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)

Cisplatinum (cis-dichlorodiammineplatinum II (NSC-119875], proven to be of therapeutic value in a variety of solid tumors, is thought to have DNA as its major target. Prior in vitro studies have suggested that it also induced cell membrane and cytoplasmic changes. To better understand glial tumor cell sensitivity to cisplatinum and to design more effective adjuvant therapy, three cisplatinum sensitive human glioma-derived cell lines, SNB-1, SNB-3, SNB-4, were examined by transmission electron microscopy for cisplatinum induced changes. Tumor cells were exposed to 25, 50, and 100 micrograms/ml cisplatinum in medium for varying time periods (4-72 hours). Four changes were consistent: cell rounding and reduced nuclear-cytoplasmic ratio, nuclear chromatin clumping, vesiculation and swelling of the golgi apparatus, and dilatation of the smooth endoplasmic reticulum. These morphologic changes are distinct for cisplatinum and unlike those induced by BCNU (plasma membrane blebbing) and AZQ (mitochondrial swelling and destruction) previously seen in our laboratory. The cellular events described here suggest that cytoplasmic, as well as nuclear, changes (occurring within the same time intervals) may both be relevant to the antitumor effects of cisplatinum.
J Neurooncol 1990 Dec
PMID:Selective cytoplasmic and membrane changes induced by cisplatinum. 208 34

Malignant glioma cells often have more epidermal growth factor (EGF) receptors than normal cells and targeting of toxic substances to the receptor might therefore be an attractive therapeutical approach. Radiation effects were analysed on human glioma cells growing as monolayers after exposure to 131I-EGF. Unspecific effects were analysed with 131I-BSA or after presaturation with nonradioactive EGF. The radiation effects were compared to the effects obtained by external 60Co gamma irradiation. Administration of the highest radioactive concentrations, 0.2-0.5 MBq/ml in the culture medium, corresponded, after 20 min incubation, to a binding of about 1.0-2.5 dpm/cell. Such an exposure to 131I decays gave effects on cell survival corresponding to about 2.5 Gy of external gamma irradiation. Somewhat less than half of this effect came from the specific bound radioactivity and the rest from nonbound radioactivity. When administrating lower concentrations of radioactivity both the binding and the radiation effects were smaller. The observations showed that it is possible to inactivate cell-proliferation of glioma cells with specific bound 131I-EGF. The possibilities to fractionate the treatments and of binding also other toxic agents than 131I to the EGF receptor are discussed.
J Neurooncol 1990 Dec
PMID:Effects of 131I-EGF on cultured human glioma cells. 208 35

The relationship between photosensitizer concentration, light dose, incubation time and cellular damage in human cerebral glioma cells in culture, was studied. Cells were incubated with hematoporphyrin derivative (Hpd) for different durations at 37 degrees C. Immediately after specified period of incubation, cells were irradiated with white light. Cellular damage was assessed by colony forming ability of cells. A progressive reduction in the surviving fraction was observed as a function of drug and light dose. The survival curves were of exponential nature with an initial shoulder. The cell survival was found to be dependent on the time of incubation with Hpd. These results suggest that photodynamic cellular damage can be enhanced at low drug and light dose by increasing the incubation time.
Indian J Med Res 1990 Dec
PMID:Interdependence of drug dose, incubation time & light dose on hematoporphyrin derivative induced photoinactivation of brain tumour cells. 215 Apr 3

Three distinct antipeptide antisera generated against synthetic peptides that represent parts of the primary sequence of the alpha-subunit of the (pertussis toxin-sensitive) guanine nucleotide binding protein G0 were used in two-dimensional immunoblots of membranes of neuroblastoma X glioma (NG108-15) cells. Each antiserum identified two distinct polypeptides of some 39 kDa. These had apparent isoelectric points of 5.5 and 5.8. Differentiation of NG108-15 cells in response separately to dibutyryl cyclic AMP (cAMP), 8-bromo cAMP, forskolin, and prostaglandin E1 produced elevated levels of G0 alpha, as has previously been noted in one-dimensional immunoblots. Two-dimensional analysis demonstrated that the cAMP-induced increases in levels of G0 alpha were only of the more acidic isoform. The two isoforms were both substrates for pertussis toxin-catalysed ADP-ribosylation and did not appear to represent differentially phosphorylated forms of the same polypeptide. Separation of the two forms of G0 alpha could be achieved in one-dimensional sodium dodecyl sulphate-polyacrylamide gel electrophoresis when 4 M deionized urea was included in the resolving gel. The more slowly migrating band was the acidic form and corresponded exactly in mobility with the major form of G0 from both rat and mouse brain. There was no equivalent in brain of the more rapidly migrating form of G0 from the cells. In agreement with the data from two-dimensional gels, only the more slowly migrating form was expressed in considerably higher amounts following cAMP-induced differentiation of NG108-15 cells. Of these two forms of "G0," the acidic species is equivalent to G0 from brain, but the basic form is not identical with G0*, which has been purified from bovine brain.
J Neurochem 1990 Dec
PMID:Identification of two distinct isoforms of the guanine nucleotide binding protein G0 in neuroblastoma X glioma hybrid cells: independent regulation during cyclic AMP-induced differentiation. 217 64

A human beta-interferon (HuIFN-beta) gene inserted into a eukaryotic expression vector (pSV2IFN-beta) was entrapped in liposomes having positive charges on their surface. Liposome-mediated transfection of the gene into cultured glioma cells (U251-MG) resulted in the secretion of HuIFN-beta into the medium. The HuIFN-beta level in the culture medium of glioma cells reached 24 +/- 8 (mean +/- SD) IU/ml after 96 h of incubation, at which level the growth inhibitory effect on the cells was found to be greater than 40 times as compared with exogenously added HuIFN-beta. When the plasmid-containing liposomes were coupled with a monoclonal antibody (G-22 MCA) against glioma-associated antigen, the level of HuIFN-beta in the medium was 178 +/- 26 IU/ml, resulting in a 7-fold increase, and the growth inhibitory effect was further elevated. Since the addition of a monoclonal antibody against HuIFN-beta to the medium did not cause the cell growth to resume, the growth inhibitory effect on the cells seems to be ascribed to HuIFN-beta produced in the cells transfected with its gene. Accordingly, the specific delivery of the HuIFN-beta gene into glioma cells by the use of such liposomes might become a useful technique for gene therapy of malignant glioma.
Cancer Res 1990 Dec 15
PMID:Growth inhibition of glioma cells transfected with the human beta-interferon gene by liposomes coupled with a monoclonal antibody. 217 34

Two major classes of mRNAs for the alpha-crystallin B chain (or alpha(B)crystallin), about 0.9 and 1.2 kilobases in length, are expressed in rat brain. To examine the structures of these mRNAs, we isolated cDNA clones from rat brain and genomic DNA from rat liver. Characterization of these clones as well as Northern blot analysis indicated that the various mRNAs differed in the lengths of their 5' leader sequences. RNase protection assays revealed that the gene for alpha-crystallin B chain contains multiple start sites. The transcriptional start sites of the longer mRNAs are preceded by a putative CAAT box and that of the shorter mRNA by a putative TATA box. The shorter mRNA encodes the alpha-crystallin B chain protein, whereas the longer mRNA contained three extra small open reading frames upstream of the AUG start codon for the protein. The shorter mRNA is abundant in lens, heart, muscle, and kidney, while the longer mRNAs are constitutively expressed at low levels in a wide variety of tissues. The shorter mRNA was increased by treatment with phorbol 12-myristate 13-acetate in rat C6 glioma cells. Since there is only a single copy of the alpha-crystallin B chain gene, our results indicate that the two classes of mRNAs are generated by alternative transcriptional initiation from different promoters and their expressions are regulated differentially.
J Biol Chem 1990 Dec 25
PMID:Multiple mRNAs of rat brain alpha-crystallin B chain result from alternative transcriptional initiation. 217 7

Twelve patients with central neurofibromatosis underwent MR examination of the head. Among these, chiasma glioma was the most common CNS tumour (6/12). Seven patients had multifocal areas of increased T2-signal without mass effect predominantly involving the region of the basal ganglia. No corresponding CT abnormalities were present. These lesions may represent multifocal dysplasia and seem to be characteristic of central neurofibromatosis.
Rofo 1990 Dec
PMID:[The MR tomographic findings in cranial manifestations of neurofibromatosis]. 217 21

We undertook a phase II study of combination chemotherapy with mechlorethamine (nitrogen mustard) 6 mg/m2 intravenously day 1 and day 8, vincristine 2 mg intravenously day 1 and day 8, and procarbazine 100 mg/m2 orally days 1 through 14 (MOP) in adults with recurrent high-grade glioma. There were 31 patients entered and 27 patients assessable for response. The median age was 49 years old. All patients had prior maximal radiotherapy, and eight had previous chemotherapy. Responses were determined based on clinical and computed tomographic (CT) scan/magnetic resonance imaging (MRI) criteria. The response rate (partial response [PR] plus objective qualitative response [OQR] plus complete response [CR]) was 52% with one CR. The response rate was higher in patients with anaplastic astrocytoma as compared with glioblastoma multiforme (P less than .05). The median duration of response was 42 weeks. Median survival for all assessable patients was 30 weeks, and for responders, it was 60 weeks. Response was correlated with ability to decrease dexamethasone doses and improved performance status. Toxicity was mainly hematologic with leukopenia being common. There was one treatment-related death from listeria meningitis, and two patients developed Pneumocystis carinii pneumonia. There were three episodes of neutropenic fever. We conclude that MOP is active and merits further investigation in adult high-grade glioma.
J Clin Oncol 1990 Dec
PMID:Mechlorethamine, vincristine, and procarbazine chemotherapy for recurrent high-grade glioma in adults: a phase II study. 223 Aug 93

To better understand the cellular mechanism of tumor invasion, the production of a cell motility-stimulating factor by malignant glioma cells was studied in vitro. Serum-free conditioned media from cultures of rat C6 and human T98G cell lines contained a factor that stimulated the locomotion of the producer cells. This factor was termed the "glioma-derived motility factor." The glioma-derived motility factor is a heat-labile protein with a molecular weight greater than 10 kD and has relative stability to acid. The factor showed not only chemotactic activity but also chemokinetic (stimulated random locomotion) activity in the two types of glioma cells studied. Although glioma-derived motility factors in conditioned media obtained from two different cell origins are likely to be the same, chemokinetic migration of T98G cells to their conditioned medium was much stronger than that of C6 cells to theirs. Coincubation of cells with cytochalasin B, which disrupts the assembly of cellular actin microfilaments, almost completely inhibited the cell migration stimulated by glioma-derived motility factor. Cytochalasin B also induced marked alterations in cell morphology, including cell retraction and arborization, while the drug did not affect cell attachment to culture dishes. These results indicate that glioma cells produce a motility factor which may play a role particularly when tumor cells are detached and migrate away from the original tumor mass, thus promoting tumor invasion. Also, glioma cell migration stimulated by the motility factor requires the normal organization of cytoskeletons such as actin microfilaments.
J Neurosurg 1990 Dec
PMID:Motility factor produced by malignant glioma cells: role in tumor invasion. 223 Sep 71

A human monoclonal antibody (CLN-IgG) was produced from a human-human hybridoma derived from lymphocytes of a patient with cervical carcinoma. The reactivities of this antibody with various human glioma tissues and cultured glioma cells and the characterization of the antigen recognized by CLN-IgG on malignant glioma cells were analyzed and reported. CLN-IgG reacted with various human glioma cells and glioma tissues, especially glioblastoma, but did not react with normal brain tissues or fetal brain tissues. A large amount of antigen recognized by CLN-IgG was expressed on cell membranes of undifferentiated glioma cells and of glioma cells at the G2/M tumor growth phase in cycling cells. Antigen recognized by CLN-IgG was detected in only one of seven samples of cyst fluid, and was not detected in 27 serum samples or 18 samples of cerebrospinal fluid from glioma patients. CLN-IgG exhibited antibody-dependent cell cytotoxicity against U-25 1 MG glioma cells and primary cultured cells of glioblastomas and anaplastic astrocytomas. These data suggest that the antigen recognized by CLN-IgG might be related to cell proliferation in malignant gliomas. Thus, CLN-IgG might be useful for immunotherapy or immunoimaging of malignant gliomas.
J Neurosurg 1990 Dec
PMID:Antigen related to cell proliferation in malignant gliomas recognized by a human monoclonal antibody. 223 Sep 72


<< Previous 1 2 3 4 5 6 7 8 9 10