Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monoclonal antibodies (MAb; DMAb, monoclonal antibodies derived at Duke Medical Center) directed against the oncofetally expressed lactotetraosyl gangliosides 3'-isoLM1 (IV3NeuAc-LcOse4Cer) and 3',6'-isoLD1 (IV3NeuAc,III6NeuAc-LcOse4Cer) were produced and their reactivity spectra compared to that of the alpha-3'-isoLM1 MAb SL-50. The IgM MAb SL-50 defines the epitope NeuAc (or NeuGc)alpha 2-3Gal beta 1-3GlcNAc, the terminal sequence of both gangliosides. SL-50 requires an unsubstituted GlcNAc residue; IgM DMAb-14 will accept the alpha 2-6 linked sialic acid to GlcNAc found in 3',6'-isoLD1. Immunohistochemical localization of 3'-isoLM1 was performed on 31 biopsy specimens of human gliomas; 15 (48%) expressed 3'-isoLM1 as defined by binding of MAb SL-50. Staining of small anaplastic cells, giant cells, and the glial component of gliosarcomas was observed. Neoplastic gemistocytes, when present, showed particularly intense staining. The 3'-isoLM1 and 3',6'-isoLD1 distribution in cultured cell lines and derived xenografts of primary tumors of the human central nervous system and of embryonal or neuroectodermal tumor derivation was determined. Six of 29 cell lines expressed 3'-isoLM1: 2/16 gliomas, 3/3 teratomas, 1/1 pancreatic adenocarcinoma. No cell line expressed detectable 3',6'-isoLD1 by immunostain analysis of ganglioside extracts. The 3'-iso-LM1-positive cell lines expressed it in xenograft form; in five xenografts, the corresponding cell lines of which were 3'-isoLM1-negative, it was a proportion of the monosialoganglioside fraction. 3',6'-isoLD1 was detected in two xenografts, D-54 MG (glioma) and PA-1 (teratoma). The demonstration of 3'-isoLM1 in gliomas in in vivo forms and the relatively infrequent expression by derived cultured cells suggest that ganglioside expression is modified by environmental forces. Expression of 3'-isoLM1 and 3',6'-isoLD1 in fetal and neonatal brain, in intense reactive astrocytosis such as polyunsaturated fatty acid lipidosis, and in primary neoplasms of the central nervous system suggests their role in cell-cell attachment during development, migration, and neoplastic transformation.
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PMID:Occurrence of lacto series gangliosides 3'-isoLM1 and 3',6'-isoLD1 in human gliomas in vitro and in vivo. 174 82

Suramin is an anti-helminthic drug that has been shown to antagonize the effects of a variety of growth factors including EGF, PDGF and TGF beta. When added to the culture medium, suramin inhibited the proliferation of both human colonic adenocarcinoma cells HT29-D4 and rat glioma cells C6. Suramin also induced the differentiation of both cell lines: appearance of cellular extensions for C6 cells, enterocyte-like epithelial differentiation for HT29-D4-cells. In the latter case, suramin probably acts at the level of glucose metabolism, which is likely to be modulated by autocrine growth factors. The permanent secretion of such factors probably stimulates HT29-D4 proliferation and simultaneously inhibits their differentiation. It is hypothesized that interfering with this autocrine loop, suramin allows HT29-D4 cells to differentiate.
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PMID:[Suramin inhibits the proliferation and stimulates the differentiation of tumoral cell lines HT29-D4 and C6]. 175 32

Flavonolignans isolated from Hydnocarpus wightiana seeds, namely hydnowightin, hydnocarpin, and neohydnocarpin, demonstrated potent hypolipidemic activity in mice, lowering both serum cholesterol and triglyceride levels at 8 mg/kg/day ip. Hydnowightin demonstrated the best lipid-lowering effect of the three compounds. Good anti-inflammatory and antineoplastic activity was demonstrated by hydnocarpin in mice in vivo. The other two derivatives were not as active in these screens. Cytotoxicity against the growth of murine and human tissue cultured cells was shown. All three compounds were moderately active against murine L-1210 leukemia growth. All three compounds demonstrated good activity against the growth of human KB nasopharynx, colon adenocarcinoma, osteosarcoma, and HeLa-S3 uterine growth. Hydnocarpin was the only compound of the three which was active against glioma growth. Hydnocarpin and neohydnocarpin demonstrated significant activity against Tmolt3 leukemia cell growth.
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PMID:Hypolipidemic, anti-inflammatory, and antineoplastic activity and cytotoxicity of flavonolignans isolated from Hydnocarpus wightiana seeds. 180 Jun 32

Boron analogues of piperidine, piperazine, morpholine, and imidazole proved to be cytotoxic against the growth of murine and human tissue culture cells. Significant activity was demonstrated for single-cell suspensions of L1210 lymphoid leukemia, Tmolt3 lymphoblastic leukemia, and HeLa-S3 cervical carcinoma. Trimethylamine-imidazole carbonyldihydroborane 17 demonstrated activity against solid tumor growth of human colorectal adenocarcinoma, KB nasopharynx, and osteosarcoma. In addition, 4-methylpiperidine-carbomethoxyborane 12, 2-methylimidazole-3-cyanoborane 16, and 1-methylimidazole-3-(N-ethylcarbamoyl)borane 19 were active against the KB nasopharynx growth. Piperidine-cyanoborane 2, piperidine-carboxyborane 4, and 1-methylimidazole-3-(N-ethylcarbamoyl)borane 19 were effective in reducing the growth of osteosarcoma cells. The imidazole derivatives 13-19, as well as 4-methylpiperidine-carboxyborane 11 and carbomethoxyborane 12, demonstrated good activity against lung bronchogenic and glioma growth. In the in vivo studies, N-methylmorpholine-carboxyborane 7,4-phenylpiperidine-carboxyborane 9, 4-phenylpiperidine-carbomethoxyborane 10, 4-methylpiperidine-carboxyborane 11, imidazole cyanoborane 14, and 1-methylimidazole-3-carbomethoxyborane 18 demonstrated the best activity against Lewis Lung growth and P388 lymphocytic leukemia growth in mice. Mode of action studies in L1210 leukemia cells demonstrated that piperidine-carboxyborane 4 and N-methylmorpholine-carboxyborane 7 inhibited DNA synthesis, purine synthesis at PRPP amido transferase and IMP dehydrogenase sites, and thymidine kinase and thymidine diphosphate kinase activities, while lowering d(NTP) pool levels. Also, DNA strand scission was evident after incubation with these drugs.
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PMID:Synthesis and antineoplastic activity of some cyano-, carboxy-, carbomethoxy-, and carbamoylborane adducts of heterocyclic amines. 181 71

Clone pTB16 has been isolated by differential screening of a human glioma cDNA library. Northern blot analysis has shown that pTB16 expression is several times (greater than 11-fold) higher in gliomas than in a primitive neuroectodermal tumor. This observation was supported by in situ hybridization and extended to nine other gliomas. Expression was virtually absent in adenocarcinoma cells metastasized to brain. Malignant gliomas showed stronger hybridization than benign gliomas, while blood capillaries did not show hybridization. pTB16 mRNA was also shown to be expressed in established glioma cell lines and at high levels in epileptic foci, indicating that expression of the gene may be limited to certain cell types and that its upregulation is not merely a consequence of cellular proliferation. Nucleotide sequence analysis identified pTB16 as the human counterpart for rat testicular sulfated glycoprotein 2 (SGP-2), whose function in the reproductive system remains unknown. Although SGP-2 transcripts, and hence pTB16, were recently shown to be increased in neurodegenerative diseases such as scrapie in hamsters and Alzheimer disease in humans, our observations with brain tumors and epilepsy are suggestive of a role for pTB16 in neuropathologies in general and support the hypothesis of its involvement in tissue remodeling and cell death.
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PMID:Human gliomas and epileptic foci express high levels of a mRNA related to rat testicular sulfated glycoprotein 2, a purported marker of cell death. 192 17

In 1986, a pilot Phase I/II project was initiated using Iodine-125 labeled anti-epidermal growth factor receptor-425 in the treatment of patients with recurrent glioblastoma multiforme of the brain. The monoclonal antibody was administered intra-arterially by the internal carotid arterial system or the vertebral arterial system depending upon the blood supply to the tumor. The treatment program was repeated at intervals for two or three times. Demonstrated was the intense localization of the monoclonal antibody in the brain tumor prior to therapy using Indium-111 labeled anti-epidermal growth factor receptor-425. This localization was demonstrated prior to any therapy as well as after failure from primary radiation therapy with or without concomitant chemotherapy. To date, 15 patients have been treated following recurrence of their glioma (1/15 metastatic adenocarcinoma) with the monoclonal antibody labeled with Iodine-125. Of the 15 patients, there has been one surgically documented complete response, two partial responders, and five patients with stable disease. The results indicate the potential activity of this radiolabeled monoclonal antibody and have prompted continued accession of patients into a Phase II study as a part of the primary treatment regimen (surgery, radiation therapy with or without chemotherapy) followed by administration of the Iodine-125 labeled anti-epidermal growth factor receptor-425.
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PMID:Iodine125 labeled anti-epidermal growth factor receptor-425 in the treatment of malignant astrocytomas. A pilot study. 196 3

Metastatic spreading of carcinoma into a pre-existing cerebral glioma is extremely rare and only a few well-documented cases have been reported in the literature. Here we report a 53-year-old man who at the age 49 was first operated on for a frontal astrocytoma (WHO-grade II). This tumour was completely resected and no post-operative radio- or chemotherapy was applied. About five years later the patient presented again with a large partially cystic space-occupying lesion at the same site, which pre-operatively appeared as a recurrence of the astrocytoma. Histologically, however, this tumour proved to be a metastatic adenocarcinoma into a recurrent astrocytoma. Further clinical examinations revealed a bronchial carcinoma as the primary lesion responsible for this unusual metastatis. The clinical and neuropathological findings of this interesting case including immunohistochemistry are presented and discussed.
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PMID:Metastatic adenocarcinoma in cerebral astrocytoma: clinicopathological and immunohistochemical study with review of the literature. 223 81

Two clones have been selected from a human fibroblast cDNA bank. By DNA sequencing the clones were shown to contain Alu elements located near the ends of the cDNA inserts. DNA of the clones was used for Northern blot hybridization analysis of a number of poly(A)-containing RNAs from normal human tissues (brain, stomach, uterus, spleen, fibroblasts) and tumors (neurinoma, glioma, neuroblastoma, liposarcoma, adrenal cortex adenocarcinoma). All RNA samples reveal a heterodisperse distribution of Alu transcripts with discrete bands in the region of 7-12 S RNA. The majority of these small poly(A)+ Alu+ RNAs contain Alu sequences only in one (canonical) orientation with functional signals including the split promoter for RNA polymerase III.
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PMID:Cloning of Alu-containing cDNAs from human fibroblasts and identification of small Alu+ poly(A)+ RNAs in a variety of human normal and tumor cells. 243 58

A nonfamilial case of Turcot syndrome (glioma-polyposis syndrome) is described. A 16-year-old male with no siblings first developed a frontal astrocytoma, and was later found to have colonic polyposis with adenocarcinoma. The family history was negative for the syndrome, but his parents were first cousins.
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PMID:Nonfamilial turcot syndrome presenting with astrocytoma--case report. 247 61

Fossel et al. have recently proposed the proton NMR examination of plasmatic lipoproteins--and more precisely the determination of an index obtained from the averaged linewidth of the CH2 and CH3 resonances--as a possible tool for detection of cancer. Many evaluations conducted on an international basis have demonstrated that initial expectations were not met and that the test lacked sensitivity, specificity, and predictive value to be accepted as a screening and diagnostic tool. In our evaluation we have collected plasma from healthy subjects, from patients with various kinds of cancer at different stages of evolution and therapy, and from patients suffering from a variety of pathologies, including benign tumors. In accordance with Chmurny et al., we observed that the linewidth index (LWI) is precise and reproducible when care is taken in the handling and storage of samples and in the fasting of subjects. After finding no predictive value to the test, we have reanalyzed the spectra and studied the variations of the ratio defined by the methylene signal area over the methyl signal area. This ratio is significantly increased in cancer. Furthermore, it offers a better separation of statistical populations permitting a more precise discrimination between cancer, other pathologies and controls. We have also found that malignant tumors arising from mesenchyma (sarcoma, leukemia, lymphoma) induce less important variations in the CH2/CH3 ratio than adenocarcinoma or glioma, when such differences cannot be documented using the LWI. These observations are particularly interesting since they might bring new information on the metabolic modifications of the LWI and the CH2/CH3 ratio might reflect the embryologic origin of the tumors and raise the issue of the heterogeneity of cancer disease.
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PMID:[Modification of the relative plasma concentrations of methyl and methylene groups in cancer: a study using proton NMR spectroscopy]. 251 67


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