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)

A human blood group B-active glycosphingolipid, belonging to the ganglio-series, was isolated from rat glioma cell line RG2 subcutaneous isografts. The oligosaccharide structure of the glycosphingolipid was completely characterized as Gal alpha 1-3(Fuc alpha 1-2)Gal beta 1-3GalNAc beta 1-4Gal beta 1-4Glc beta 1- 1'ceramide by NMR spectrometry, negative fast atom bombardment-mass spectrometry, sequential degradation by glycosidases and methylation analysis. Human blood group B antigenicity and the activity of this glycosphingolipid were confirmed by immunostaining on thin-layer chromatography and the inhibition of hemagglutination, respectively. Although the lipid has been detected in rat granuloma, bone marrow cells, spleen, thymus, ascites hepatoma cells and gastric mucosa, this is the first report of the occurrence of the B-active lipid in glioma.
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PMID:Human blood group B-active ganglio-glycosphingolipid in rat glioma. 839 23

Radiolabeled monoclonal antibodies have been used for radioimmunotherapy studies with human tumor spheroids and murine and human tumor xenografts in experimental animals. This paper reviews the work that has been performed in these models with different types of cancer, and highlights those papers that have presented dosimetry estimates and attempts to correlate the findings. Radioimmunotherapy studies in multicell spheroids, as a model for micrometastases, have been performed in human neuroblastoma, colon cancer, and melanoma cell lines using 131I-, 125I-, 186Re-, and 212Bi-labeled antibodies. The uniform geometry of the spheroid has allowed radiation dose estimates to be made. Up to three logs of cell kill have been achieved with 131I- and 186Re-specific antibody with minimal toxicity from labeled nonspecific antibody, but 212Bi-antibody had little effect because of its short half-life as shown by Langmuir. It appears that the two most important factors for therapeutic efficacy in this model are good penetration of the radiolabeled antibody and an adequate radionuclide half-life to allow penetration of the immunoconjugate prior to significant radionuclide decay. Radioimmunotherapy studies in animals bearing transplants of colon cancer, leukemia, lymphoma, hepatoma, renal cell carcinoma, neuroblastoma, glioma, mammary carcinoma, small cell lung carcinoma, cervical carcinoma, ovarian carcinoma, and bladder cancer have been performed with 131I, 90Y, 186Re, 153Sm, and 177Lu beta emitting, and 212Bi alpha emitting radionuclides conjugated to monoclonal antibodies. A few studies compared different radionuclides in the same model system. The approaches that have been used in these studies to estimate tumor dosimetry include the MIRD approach, thermoluminescent dosimetry, autoradiography, and comparison to external irradiation. The majority of investigators have estimated the dose to tumor and normal organs using MIRD-based calculations (time-activity curve and equilibrium dose constant method). The range of tumor doses has been between 17 and 11 171 mGy/MBq of administered radioactivity. The effectiveness of radiolabeled monoclonal antibody therapy depends on a number of factors relating to the antibody such as specificity, affinity, and immunoreactivity. The density, location, and heterogeneity of expression of tumor-associated antigen within tumors will affect the localization and therapeutic efficacy of radiolabeled antibodies, as will physiological factors such as the tumor vascularity, blood flow, and permeability. These factors are discussed and examples are presented.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Experimental radioimmunotherapy. 849 64

Schwannoma-derived growth factor (SDGF) is a member of the epidermal growth factor (EGF) family, having mitogenic activity on rat astrocytes, fibroblasts and Schwann cells. The SDGF gene is significantly expressed in the newborn rat lung and in the adult rat sciatic nerve. However, except for one rat schwannoma cell line, from which SDGF and its cDNA were isolated, nothing is known about SDGF expression in established tumor cell lines. We examined the expression level of the SDGF gene in a variety of rat tumor cell lines by Northern blotting and found that it was increased in 11 of 25 established lines. The most abundant SDGF mRNA, which was about 50-fold higher than in the newborn rat lung, was expressed in rat liver adenoma dRLa74 cells. In rat glioma cell lines, such as C6, 9L and T9, and in the rat hepatoma dRLh84 and H411E cells, the SDGF expression level was about 10-fold higher than in the newborn rat lung. In 8 of 13 cell lines expressing SDGF mRNA, the EGF receptor (EGFR) gene, the product of which is regarded as a functional receptor of SDGF, was co-expressed. In addition, transfected gene-dependent anti-sense SDGF RNA expression under the control of the human metallothionein promoter significantly suppressed the in vitro growth as well as in vivo tumorigenicity of 9L glioma cells. Our results suggest that SDGF acts as an autocrine growth factor in the development and growth of rat tumors such as gliomas.
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PMID:Increased expression of schwannoma-derived growth factor (SDGF) mRNA in rat tumor cells: involvement of SDGF in the growth promotion of rat gliomas. 862 Dec 57

Gliomas are tumors which have been found to exhibit consistent genetic changes. Recent studies have shown mitochondrial DNA is also altered in these tumors, and include large deletions and gene amplification. Other studies of the mitochondrial genome in cancer have revealed a variety of different alterations, including the localization and insertion of mitochondrial DNA into the nucleus and nuclear genome in HeLa cells and diethylnitrosurea-induced hepatoma cells. Whether these changes are ontogenically early in the multistep pathway to the development of malignancy, or if this phenomenon occurs in human glial tumors is unknown. I sought to study these questions in a panel of unselected primary glial tumors of pathologically low grade. Fifteen tumors were assessed with a mitochondrial cDNA probe with homology to positions 1679-1948, and 2017-2057. All low-grade tumors revealed increases in copy number when compared to a normal brain control. Nuclear suspensions of these tumors were evaluated by fluorescent in situ hybridization (FISH), using the entire mitochondrial genome as a probe after labeling with rhodamine. All tumors showed evidence of mitochondrial sequence localization within the nuclei. A corresponding glioblastoma and two normal brain specimens were also evaluated which did not have amplification of the mitochondrial genome; FISH with the mitochondrial probe revealed minimal hybridization signal within the nuclei of these samples. Mitochondrial DNA nuclear localization can be found in primary low-grade brain neoplasms, and is correlated to increases in mitochondrial DNA.
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PMID:Evidence for association of mitochondrial DNA sequence amplification and nuclear localization in human low-grade gliomas. 869 3

Current treatment for disseminated prostate cancer, whether progressive or hormone-resistant, do not improve survival. Insulin growth factors (IGFs) are potent stimulants of prostate epithelial cells growth, their presence having been demonstrated in high quantities in several tumours such as lung, hepatoma, pheochromocytoma, malignant glioma and breast cancer. Local management of growth factors production could improve the results of second line therapy in hormone-resistant prostate cancer. Levels of IGF-I were determined by radioimmunoassay (RIA) in normal (n = 5), hyperplastic (n = 5) and tumoral (n = 8) prostate tissue. Presence of IGF-I is confirmed in all tissues (9.62 +/- 5.81; 8.32 +/- 7.81 and 6.02 +/- 1.42 ng/mg protein, respectively) but no significant differences are displayed among the three groups.
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PMID:[Insulin growth factor I (IGF-I) in normal, hyperplastic, and tumor prostatic tissue]. 876 97

Recently we demonstrated that rat glioma cells when transfected with a vector encoding antisense IGF-I c-DNA lost tumorigenicity and induced a tumor specific immune response involving CD8+ lymphocytes. Here we showed, using immunostaining flow cytometry analysis, that the transfected cell lines, rat C-6 glioma and rat LF hepatoma, expressed an increase level of MHC-class I, and even the amount of MHC-I was found to be higher in the transfected hepatoma, than in the transfected glioma cells. This increased expression of MHC-I could contribute to the final immune recognition of tumour immunogenicity.
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PMID:[Immunotherapy of tumors expressing IGF-I]. 888 Dec 77

The influence of aniso-osmolarity on the activity of the MAP kinases Erk-1 and Erk-2 was studied in C6 glioma cells. Hypo-osmotic treatment (205 mosmol/l) led to an increased activity of Erk-1 and Erk-2 within 3 min, which became maximal at 10 min and returned to basal level within 120 min. In contrast, Erk activity was reduced under hyper-osmotic conditions (405 mosmol/l), compared to the normo-osmotic control (305 mosmol/l). Erk activation was accompanied by a mobility shift of Raf-1. Hypo-osmotic exposure increased the cytosolic Ca2+ concentration ([Ca2+]i). Absence of extracellular Ca2+ largely abolished the [Ca2+]i response to hypo-osmolarity, whereas Erk activation following hypo-osmotic stimulation remained unaffected, suggesting a Ca2+ independence of the osmosignalling pathway to the MAP kinases. Both the Ca2+ response as well as the Erk activation following hypo-osmotic exposure were maintained in the presence of the phospholipase C inhibitor U73122. Application of 8-CPT cAMP, forskolin/isobutylmethylxanthine or isoproterenol blocked Erk activation following hypo-osmotic treatment of the cells, suggesting a role of the Ras/Raf pathway upstream from Erk-1 and Erk-2. Protein kinase C (PKC) is unlikely to play a role in the hypo-osmolarity- induced signalling towards MAP kinases, as revealed by inhibition of PKC with Go6850. Inhibition of pertussis- or cholera toxin-sensitive G-proteins as well as inhibition of tyrosine kinases with genistein and of PI3 kinase by wortmannin had no effect on the Erk response to hypo-osmolarity. It is concluded that osmosignalling in C6 glioma cells differs upstream of the MAP kinases from that observed in primary rat astrocytes, H4IIE rat hepatoma cells and isolated rat hepatocytes.
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PMID:Osmosignalling in C6 glioma cells. 900 90

Tamoxifen has been used most commonly to treat breast and endometrial cancer, two malignancies in which the antiestrogenic properties of tamoxifen have substantial therapeutic benefit. However, tamoxifen has been used in the treatment of other cancers as well, some in which an antiestrogen may be effective, but others in which estrogen receptor is not expressed. In estrogen receptor-negative cancers, tamoxifen has been shown to have therapeutic activity at doses approximately fourfold to eightfold above those used for estrogen receptor inhibition. It is thought that the primary mechanism of tamoxifen in estrogen-negative tumors is inhibition of protein kinase C. Clinical trials of tamoxifen in ovarian cancer, hepatocellular carcinoma, desmoid tumors, malignant glioma, pancreatic carcinoma, melanoma, and renal cell carcinoma are reviewed.
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PMID:Tamoxifen for the treatment of malignancies other than breast and endometrial carcinoma. 904 18

Laminin is a major glycoprotein specific to basement membranes. Hepatocellular carcinoma tissue synthesize and secrete abundant laminin. By DNA-protein interaction assays, we have identified nuclear factors specific to hepatocellular carcinoma cells. The comparison of nuclear factor binding by Southwestern analysis with B1 and B2 laminin promoters revealed different patterns of nuclear factor binding in different cells types. In hepatocellular carcinoma, HepG2 cells, a specific pair of proteins (P105 and P98) consisting of 105 and 98 kDa were identified as common nuclear factors for both B1 and B2 laminin promoters, while in completely diverse human glioma cells (U251), various different and greater number of nuclear proteins ranging from 212 to 68 kDa were detected to interact separately with laminin B1 and B2 genes.
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PMID:Hepatocellular carcinoma cell type specific interaction of P105 and P98 nuclear factors with laminin B1 and B2 genes. 905 41

A series of 120 pathologically verified intraspinal tumors was analyzed for the relative incidence and location of the tumors as well as the distribution of age and sex. These data were compared to series from Taiwan, mainland China, Thailand, Korea, Japan, Iran, India, and countries in the West. The ratio of brain to intraspinal tumors was about 5:1 in Taiwan, higher than those reported in China, Korea, and in the West. The male to female ratio is about six to five. For most tumors, male predominance is noted except for meningioma. The incidence of intraspinal tumors in the order of frequency is nerve sheath cell tumor(NSCT), metastatic tumors, meningioma, glioma, congenital tumors, and vascular tumors. In the East, the incidence of NSCT is about 40%, and meningioma is about 10%. In the West, they are both about 20%. Congenital tumors accounted for only 3.3%. In China, it was about 12% and this is the highest incidence of dysembryoplastic tumors in the world. Glioma has similar incidence (about 10%) in Taiwan, China, Thailand, Japan, and Iran (about 10%), whereas it is about 15% in the West and India. Korea has the highest incidence of glioma, (32.3%). Low incidences of metastatic intraspinal tumors (4.6-5.5%) were noted in China and Japan, but a higher incidence (14.2-24.2%) was seen in Taiwan, Iran, and the West. The most common metastatic tumors in the order of frequency is tumors of unknown origin, lung cancer metastasis, hepatoma, and breast cancer. The high percentage of unknown origin of metastasis may have resulted from loss of follow-up and lack of postmortem studies.
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PMID:An analysis of intraspinal tumors in south Taiwan. 917 84


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