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)

The 5' flanking region of the alpha isoform of the rat Ca2+/calmodulin-dependent protein kinase II (alpha CaM kinase II) gene was isolated in 2.3 kbp of genomic sequence. Functional analysis of alpha CaM kinase II promoter deletion mutants fused to a reporter gene in neuroblastoma, including N18TG2, NG108-15, and CAD cells revealed strong transcriptional activity localized 100-145 bp, and a potent silencer 199-275 bp upstream of the transcription start site. The promoter is inactive in non-neuronal cells including BALB/c 3T3, Chinese hamster ovary, HT1080, and C6 glioma cells. These results indicated that the alpha CaM kinase II gene is transcribed from a tissue-specific promoter which is under intense negative control.
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PMID:Characterization of 5' flanking region of alpha isoform of rat Ca2+/calmodulin-dependent protein kinase II gene and neuronal cell type specific promoter activity. 1142 14

ICAD / DFF is a downstream molecule of caspases, participating in nuclear DNA fragmentation during apoptosis. ICAD / DFF binds CAD / DFF40 and inhibits its DNase activity. ICAD / DFF has two alternative isoforms, long isoform (ICAD-L / DFF45) and short isoform (ICAD-S / DFF35). We have studied the presence and functional status of ICAD / DFF in human glioma cell lines. All cell lines tested expressed both ICAD-L and ICAD-S. When the cultured glioma cells were exposed to anti-Fas antibody, these isoforms were degraded prior to the fragmentation of the nuclear DNA, indicating that the ICAD / DFF expressed in cultured glioma cells was potentially functional. In primary brain tumors and normal brain tissues, there was a difference in the expression level between ICAD-L and ICAD-S. In glioblastomas, ICAD-S was more abundant than ICAD-L. In contrast, ICAD-L was more abundant than ICAD-S in medulloblastomas. The present findings suggest that primary brain tumors and normal brain constitutively express ICAD / DFF, and that there is a difference between the expression levels of ICAD-L and ICAD-S.
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PMID:Expression of ICAD-l and ICAD-S in human brain tumor and its cleavage upon activation of apoptosis by anti-Fas antibody. 1147 33

We have previously demonstrated the effectiveness of simultaneous RNA interference (RNAi)-mediated downregulation of urokinase-type plasminogen activator receptor (uPAR) and matrix metalloproteinase-9 (MMP-9) in inhibiting tumor invasion in vitro and in vivo. In particular, we have shown that the downregulation of uPAR and MMP-9 inhibits intracranial tumor growth. The mechanism of the inhibition of tumor growth has not yet been determined. In this study, we have attempted to explain the mechanisms involved in the inhibition of invasiveness and tumor growth in vitro. SNB19 glioma cells were transfected with scrambled vector plasmid (pSV) and a siRNA-expressing plasmid targeting either uPAR (pU) or MMP-9 (pM) singly or in combination (pUM). Untransfected cells were also used as a control. Western blotting and RT-PCR analyses showed the downregulation of uPAR in pU-transfected cells and MMP-9 in pM-transfected cells. In cells transfected with pUM, we observed down-regulation of both uPAR and MMP-9, thereby indicating the specificity of the siRNA-expressing plasmids. An increase in caspase 9 expression was observed in cells transfected with pUM whereas no change in the level of caspase 9 was observed in pU or pM-transfected cells. Additionally, no change in the expression level of caspase 8 was observed. However, an increase in the expression level of cleaved PARP was observed in the case of cells transfected with pU, pM and pUM. Cells transfected with pUM showed the highest levels of cleaved PARP expression. Expression levels of APAF-1 were also higher in pUM-transfected cells with no change in expression levels of controls and in pU and pM-transfected cells. Total CAD expression levels did not change under any of the transfection conditions. However, immunohistochemical studies demonstrated that CAD was translocated to the nucleus, thereby indicating DNA damage. As determined by Western blot analysis of subcellular fractions, cytoplasmic levels of cytochrome c were also increased. We determined the extent of DNA damage using the TUNEL assay (poly-A termination of free -OH ends of degraded nuclear DNA). Based on our results we conclude that the simultaneous downregulation of uPAR and MMP-9 induces apoptosome-mediated apoptosis.
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PMID:Simultaneous downregulation of uPAR and MMP-9 induces overexpression of the FADD-associated protein RIP and activates caspase 9-mediated apoptosis in gliomas. 1881 92

Gliomas are the most common primary brain tumors, and the objective grading is of great importance for treatment. This paper presents an automatic computer-aided diagnosis of gliomas that combines automatic segmentation and radiomics, which can improve the diagnostic ability. The MRI data containing 220 high-grade gliomas and 54 low-grade gliomas are used to evaluate our system. A multiscale 3D convolutional neural network is trained to segment whole tumor regions. A wide range of radiomic features including first-order features, shape features, and texture features is extracted. By using support vector machines with recursive feature elimination for feature selection, a CAD system that has an extreme gradient boosting classifier with a 5-fold cross-validation is constructed for the grading of gliomas. Our CAD system is highly effective for the grading of gliomas with an accuracy of 91.27%, a weighted macroprecision of 91.27%, a weighted macrorecall of 91.27%, and a weighted macro-F1 score of 90.64%. This demonstrates that the proposed CAD system can assist radiologists for high accurate grading of gliomas and has the potential for clinical applications.
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PMID:Computer-Aided Grading of Gliomas Combining Automatic Segmentation and Radiomics. 2985 28