-lysine, poly-L-arginine, and protamine (free base), were also effective inhibitors, whereas the basic proteins cytochrome c and lysozyme had no effect. Poly-L-histidine, poly-L-glutamic acid, poly-L-aspartic acid, and dextran blue also had no inhibitory effect.
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PMID:Protamine sulfate inhibition of serum-induced mitogenic responses: differential effects on normal and neoplastic cells. 621 Mar 90


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