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

Necdin is a polypeptide sequence encoded by neural differentiation-specific mRNA derived from embryonal carcinoma cells. We have examined the expression of necdin and its mRNA in cultured cells and mouse brain by Northern blot analysis and immunohistochemistry. Among various established cell lines including neuroblastoma and glioma cells, only differentiated embryonal carcinoma cells (P19 and F9) expressed necdin mRNA. Necdin immunoreactivity was localized in the nuclei of differentiated neurons derived from P19 cells. Necdin mRNA was detected throughout brain regions of adult mouse; the relative abundances in the hypothalamus and midbrain were the highest, whereas those in the olfactory bulb and cerebellum were the lowest. In developing mouse brain, necdin mRNA was expressed during early periods of neuronal generation and differentiation, and the peak levels were attained during postnatal days 1-4. Necdin immunoreactivity was not detected in the neural stem cells on embryonic day 10, but was concentrated in the nuclei of brain cells, mostly neurons, at advanced stages of differentiation. The majority of differentiated neurons in the brain had necdin-immunoreactive nuclei on postnatal day 33. Thus, necdin may represent a valuable molecular marker for differentiated neurons both in vitro and in vivo.
 ...
PMID:Expression of necdin, an embryonal carcinoma-derived nuclear protein, in developing mouse brain. 139 72

The ganglioside composition of 15 cases of meningioma, 15 cases of astrocytoma, 5 cases of neurinoma, 4 cases of ependymoma, 3 cases of metastatic brain tumor and 1 case each of mixed glioma, oligodendroglioma, medulloblastoma, embryonal carcinoma, and cultured glioma cell line were analyzed by thin-layer chromatography. The GM2, GD3, and GD2 content of the tumors was determined using specific monoclonal antibodies (MAb). Cases were grouped according to the difference in ganglioside pattern and various clinical features. In meningiomas and astrocytomas, GM3 and GD3 were the major gangliosides. The tumor content of the rather simple gangliosides (GM3, GM2, GD3, GD2) increased or was almost equal to that of normal tissue (leptomeninges tissue in the case of meningiomas, and brain tissue in the case of astrocytomas), while the tumor content of complex gangliosides (GM1, GD1a, GT1a, GT1b) decreased as compared with normal tissue. The GM3 content of meningiomas increased in middle-aged patients, who comprised the majority of the patients with these tumors. The GD2 content decreased in middle-aged patients with initial symptoms of meningioma within a year. The GM3 content of astrocytomas decreased in patients who underwent radiotherapy. The amount of GM3 and GD3 increased in small tumors. GM3 may be related to the early proliferative stage. The ganglioside patterns of brain tumors are shown in this study to differ according to clinical features and also to be changeable in their clinical courses.
 ...
PMID:Ganglioside composition and its relation to clinical data in brain tumors. 140 35

Antitumor activity of Cisplatin (cis-diamminedichloroplatinum) against malignant brain tumors was investigated from both experimental and clinical points of view. With glioma and neuroblastoma cell lines we studied inhibition of cell growth was studied and DNA histogram analyzed with flow cytometry to determine its antitumor activity in vitro. At the concentration of 1.25 micrograms/ml, DNA accumulation is S or G1-S phase and mild inhibition of cell growth were demonstrated; at the concentration of 12.5 micrograms/ml, cessation of cell cycle was observed. In the clinical study, four glioma patients were treated by intravenous administration of Cisplatin 10 mg/sqm for 5 days q 4 weekly. There were one complete response, one minor and two stable responses. Three patient with intracranial embryonal carcinoma were treated by cisplatin. One patient showed partial response and the others were stable.
 ...
PMID:[Antitumor activity of cisplatin against malignant brain tumors]. 608 69

Murine embryonal carcinoma tumors were induced to differentiate in vivo by administration of retinoic acid. Six long-term surviving animals had seven slowly growing tumors which were transplanted s.c. into strain 129 mice. Untreated embryonal carcinomas were transplanted as controls. All of the 16 control transplants grew rapidly and killed their hosts within 25 days. All of the 24 transplants of retinoic acid-differentiated tumor survived. Sixteen experimental transplants originating from five original tumors showed no or slow growth for up to 16 weeks and were found to be histologically benign cystic teratomas. Two original tumors gave rise to eight relatively rapidly growing transplants. One tumor resulted in four histologically similar solid tumors which resembled chondrosarcomas, and the second tumor gave rise to four histologically similar solid tumors which proved to be a mixture of glioma and chondrosarcoma. Examination of the tumor sources of these latter transplants showed benign cystic teratomas with focal solid, mitotically active cellular areas which were histologically similar to the transplants. These data confirm that retinoic acid-induced differentiation of murine embryonal carcinoma cells results in altered biological potential of these cells and usually the formation of a benign teratoma. Rarely (about 1 per 2 X 10(8], the resulting differentiated cells will give rise to rapidly growing, histologically malignant tumors. One can predict such biological propensity when solid, mitotically active areas in the original tumor are found.
 ...
PMID:Chemically induced differentiation of murine embryonal carcinoma in vivo: transplantation of differentiated tumors. 620 Dec 66

Seventeen patients, aged 9 to 63 years (mean age 38.2 years), with 6 recurring malignant glioma, 5 malignant meningioma, 4 metastatic brain tumor, one endodermal sinus tumor and one embryonal carcinoma were postoperatively treated with adriamycin (ADM). As a rule, 20 mg of ADM (to 960 mg in a total dosis) were given by means of intra-carotid administration every two weeks (to 250 months in duration). According to Karnofsky's evaluation, 4 of 6 glioblastoma patients(66.7%), 4 of 5 malignant meningioma (80%), 2 of 4 metastatic brain tumor (50%) and one embryonal carcinoma had improvement of clinical condition, at least during two months after the beginning of the treatment, and/or remission of more than 50% of the enhanced area on CT scan. Consequently, allover response rate was 64.7%. Tumor tissue concentration of ADM administered intraoperatively by the same regimen, was estimated by fluorescence assay, twenty times in sixteen patients. The level of the concentration was higher in malignant tumor (3.6 to 6.2 micrograms/g) than in low grade astrocytoma (1.5 microgram/g in maximum) during sixty minutes after ADM administration. On the other hand, when ADM of same dosis was given intravenously, maximum serum level was 2.8 microgram/ml, which was less than half in comparison with tissue level of intracarotid administration. There was a serious myelosuppression in two cases in our series, but no cardiomuscular damage was observed in any cases. In conclusion, ADM concentration of brain tissue such as malignant meningioma, metastatic brain tumor and, even glioblastoma, was highly obtained. Further, intermittent intra-carotid administration of ADM was more effective than intravenous dripping in treating malignant intracranial tumor, although side effects should be carefully avoided.
 ...
PMID:[Postoperative treatment for malignant intracranial tumors--especially concerning intermittent intra-carotid administration of adriamycin]. 646 30

Murine embryonal carcinoma tumors were induced to differentiate in vivo using retinoic acid. Six mice bearing seven tumors survived more than 100 days after treatment. Histological samples of these tumors showed no residual embryonal carcinoma cells, and, for the most part, they were benign cystic teratomas. Three tumors, in addition to the benign tissue, had solid, mitotically active areas. Two of these tumors upon transplantation gave rise to progressively growing, potentially lethal tumors which have proven to be permanently transplantable cell lines. Using techniques of light and electron microscopy, immunohistochemistry, flow microfluorometry, and cytogenetics, we have characterized these lines. One is a chondrosarcoma, and one is a glioma:chondrosarcoma mixture. Both are chromosomally different from the parent embryonal carcinoma stem cell line, but both were clearly derived from it.
 ...
PMID:Malignant neoplasms of differentiated cells occurring after retinoic acid treatment of murine embryonal carcinomas in vivo. 671 3

We isolated a neurotropic retrovirus, FrC6-V, from Friend leukemia virus complex after the adaptation of the original virus to newborn rat brain followed by the long-term infection of rat glioma cell line C6. When rats were infected with FrC6-V, the virus was isolated mainly from the brain and from the thymus of the infected animals regardless of the age of the animals at the time of inoculation. Neurological and neuropathological manifestations became apparent, however, only when the newborn rats were infected. The lesions in the brain were characterized by spongiform degeneration accompanied by the loss of neurons in the hypothalamus, cerebral cortex, and cerebellum. There was almost no inflammatory cell infiltration. In primary culture of brain, the astrocytes and the neuron specific enolase antigen-positive cells were infected with FrC6-V, but the viral antigen was not detected in neurofilament antigen-positive neurons. Furthermore, our virus inhibited the differentiation of embryonal carcinoma (EC) cell line P19 into neurons.
 ...
PMID:Gene expression of neurotropic retrovirus in the CNS. 756 85

We have found that the gene expression of the ninth member of the fibroblast growth factor (FGF) family, FGF9 was induced during retinoic acid(RA)-induced neuronal differentiation of murine embryonal carcinoma P19 cells. We have reported here the nucleotide sequence of the mouse FGF9 cDNA. The murine cDNA showed 92.4% nucleotide sequence homology to the human FGF9 cDNA and 98.2% homology to that of rats. This mouse FGF9 cDNA encoded a polypeptide consisting of 208 amino acids with amino acid sequence identical to that of rats. Only one amino acid was replaced compared to the human homolog. The highly conserved sequence homology of FGF9 suggests its functional importance. FGF9 was originally isolated from a culture medium of a human glioma cell line as a growth-promoting factor for glial cells [5]. Upon induction of neuronal differentiation by forming cell aggregates with 10(-6) M RA, the gene expression of FGF9 was increased biphasically during the first 96 hours when cells were aggregating and from 168 hours to 192 hours followed by plating onto a tissue culture dish as glia-like cells proliferated. Neither undifferentiated P19 cells nor the cells aggregated without RA remaining undifferentiated expressed FGF9. This indicates that RA regulates the gene expression of FGF9 that may play an important role in neuronal differentiation in both early and late developmental process.
 ...
PMID:Retinoic acid induces gene expression of fibroblast growth factor-9 during induction of neuronal differentiation of mouse embryonal carcinoma P19 cells. 765 83

The oncogene GLI is amplified and expressed in some cases of human malignant glioma and undifferentiated childhood sarcoma and is the prototype for a gene family characterized by a highly conserved set of five tandem zinc fingers and a consensus cysteine-histidine link. This zinc finger motif has been shown to bind DNA with sequence specificity and may mediate transcriptional regulation. Since GLI is expressed in embryonal carcinoma cell lines but not in most normal adult tissues and shows significant sequence similarity within its zinc finger domain to cubitus interruptus dominant (ciD), a Drosophila segmentation gene known to be important in the morphogenesis of the posterior portion of each larval segment, we established the temporal and tissue expression patterns of the mouse homologue of human GLI in day 10 through 18 mouse embryos with Northern blotting, reverse transcriptase coupled PCR, and in situ hybridization. gli transcripts were demonstrated on days 10 through 18 of mouse embryonic development as well as in normal adult uterus, brain, testis, and limb. Tissue expression of gli during gestation was demonstrated in Meckel's precartilage mesenchyme, the basis occipitus, rib mesenchymal condensations, primordial vertebral bodies, digital mesenchymal condensations in forefoot and hindfoot plates, the ependymal layer of the spinal cord, and the mesoderm of the gastrointestinal tract. Expression persisted throughout gestation in developing bone and cartilage of the extremities, the ribs, and the vertebral bodies, as well as the gastrointestinal tract mesoderm. These findings support a role for gli family genes in normal craniofacial and digital development in mammals first suggested by the demonstration of translocation breakpoints within the GLI3 gene in families with the Greig cephalopolysyndactylyl syndrome and subsequently by reduced gli3 expression in the mouse mutant extra toes. It is surprising that a single gene would be expressed in such a wide range of mesenchymal structures.
 ...
PMID:gli, a zinc finger transcription factor and oncogene, is expressed during normal mouse development. 836 25

Numerous eukaryotic mRNAs contain sequences complementary to segments of the 18S and 28S rRNAs. Previous studies raised the possibility that these complementarities might allow mRNA-rRNA interactions and affect rates of translation. In the present study, we investigated the mRNA encoding the mouse Gtx homeodomain protein. This mRNA contains within its 5' untranslated region (UTR) a segment that is complementary to two regions of the 18S rRNA, located at nucleotides 701-741 and 1104-1136. A Gtx RNA probe containing this complementarity could be photochemically cross-linked to ribosomal subunits through a linkage to 18S rRNA but not to 28S rRNA. Oligonucleotide-directed RNase H digestion of the rRNA and a reverse transcription analysis localized the cross-linked probe to the complementary segment of 18S rRNA at nucleotides 1104-1136 but not at nucleotides 701-741. To determine whether complementarity in the Gtx mRNA affected translation, a mutational analysis was performed with a Gtx-luciferase fusion construct and four related constructs with altered complementarity to the 18S rRNA. These constructs were examined for their ability to be translated in cell-free lysates prepared from P19 embryonal carcinoma and C6 glioma cell lines and after cellular transfection into these same cell lines. In both cell-free translation and transfection studies, the rate of translation decreased more than 9-fold as the degree of complementarity to nucleotides 1104-1136 of the 18S rRNA increased. We hypothesize that segments complementary to rRNA, such as those contained within the Gtx mRNA, form a category of cis-acting regulatory elements in mRNAs that affect translation by base pairing to rRNA within ribosomes.
 ...
PMID:rRNA-complementarity in the 5' untranslated region of mRNA specifying the Gtx homeodomain protein: evidence that base- pairing to 18S rRNA affects translational efficiency. 999 25


1 2 Next >>