Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0017636 (
glioblastoma
)
18,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The authors investigate the expression of enzyme cathepsin D in human astrocytic neoplasias revealing the dependency on the grade of anaplasia of the tumor. This investigation has shown that there is a significant difference of cathepsin D-expression between the group of low malignant astrocytomas (G1 and G2) and the group of highly malignant astrocytomas (G3 and
glioblastoma
). Enzyme expression decreases when the grade of anaplasia increases. Parallel experiments have shown that in the investigated tumors the expression of
GFAP
also decreases when the grade of anaplasia increases. These results are related to the role of cathepsin D in the protein metabolism of healthy human CNS. The authors assume that in low malignant tumors, owing to the persisting and well-developed cytoskeleton, the investigated enzyme cathepsin D expresses more strongly than in highly malignant tumors, which are characterized by a heavier loss of their capability to express regular structures so that cathepsin D finds less substrate and, correspondingly, expresses less strongly.
...
PMID:Expression of cathepsin D in human astrocytic neoplasias. 854 99
A
glioblastoma
that retained
glial fibrillary acidic protein
(
GFAP
) in culture has a break in the long arm of chromosome 17 at band 17q11.2. DNA inserted at this breakpoint came from chromosome bands 3p21, 3q23, 16q11.2, and 22q11.2. These chromosome fragments were inserted in band 17q11.2 proximal to the neurofibromatosis-1 (NF-1) gene and neu (HER2; erbB2) oncogene loci. The
glioblastoma
also contained a reciprocal translocation between 16p12 and 20p12. These structural abnormalities, previously undescribed in gliomas, were demonstrated by high-resolution chromosome banding, microdissection, and fluorescence in situ hybridization (FISH). Numerical changes typical of
glioblastoma
were present: gain of chromosome 7 and losses of chromosomes 10, 13, and 22. The complex chromosome origin of DNA inserted in this glioma chromosome is described. The association of two infrequent events in this single
glioblastoma
line, this complex insertion and retention of
GFAP
expression, is not likely to be a chance occurrence. It raises the possibility of an association between the two events.
...
PMID:Chromosome breakpoint at 17q11.2 and insertion of DNA from three different chromosomes in a glioblastoma with exceptional glial fibrillary acidic protein expression. 864 40
A 50 y.o. male presented with a right parietal tumor which was a
glioblastoma
on stereotactic biopsy. He was treated by radiation and steroids, with clinical improvement. Four months later, he presented with a left preauricular mass and cervical lymphadenopathy. CT scan showed destruction of the left mastoid and filling of the left tympanic cavity. One month later, he suffered progressive dyspnea. Chest X ray showed a mediastinal mass on the right side and numerous bilateral interstitial opacities in the lungs. A bronchial biopsy was inconclusive. His general condition worsened, and he died. Postmortem showed continuous neoplastic infiltration of the left part of the base of skull, extending into the neck. Numerous metastases were present in mediastinal lymph nodes, lung parenchyma, pleura and pleural aspect of the diaphragm. There were no subdiaphragmatic metastases. Neuropathological examination confirmed a poorly differentiated highly malignant
glioblastoma
with severe necrosis involving the internal part of the parietal lobe extending to the dura mater of the convexity and falx cerebri with invasion of the superior longitudinal sinus which was entirely occluded. The biopsy scar was not infiltrated. Visceral tumors were morphologically identical to the brain tumor. They were strongly
GFAP
positive and cytokeratin negative. Extraneural metastases of
glioblastoma
in the absence of surgery are uncommon in adults. Involvement of the dura mater and/or superior longitudinal sinus is an almost constant feature. In our case, this may have led to invasion of the base of skull and secondary regional, lymphatic, and hematogenous spread.
...
PMID:[Extracerebral metastases of a glioblastoma, in the absence of surgery]. 872 51
We investigated the expression of glutamine synthetase (GS), an enzyme involved in astroglial metabolism and marker of astroglial functional maturity, in a
glioblastoma
cell-line (GL-15) of clonal origin. In spite of their phenotypic immaturity, evidenced in a mosaic fashion by a poor
glial fibrillary acidic protein
(
GFAP
) expression, the level of GS-mRNA is high in GL15 cells and the considerable amount of GS biological activity can be further induced and stabilized by glucocorticoids. A correlation between the induction by dexamethasone of the GS-mRNA level and the GS biological activity suggests a transcriptional regulation of GS expression by the aforesaid hormone. Under this hormonal action, changes in cell morphology occur and they are correlated with an overexpression of the
GFAP
, a marker of astroglial differentiation. On the contrary, dibutyryl cyclic AMP (dbc AMP) down-regulates the GS-mRNA expression and decreases GS activity. These results suggest that GL-15 cells have a common glucocorticoid dependent mechanism able to induce GS and
GFAP
as well as morphological changes. However in these cells AMPc responsive elements are involved in the negative modulation of the GS expression, contrary to what occurs in normal astroglial cells.
...
PMID:Glutamine synthetase gene expression in a glioblastoma cell-line of clonal origin: regulation by dexamethasone and dibutyryl cyclic AMP. 874 97
The transmission of donor-related malignancies by organ transplantation is a rather rare event. There has only been one report on the development of a brain tumor metastasis in liver transplantation. From September 1988 to January 1993, 342 donor hepatectomies with subsequent transplantation were performed at our center. The main donor diagnoses included subarachnoidal bleeding (n = 128; 37.4%), isolated head injury (n = 114; 33.3%), multiple injuries (n = 55; 16.1%), primary cerebral neoplasia (n = 13; 3.8%), and other (n = 32; 9.4%). Primary cerebral neoplasia included
glioblastoma
(n = 4), meningioma (n = 3), astrocytoma (n = 2), angioma (n = 2), neurocytoma (n = 1), and ependymoma (n = 1). In the group of donors suffering from primary cerebral neoplasia, procured organs other than the liver included kidneys (n = 20), combined kidneys and pancreata (n = 1), pancreata (n = 2), hearts (n = 8), combined hearts and lungs (n = 1), and single lungs (n = 1). Follow-up of the respective graft recipients ranged from 28 to 68 months (median 43 months). Recurrent malignancy was observed once, in a liver graft recipient. The donor, a 48-year-old female, had undergone surgical resection of an intracerebral multiform
glioblastoma
and died 4 months later of a relapse in the brain stem. The 28-year-old female recipient had undergone transplantation for an autoimmune-hepatitic cirrhosis. Four months later, histopathological examination of an intraperitoneal and intrahepatic mass revealed a poorly differentiated, small-cell pleomorphic cancer, identified as a glioma metastasis by S100- and
glial fibrillary acidic protein
immunohistochemical staining. The patient died 6 months post-transplantation. On autopsy, no further neoplastic lesions were detected. Our review adds a second reported case of a liver graft-transmitted brain tumor to the literature and the fourth donor-related malignancy after hepatic transplantation in general.
...
PMID:Liver graft-transmitted glioblastoma multiforme. A case report and experience with 13 multiorgan donors suffering from primary cerebral neoplasia. 900 60
To elucidate the morphological characteristics of glioma in children, we investigated 83 tumors that occurred in patients under the age of 20 years old. Seven of 20 histologically malignant tumors were adult-type anaplastic astrocytoma and
glioblastoma
. Eleven tumors were composed of small undifferentiated or poorly differentiated cells. The tumors usually had no fibrillary stroma or if present, the stroma was scanty. A few tumors exhibited ependymal differentiation. One tumor showed rhabdoid features. In 63 benign tumors, including 28 pilocytic astrocytomas and 15 ependymomas, there were 6 plemorphic tumors. Four were regarded as pleomorphic xanthoastrocytoma (PXA), and contained a few neurofilament-positive cells. Further-more, an unclassified glioma composed of eosinophilic plump cells coexpressed
glial fibrillary acidic protein
and neurofilament protein in identical cells. There were 6 tumors associated with desmoplasia including PXA and desmoplastic infantile astrocytoma (DIA). Characteristics of gliomas in children were considered to be the presence of tumors showing insufficient expression of glial phenotype, expression of neurofilament in some types of gliomas, and the presence of a special type of glioma with conspicuous desmoplasia, including PXA and DIA.
...
PMID:Morphological features of gliomas in children. 891 25
The effects of transforming growth factor-beta1 (TGFbeta) on two human neuroblastoma cell lines, LAN-5 and SK-N-AS, and one human
glioblastoma
cell line, GL15, were evaluated. Of the three cultures, only two, SK-N-AS and GL15, had a complete response to TGFbeta, with induction of the following effects: (i) inhibition of cell proliferation; (ii) up-regulation of the extracellular matrix glycoprotein fibronectin, together with down-regulation of the VLA5 integrin receptor; (iii) up-regulation of histotype-specific cytoskeletal intermediate filaments (neurofilaments for neuroblastoma and
GFAP
for
glioblastoma
); and (iv) increase in the glycoprotein CD44, only in SK-N-AS. In the third cell line, neuroblastoma LAN-5, the effects exerted by TGFbeta consisted only of (i) neurofilament increase and (ii) morphological differentiation. The TGFbeta receptor pattern was different in each culture: SK-N-AS expressed low rates of type I and type II receptors and high rates of type III receptor; LAN-5 expressed high rates of type I, low rates of type II, and no type III; GL15 expressed high rates of all three receptors. These data suggest that TGFbeta can induce a histotype-specific cell maturation and that the neuroblastoma expressing low type II and at the same time lacking type III receptor responds only partially to TGFbeta, with induction of neural differentiation but without inhibition of cell growth.
...
PMID:Transforming growth factor beta regulates differentiation and proliferation of human neuroblastoma. 894 Feb 58
To prognosticate the implications of various allelic losses on chromosome 17 in the morphology and biology of astrocytic tumors, we have examined loss of heterozygosity (LOH) at 14 microsatellite loci on chromosome 17 in a series of 19 astrocytic tumors (3 astrocytomas, 5 anaplastic astrocytomas, and 11 glioblastomas). The DNA samples extracted from tumor and matched normal brain tissue were amplified by polymerase chain reaction (PCR) followed by polyacrylamide gel electrophoresis and photography under UV transillumination. The molecular genetic data were compared with immunohistochemistry performed with antibodies to
glial fibrillary acidic protein
(
GFAP
), MIB-1 and p53 protein. LOH was observed in 11/19 (58%) instances with frequent involvement of TP53, NF1, and D17S795 loci, LOH at D17S578 and D17S520 occurred in recurrent tumors exclusively. Allelic status of D17S795 in all 12 informative instances were concordant with
GFAP
immunoreactivity (p < 0.01, Fisher's test). p53 immunopositivity (> 25% of tumor cell nuclei) was seen in 11 (58%) tumors, of which 6 were informative of TP53 locus with 2 (33%) demonstrating LOH. The MIB-1 staining indexes in astrocytomas, anaplastic astrocytomas, and glioblastomas were 1.9 +/- 0.9, 8.4 +/- 4.0, and 17.1 +/- 7.1% (mean +/- SD), respectively, and their differences were statistically significant (p < 0.05, Student's t test). A trend of inverse relationship between patient survival and the number of tumor cell nuclei with immunohistochemically detectable p53 protein was seen in
glioblastoma
cases: 20.5 +/- 12.7 versus 13.7 +/- 6.3 months (mean +/- SD) in instances with > or > or = 25% positive cells, respectively. We conclude, the intriguing correlation between allelic status of D17S795 microsatellite locus and
GFAP
immunoreactivity suggests the possible involvement of q21.2 segment of chromosome 17 in the morphology and biology of astrocytic tumors.
...
PMID:Chromosome 17 allelic loss in astrocytic tumors and its clinico-pathologic implications. 926 49
In order to study the clinicopathological features, histogenesis and prognosis, 12 cases of gliosarcoma were reported representing 0.4% of a series of 2743 patients undergoing biopsy for CNS tumors. All the tumors originated from the cerebral hemispheres with a predilection for the temporal lobes. Half of the cases show more firm consistency and are rather well demarcated from brain tissue. Clinically, they are sometimes mistaken for meningiomas. Of the 10 patients with follow-up, 9 have died. The mean survival period after operation was 8 months, 1 cases is still alive and well for 3.2 years. There were some cases in which the origin of spindle cell populations could not be determined by H & E staining.
Glioblastoma
and malignant fibrous histiocytoma (MFH) element of the tumor was confirmed by electron microscopical examination and immunohistochemical stains for
GFAP
, Mac 387, VIM, FV III RA, etc. Osteosarcoma component in the tumor was detected in one case. It was accepted that MFH arose from the primitive uncommited mesenchyme.
...
PMID:[A clinical and pathological study of gliosarcoma]. 927 62
A human glioma cell line, SA146, was initiated on precoated extracellular matrix from a stereotactic biopsy of a
glioblastoma
. We report modulation in the expression of
glial fibrillary acidic protein
(
GFAP
) by SA146 passed in vitro before or after xenogenic transplantation into nude mice. Immunofluorescence data show a decrease in the percentage of
GFAP
-expressing cells with increasing in vitro passages but a full reexpression (100% of
GFAP
-positive cells among vimentin-positive cells) was observed in cultures just derived from the xenotransplanted tumor. These changes are correlated with the mRNA content (Northern blot probed with a cDNA for
GFAP
) and with the protein level (cytoskeletal fraction analyzed by two-dimensional gel electrophoresis and Western blots probed with a monoclonal antibody). At the optimal level of
GFAP
expression, a large range of micro-heterogeneity in
GFAP
isoforms is reached for which post-translational events are clearly involved since mRNA translation in cell free system would provide at best three isomers. We suggest that SA146 would be an appropriate model to study the regulation of
GFAP
expression in the context of human glial tumor biology.
...
PMID:Glial fibrillary acidic protein expression in a new human glioma cell line in culture before and after xenogenic transplantation into nude mice. 934 40
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>