Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-three patients with inoperable and/or recurring malignant gliomas and 30 patients with multiple recurring brain metastases were treated with a combination of adriamycine (45 mg/m 2 and 4-dimethyl-epipodophyllotoxin D-thenylidene (VM 26) (60 mg/m 2 for 2 days) and 1-(2-chloroethyl)-3-cyclohexyl-1-nitroso-urea (CCNU) (60 mg/m 2 for 2 days). These cycles of treatment were repeated as soon as the hematologic restoration was complete. The treatment was well-tolerated and the clinical condition of 31 out of 43 glioblastoma patients improved during the 2 months after the beginning of the treatment. Six out of eight patients with breast cancer metastases, one out of 13 with bronchial cancer metastases, and three out of nine with other types of cancer metastases also benefitted from the treatment. Examination of the results reveals the following characteristics: 1. A low degree of efficiency of this combination in the treatment of brain metastases, except for breast cancer metastases. 2. Absence of complete correlation between the clinical results observed and the cinegammagraphic developments 3. Similarity of the results independent of the initial localization 4. Establishment of a 6-month median survival period, with ten patients at present in a state of apparently complete remission, 180-506 days after beginning of the treatment.
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PMID:Treatment of malignant gliomas and brain metastases in adults using a combination of adriamycine, VM 26, and CCNU. Results of a type II trial. 34 Dec 49

Forty-three patients with inoperable and/or recurring malignant gliomas, and 30 patients with multiple recurring brain metastases were treated with a combination of adriamycine (45 mg/m2) and 4-dimethyl-epipodophyllotoxin D-thenylidene (VM 26) (60 mg/m2 for 2 days) with 1-(2-chloroethyl) -3-cyclohexyl-1-nitroso-urea (CCNU) (60 mg/m2 for two days). These cycles of treatment were repeated as soon as the hematological restoration was complete. The treatment was well tolerated and the clinical condition of 31 out of 43 glioblastoma patients improved during the two months after the beginning of the treatment. Six out of eight patients with breast cancer metastases, one out of 13 with bronchial cancer metastases and three out of nine with other types of cancer metastases also benefitted from the treatment. Examination of the results obtained reveals the following characteristics: -A low degree of efficiency of the combination in the treatment of brain metastases, except for breast cancer metastases. -Absence of complete correlation between the clinical results observed and the cinegammagraphic developments. -Similarity of the results independent of the initial localization. -Establishment of a six-months median survival period, with ten patients at present in a state of apparently complete remission, 180 to 506 days after beginning of the treatment.
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PMID:[Trial treatment of glioblastomas in adults and cerebral metastais by adriamycin, VM 26 and CCNU combination. Result of a type II trial]. 77 98

Forty-three patients with inoperable or recurring malignant gliomas, and 30 patients with multiple recurring brain metastases were treated with a combination of Adriamycin (45 mg/m2) and 4-dimethyl-epipodophyllotoxin D-thenylidene (VM 26) (60 mg/m2 for 2 days) with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) (60 mg/m2 for 2 days). These cycles of treatment were repeated as soon as the hematologic restoration was complete. The treatment was well tolerated and the clinical condition of 31 of 43 glioblastoma patients improved during the 2 months after the beginning of the treatment. Six of eight patients with breast cancer metastases, one of 13 with bronchial cancer matastases, and three of nine with other types of cancer metastases also benefitted from the treatment. Examination of the results obtained revealed the following characteristics: 1) This combination had a low degree of efficiency in the treatment of metastases to brain, except for breast cancer metastases; 2) there was no complete correlation between the clinical results observed and the cinegammagraphic developments; 3) the results obtained were similar, independent of the initial localization; and a 6-month median survival period was established, with 10 patients now in a state of apparently complete remission, 180 to 506 days after beginning of the treatment.
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PMID:Treatment of malignant gliomas and brain metastases in adults with a combination of adriamycin, VM 26, and CCNU. Results of a phase II trail. 103 28

The neu gene in rat neuro/glioblastoma was found to be activated by a single point mutation in the DNA sequence encoding the transmembrane region of the neu-encoded p185 protein. The human homologue of the rat neu gene, termed c-erbB-2 or HER-2, can also be activated in vitro by a similar mutation in the corresponding region. Although the human neu gene was shown to be amplified/overexpressed in a large portion of human breast and ovarian cancer, no reports indicate that the human neu gene is activated by a point mutation in human tumor. To study the possible point mutation of neu gene in human tumors, we characterized the genomic structure in the transmembrane region of human neu gene, which in turn allowed us to determine DNA sequence in this region directly following DNA amplification by polymerase chain reaction. We analyzed 7 tumor cell lines (2 breast cancer, 1 neuroblastoma, 1 rhabdomyosarcoma, and 3 glioma) and 11 tumor tissue samples (8 breast and 3 ovarian cancers). No mutation was found in the transmembrane region of human neu gene. Our results suggest that unlike the rat neuro/glioblastoma, the single point mutation in the transmembrane region of the human neu gene is a rare event in human tumors. In this study, we developed a technique for direct DNA sequencing of the transmembrane region of the human neu gene. This technique makes it possible to screen a large number of tumor samples.
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PMID:Direct sequencing analysis of transmembrane region of human Neu gene by polymerase chain reaction. 220 83

A combination of multiple primary neoplasm (MPN) with glioblastoma and cancer of other organs is extremely rare but might be spurred up in the field of neurosurgery because of increasing number of cured patients from cancer or malignant brain tumor. Four such cases are presented. Two of them are of heterochronous occurrence of tumors. One has survived for 17 years after treating four malignancies: uterus, stomach, breast cancer and glioblastoma multiforme in this order and free of brain tumor for 4 years. The other has survived 18 years after three malignancies: uterus, stomach cancer and glioblastoma but is in morbid neurological state for a year. A case of synchronous primary tumors is a combination with glioblastoma and maxillary cancer and the patient died of brain tumor after 4 years and two months. The other case is an old man with glioblastoma and stomach cancer but died of severe general and neurological condition for three months before treatment was started. The pathogenesis of MPN is unknown. Regarding intrinsic factors, heredity, age, genetic or immunological state have been proposed for possible mechanism of the synchronous occurrence of MPN. While extrinsic factors such as environmental changes due to irradiation or chemical exposure to host might also be important for heterochronous MPN. Discussions based on these cases and literature were also made on the biological nature and clinical characteristics of MPN malignant brain tumor combined with cancer of other organs.
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PMID:[Multiple primary neoplasm--glioblastoma combined with cancer of other organs]. 282 47

We studied two children who had rhabdomyosarcoma and glioblastoma and who were from a family with a hereditary cancer syndrome that was characterized by sarcoma, breast cancer, brain tumors, lung cancer, laryngeal carcinoma, leukemia, and adrenocortical carcinoma. The deleterious genotype has now been expressed through the fourth generation of this large kindred. The pedigree emphasizes the need for an extended history of several generations to arrive at a hereditary-syndrome diagnosis. A limited pedigree may result in nonappreciation of the genetic component. The pedigree illustrates that, in certain circumstances, the highly specific varieties of cancer may occur in children before it is expressed in the parent who carries the putative gene. Pediatricians, in evaluating the causes of childhood cancer, must be cognizant of cancer among adult relatives, since this recognition may aid in the diagnosis of those hereditary cancer syndromes that are characterized by cancer occurrence in children as well as adults.
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PMID:The sarcoma, breast cancer, lung cancer, and adrenocortical carcinoma syndrome revisited. Childhood cancer. 397 85

Activities of pyrimidine nucleoside phosphorylase in brain tumors were measured and their relationship to a clinical course of the patients was investigated. Pyrimidine nucleoside phosphorylase is said to exist more quantitatively in malignant tumors such as Sarcoma 180, Ehrlich ascites carcinoma, Walker 256, and hepatoma, and very little in normal tissues. In brain tumors the activities were measured by bioassay and compared to that of Sarcoma 180. When the activity of Sarcoma 180 was expressed to be 100%, those of brain tumors were as follows: ten cases of normal brain less than 8.5; six cases of glioblastoma 39.3 +/- 30.7; five cases of astrocytoma 22.0 +/- 13.8; five cases of meningioma 22.4 +/- 13.7; two cases of oligodendroglioma 8.1 and 11.3; two cases of sarcoma 94.3 and 145.4; chordoma 48.0; ependymoblastoma 3.7; plexus papilloma 22.5; parotid cancer 43.4; ten cases of metastatic brain tumors from lung cancer 61.5 +/- 41.6; two cases from breast cancer 28.0 and 68.8; that from thyroid cancer 10.0; that from gastric cancer 13.5; malignant melanoma 77.2. In 12 cases of gliomas (glioblastoma, astrocytoma, oligodendroglioma) the mean activity was highest in glioblastoma (39.3), followed by astrocytoma (22.0) and oligodendroglioma (9.7). The postoperative survival time became shorter in gliomas with the higher activities. In metastatic brain tumors from lung, breast, and gastric cancer, the average time from the diagnosis of primary cancer to brain metastasis was shorter in cases with high activities and longer in cases with low activities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Activities of pyrimidine nucleoside phosphorylase in brain tumors and antitumor effect of 5'-DFUR]. 622 41

A blocking microcytotoxicity assay was used to detect soluble astrocytoma-associated antigen. The richest source of soluble antigen was found in spent culture media from an established glioblastoma (GF) tissue culture line. Also assayed were fractions of sonicated membrane antigen from another (GM) glioblastoma and pellets of GF and GM cultured glioblastoma tissue. Blocking by media conditioned by cultured normal human brain, breast cancer, neuroblastoma, meningioma, or 2-year-old astrocytoma cell lines was 41-82% lower. A monomer was isolated that blocked cytotoxicity and migrated in molecular exclusion chromatography with alpha-macroglobulins rather than the beta-2-microglobulins usually associated with histocompatibility antigens.
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PMID:Microcytotoxicity blocking assay for the detection and isolation of soluble astrocytoma association antigen. 654 96

Antipsychotic drugs that bind to and inhibit the action of calmodulin also inhibit cellular proliferation. In addition these drugs are cytotoxic to most malignant cells and can augment the antiproliferative and cytotoxic effects of bleomycin. They are attractive candidates for use against tumors of the central nervous system since they readily pass the blood-brain barrier and accumulate in the brain. To identify more active derivatives, we studied the effect of a series of phenothiazines and a group of related compounds alone or in combination with bleomycin against rat glioblastoma cell lines. C6 cells were grown for 24 hours prior to a 48 hour exposure to anti-psychotic drug alone or to an IC20 concentration of antipsychotic drug with bleomycin. Cells were stained with methylene blue and enumerated spectrophotometrically. Eight phenothiazines were found to augment the effect of bleomycin by > or = 3-fold. These included 1-chlorpromazine (3.8x), chlorpromazine (3.2x), 3-chlorpromazine (3.0x), 4-chlorpromazine (3.4x), thiomethylpromazine (3.3x), didesmethylchlorpromazine (11x), fluphenazine (5.5x) and trifluoperazine (3.2x). Structurally similar compounds also having activity included trans-flupenthixol (6.0x), 2-chloroimipramine (6.0x), desipramine (22x), and penfluridol (24x). There was a direct correlation between the antiproliferative effect of anticalmodulin compounds and the ability of these drugs to inhibit the activation of calmodulin-sensitive phosphodiesterase. However, there was no correlation between the inhibition of calmodulin and the augmentation of the antiproliferative activity of bleomycin. Penfluridol, one of the most active compounds, was chosen for further study. It increased the activity of bleomycin against L1210 leukemic cells by 90-fold and MCF-7 human breast cancer cells by 4-fold. The effect of penfluridol in combination with bleomycin was due to increased cytotoxicity as measured by clonogenic assay.
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PMID:Effect of anti-calmodulin drugs on the growth and sensitivity of C6 rat glioma cells to bleomycin. 753 9

Human astrocytoma cells were studied using whole-cell patch-clamp recording. Voltage-dependent outwardly-rectifying anion currents were identified in primary cultures of six freshly resected human brain tumors and in seven established anaplastic astrocytoma/glioblastoma cell lines (U251MG, CH235MG, U373MG, U105MG, D54MG, SK-MG-1, and STTG1). Anion currents were not observed in normal, non-neoplastic glial cells, nor in human tumor-derived cells of non-glial origin (melanoma, breast cancer, neuroblastoma, rhabdomyosarcoma). Currents activated at potentials > 50 mV and showed large transients upon termination of voltage steps. Currents reversed at the predicted equilibrium potential for chloride ions and could also be recorded when Cl- was replaced by F-, Br- or I-. Currents were inhibited by the Cl- channel blockers chlorotoxin, DIDS, and DNDS. These Cl- currents may play a role in the growth control of astrocytoma cells.
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PMID:Human astrocytoma cells express a unique chloride current. 874 85


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