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 neutral red (NR) cell viability assay was used with various cell types of human origin to quantitate the potency of T-2 mycotoxin and its metabolites. The human melanoma SK-Mel/27 cell line was the most sensitive, with a midpoint cytotoxicity value of 2.8 ng of T-2 per ml. With the human hepatoma cell line, HepG2, the sequence of potency for a series of mycotoxins was T-2 greater than HT-2 greater than T-2 triol greater than T-2 tetraol.
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PMID:Cytotoxicity of T-2 toxin and its metabolites determined with the neutral red cell viability assay. 189

This article contains a survey of works, published in the last few years on plasminogen activators inhibitors in neoplastic tissues. These inhibitors belong to a heterogenous group of proteins, having different molecular weights and specific ways of acting. They exemplify immunological relationship to known inhibitors of fibrinolysis from normal tissues--i.e. the inhibitors from endothelial cells--(PAI-1) and placental inhibitor--(PAI-2). To PAI-1 type belong: acid-stabile inhibitor of fibrinolysis with Mr 50,000 from HTC hepatoma cells in rats, acid-labile inhibitor Mr 42,770 produced by HepG2 human hepatoma cells; the inhibitor with Mr 54,000 from HT 1080 human cells from fibrosarcoma and single-chain acid-stabile inhibitor with Mr 50,000 from MJZJ melanoma cells. In PAI-2 type we can mention the inhibitor with Mr 47,000 from U-937 histiocytic lymphoma cells.
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PMID:[Plasminogen activator inhibitors from neoplastic tissues]. 192 93

Bradykinin was found to induce production of IL-6 in human diploid fibroblasts, as well as in a hepatoma-derived cell line, but not in a human melanoma or an osteosarcoma cell line. With the exception of the melanoma cell line, these cells were also found to be responsive to IL-1 beta. The response to bradykinin was faster but less high than that induced by IL-1. Experiments in which IL-1 (-alpha or -beta) and bradykinin were applied simultaneously revealed a synergistic interaction. Of the other cytokines tested, TNF-alpha and IFN-gamma weakly induced IL-6. Neither IL-2, IFN-alpha, nor IFN-beta was able to induce IL-6, either in the absence or the presence of bradykinin. These observations constitute further evidence for the existence of interactions between cytokine and noncytokine peptides, thus linking the neuroendocrine and immune systems.
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PMID:Bradykinin induces interleukin-6 and synergizes with interleukin-1. 193 73

A new murine monoclonal IgG3 antibody (Mab 1H10) was developed with specificity for human cervical carcinoma and several other tumor types. Antibody reactivity against a panel of tumor cell lines was examined by indirect immunofluorescence and quantified by flow cytometry. Mab 1H10 reacted with cervical, colorectal and bladder carcinoma cells and to a lesser extent melanoma and hepatocellular carcinoma cells but did not react with human fibroblasts, lymphocytes or RBCs. Mab 1H10, as assessed by immunohistochemical staining, bound 40/97 cervical carcinoma tissue samples, 8/16 colorectal carcinoma samples as well as a population of osteogenic sarcoma and lung, ovarian and bladder carcinoma tissues. Mab 1H10 did not react with any normal tissue or cell samples tested including cervix, ovary, breast, liver, colon, bladder, lung, spleen, cerebrum, lymphocytes or RBCs. Mab 1H10 may be useful for the targeting of drugs, toxins or radioisotopes to cervical carcinoma in humans.
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PMID:New monoclonal antibody against human cervical carcinoma with diagnostic and therapeutic potential. 193 67

Cytosolic extracts prepared from perfused whole liver or purified hepatocytes of C57BL/6 mice inhibited interleukin-2--and concanavalin A--induced spleen cell proliferation in vitro. In contrast, cytosolic extracts from purified nonparenchymal liver cells had no effect. Arginase and very-low-density lipoprotein were previously identified as two immuninhibitory substances present in liver cytosolic extracts. We demonstrated, however, that inhibitory activity remained after removal of very-low-density lipoprotein and arginase from liver cytosolic extract by repeated ultracentrifugation and gel filtration chromatography, respectively, suggesting the presence of another inhibitor. Further purification by anion-exchange chromatography and chromatofocusing led to the isolation of a novel liver-derived immunohibitory factor. This liver-derived immunoinhibitory factor is sensitive to pronase digestion and heat and acid treatment; it has an estimated isoelectric point of 8.25. The Mr of liver-derived immunoinhibitory factor is 28 kD as estimated from its migration on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, which is identical under both reducing and nonreducing conditions, indicating a monomeric nature of this protein. Amino acid composition analysis discloses that liver-derived immunoinhibitory factor is relatively rich in glycine and proline residues. Interleukin-2--induced spleen cell proliferation in vitro is inhibited by ths liver-derived immunoinhibitory factor, with a 50% inhibitory dose of 1.4 nmol/L. Furthermore, the biological activity of the liver-derived immunoinhibitory factor is not confined to mouse spleen cells, since the growth of B16 mouse melanoma and H35 rat hepatoma cells is also inhibited. A comparison with other liver-derived immunoinhibitors reported previously supports our claim that the liver-derived immunoinhibitory factor is a novel inhibitory protein.
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PMID:Isolation and characterization of a novel liver-derived immunoinhibitory factor. 193 91

Experiments were done to determine the effect of interleukin-1-beta (IL-1 beta) on metastasis formation in different tumor systems. Intravenous administration of 1 microgram of human recombinant IL-1 beta given 1 hour before tumor cell injection augmented lung colony formation (experimental metastases) by the human A375 melanoma variants, the human HT-29M colon carcinoma, the SN12-K1 renal carcinoma in nude mice, the murine B16 melanoma variants, and the murine UV-2237M fibrosarcoma in syngeneic recipients. The same treatment did not induce lung colony formation by a human rectal carcinoma (HCC-P2988) or by a murine reticulum cell sarcoma (M5076), both of which are not metastatic to the lung. Spontaneous metastases were studied in C57BL/6 mice bearing the B16-BL6 melanoma (metastatic to the lung) in their footpad and the M5076 reticulum cell sarcoma (metastatic to the liver) subcutaneously. Daily intraperitoneal treatment with 1 microgram of IL-1 beta increased lung and liver metastases. These findings indicate that treatment of mice with IL-1 beta can increase the number of artificial or spontaneous metastases and that this effect is not limited to a single tumor type or to a specific organ.
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PMID:Effect of interleukin-1-beta on metastasis formation in different tumor systems. 198 86

This study examined the pathophysiological role of parathyroid hormone-related protein (PTHrP) in humoral hypercalcaemia of malignancy (HHM). Seven human tumour xenografts were analysed in nude mice; five tumours (KEsC-2, oesophageal carcinoma; FA-6, pancreatic carcinoma; SEKI, melanoma; Lu-65A and Lu-61, lung carcinomas) were associated with hypercalcaemia and two tumours (MIA PaCa-2, pancreatic carcinoma; PLC/PRF/5, hepatocellular carcinoma) with normocalcaemia. Northern blot analyses, radioimmunoassay and bioassay confirmed the synthesis of PTHrP-like peptides by all five tumours associated with hypercalcaemia, but not by the two associated with normocalcaemia. These observations indicated a very close relationship between the production of PTHrP and the development of HHM. Gel filtration studies of three tumour tissue extracts revealed at least two different molecules with both PTHrP-like immunological and biological activities. One peak eluted at a position between PTHrP (1-141) and cytochrome C and the other at a position identical to cytochrome C. These results suggest that PTHrP molecules with a molecular size equal to or greater than cytochrome C participate as causative agents of HHM. All five tumour xenografts caused hypercalcaemia when grown to a size of 1.5 g in nude mice. Under cell culture conditions, four original cell lines, KEsC-2, FA-6, SEKI and Lu-65A secreted 450.0, 45.0, 3.6 and 3.0 pmol of immunoreactive PTHrP/1.5 x 10(9) cells (approximately equivalent to 1.5 g wet weight) 24 h-1 into their respective culture media. Since a subcutaneous infusion of 100 pmol 24 h-1 of PTHrP (1-34) into nude mice was sufficient to induce significant hypercalcaemia, we speculate that PTHrP alone released from tumour cells could induce hypercalcaemia at least in the case of KEsC-2, and possibly in FA-6. With regard to other tumours associated with hypercalcaemia, further examination of PTHrP and other compounds with bone-resorbing activity in these transplantable tumours is required to obtain a better understanding of this morbidity.
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PMID:Production of parathyroid hormone-related protein in tumour xenografts in nude mice presenting with hypercalcaemia. 199 2

We have shown the in vivo usefulness of a novel chimera tumor necrosis factor (TNF), called rTNF-STH, which was constituted with human thymosin beta 4 and recombinant human TNF-SAM1. Tumor necrosis was induced by intravenous injection of a smaller amount of rTNF-STH (1 x 10(3) U/mouse, 0.67 microgram/mouse) than rTNF-alpha or rTNF-S (1 x 10(4) U/mouse, 2.5-5 micrograms/mouse). Significant antitumor effects of rTNF-STH to Meth A fibrosarcoma, B16 melanoma, MH134 hepatoma, or Lewis lung carcinoma (3LL) were observed by systemic injection of rTNF-STH at the maximum tolerable dose of 1 x 10(4) U/mouse (6.7 micrograms/mouse); this dose did not cause regression of tumors by conventional rTNF-alpha. rTNF-STH showed a significant prolongation of its half-life in serum. The average calculated half-life of the chimera protein is about 110 min, which is 15 times longer than that of original TNF-SAM1 (7.5 min). On the basis of this prolongation of half-life of rTNF-STH and its efficient hemorrhagic necrotic activity, the antitumor effect of rTNF-STH--as compared with that of the known TNF species--is discussed. Findings indicate that use of the chimera protein to alter the N-terminal region of TNF may be a promising approach to obtain molecules that more favorably attack tumors and other diseases than conventional rTNFs.
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PMID:Antitumor activity of a novel chimera tumor necrosis factor (TNF-STH) constructed by connecting rTNF-S with thymosin beta 4 against murine syngeneic tumors. 204 90

One hundred twenty-six dogs with histologically confirmed, measurable malignant tumors were evaluated in a prospective study to determine the response to the antineoplastic drug mitoxantrone. Ninety-five dogs had been refractory to one or more treatment modalities (surgery, n = 57; chemotherapy other than mitoxantrone, n = 37; radiation, n = 4; whole body hyperthermia, n = 1). The extent of neoplastic disease was determined immediately before each dose of mitoxantrone was administered (1 to 10 doses, 2.5 to 5 mg/m2 of body surface area, IV) 21 days apart. Each dog was treated with mitoxantrone until the dog developed progressive disease or until the dog's quality of life diminished to an unacceptable level as determined by the owner or attending veterinarian. A partial or complete remission (greater than 50% volume reduction) was obtained in 23% (29/126) of all dogs treated. Tumors in which there was a partial or complete remission included lymphoma (11/32), squamous cell carcinoma (4/9), fibrosarcoma (2/9), thyroid carcinoma (1/10), transitional cell carcinoma (1/6), mammary adenocarcinoma (1/6), hepatocellular carcinoma (1/4), renal adenocarcinoma (1/1), rectal carcinoma (1/1), chondrosarcoma (1/2), oral malignant melanoma (1/12), cutaneous malignant melanoma (1/1), myxosarcoma (1/1), mesothelioma (1/1), and hemangiopericytoma (1/1). Our results indicated that mitoxantrone induces measurable regression in various malignant tumors in dogs.
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PMID:Efficacy of mitoxantrone against various neoplasms in dogs. 206 Nov 77

Predisposing factors to cervical cancer development are age, smoking, socioeconomical status, parity, and number of sex partners. Long-term oral contraceptive (OC) use and less than 50 mg estrogen dose have been weakly linked to increased cancer risk. Regular examination and switching to other contraception in case of cervical intraepithelial neoplasia is recommended. Estrogen in sequential pills (Ovacon) increases the risks of uterine cancer by affecting the mucosa. Predisposing factors are: absence of pregnancy (nulliparity), postmenopause, hypertension, and diabetes. Parity reduces the risk. The risk is reduced in combined pills and after use of 1 year. Protection is offered by the progesterone component for 10-20 years after cessation of use. Ovarian cancer is prevented by parity and OC use even 10 years later. High estrogen levels inducing frequent ovulation damage the ovaries. Promoting factors are: old age, avoidance of breast feeding, and overweight. Breast cancer promoters are 1st pregnancy in older age, early menarche, and no pregnancy at all. OC use under age 25 and before 1st pregnancy are significant risk factors. High progesterone levels are associated with increased mitotic activity in the breast. Rare benign fibrocysts can develop into breast cancer. OC use is connected to hepatoma development mainly estrogen-induced. Liver cancer was found twice as high in OC users. Hepatoma often ruptures causing hemorrhage. 8% of liver tumors are malignant with a survival rate of 50% of patients to 4.8 years. The possible association of OCs to skin melanoma and hypophysial tumors could not be confirmed. OCs regulate menstruation, reduce bleeding, protect against uterine and ovarian cancer, but cervical and breast cancers have been influenced by them.
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PMID:[The contraceptive pill and cancer]. 207 68


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