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

In order to understand if antiplatelet drugs possess direct antineoplastic property, we tested the apoptotic effect of 5 popularly marketed antiplatelet drugs in Taiwan in 6 cultured cancer cell lines (Hep 3B hepatocarcinoma, U87-MG malignant glioma, PC-3 prostate adenocarcinoma, HeLa cervical adenocarcinoma, HL-60 preleukemia and K-562 chronic myelogenous leukemia). While acetylsalicylate and flunarizine exerted no effect on these cancer cells, pentoxifyline (PTX), dipyridamole (DYA) and ticlopidine hydrochloride (T. HCl) displayed a time and dose-dependent apoptotic effect on them except for HL-60 and K-562 cells. PTX induced apoptosis in U87-MG, Hep 3B and HeLa cells, DYA in HeLa cells, while T. HCl in U87-MG, Hep 3B, PC-3 and HeLa cells. Adriamycin also provoked apoptotic effect in all 6 cell lines but neither PTX, DYA nor T. HCl acted synergy with adriamycin to HeLa cells, implicating that they may share a similar pathway for inducing apoptosis. Therefore, our results show that the antiplatelet drugs do possess antineoplastic property in vitro. A co-administration of antiplatelet drugs is noteworthy for an alternative adjunctive therapy in cancer patients.
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PMID:Antiplatelet drugs induce apoptosis in cultured cancer cells. 938 74

The authors report a rare case of a cystic metastasis in the midbrain that was successfully treated by brachytherapy following stereotactic biopsy and aspiration of the intratumoral cyst. Stereotactic aspiration of cystic lesions can lead to clinical improvement and brachytherapy prevents cyst recurrence. A 46-year-old man was referred to the authors' institution with a 2-month history of a left hemisensory disturbance and a 1-month history of progressive hemiparesis. Magnetic resonance (MR) imaging revealed a ring-enhancing cystic mass in the midbrain. On the basis of this imaging study, a differential diagnosis that included brainstem abscess, glioma, and metastatic tumor was made. Magnetic resonance imaging-guided stereotactic biopsy and aspiration of the intratumoral cyst were performed, yielding 5 ml of yellowish-white fluid. Histological examination provided a diagnosis of adenocarcinoma. During the surgery, a catheter through which brachytherapy would be delivered was inserted at a predetermined target. The patient's left hemiparesis and sensory disturbance were markedly improved and brachytherapy was begun 2 days postoperatively. Three radioactive isotopes composed of iridium-192 were implanted to irradiate the tumor tissue. The total dose at the tumor periphery was 30 Gy, which was administered over 100 hours. External-beam radiotherapy (20 Gy) was added after completion of the brachytherapy. At discharge from the hospital, the patient was alert and all his neurological symptoms had resolved. Follow-up MR imaging revealed stabilization of the cyst and no recurrence of the tumor. The patient is alive and well 18 months following the brachytherapy. This case suggests that brachytherapy can delay cyst recurrence, suppress tumor growth, and prolong survival in patients with cystic brainstem metastasis.
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PMID:Stereotactic brachytherapy for a cystic metastatic brain tumor in the midbrain. Case report. 942 88

Temozolomide (SCH 52365) is an imidazotetrazine derivative which exhibits broad spectrum activity against murine tumors and is structurally related to dacarbazine (DTIC). Temozolomide cytotoxicity is schedule dependent in vivo with a daily x 5 schedule showing the highest activity. Oral temozolomide is rapidly and completely absorbed with minimal interpatient and intrapatient variability in pharmacokinetics. Clinical studies have demonstrated activity against melanoma and glioma. The present study examined the activity of oral temozolomide against patients with pancreatic cancer. Patients with advanced pancreatic adenocarcinoma previously untreated with chemotherapy received temozolomide 200 mg/m2/day once daily orally for 5 days with cycles repeated every 28 days. There were 16 patients entered on study with 15 evaluable for response and toxicity. There were no responses seen in 15 evaluable patients with 14 manifesting progressive disease within 2 months of starting therapy. Toxicity was primarily hematological with 3 patients experiencing > or = grade 3 neutropenia and thrombocytopenia respectively. Other toxicities were relatively modest. In conclusion, temozolomide in the once daily x 5 schedule is inactive against adenocarcinoma of the pancreas.
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PMID:A phase II study of temozolomide in advanced untreated pancreatic cancer. 974 May 47

Fifty-eight skin biopsies and three primary internal tumors from patients affected by the rare hereditary disease xeroderma pigmentosum (XP) were studied by an improved PCR-single strand conformation polymorphism analysis to detect the mutations of the tumor suppressor gene p53. The results from cutaneous XP tumors, including 27 squamous cell carcinomas and 6 basal cell carcinomas, show a very high level (86%) of p53 mutations. The analysis of mutations found in XP skin cancers according to the complementation group of the patients shows that tandem CC-->TT transitions are a characteristic of XP-C patients with a frequency much higher in their skin tumors (85%) compared with tumors in XP patients who do not belong to group C (33%). In all XP-C biopsies, mutations were due to replication of unrepaired DNA lesions on the nontranscribed strand of the p53 gene, substantiating the preferential repair in vivo of the transcribed strand of this gene in human tissues. For the first time, we were able to analyze three primary internal tumors (a neuroendocrine tumor of the thyroid, a gastric adenocarcinoma, and a glioma of the brain) of young XP children. All of them contained one mutation on the p53 gene, which were different from the ones found in the XP skin tumors and could have resulted from unrepaired lesions caused by oxidative damage.
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PMID:p53 mutations in skin and internal tumors of xeroderma pigmentosum patients belonging to the complementation group C. 976 70

Recently, we have demonstrated that a spectrum of human adenocarcinoma cell lines express binding sites for interleukin 13 (IL-13). These cells are killed by a chimeric protein composed of human (h) IL-13 and a derivative of Pseudomonas exotoxin, PE38QQR (Debinski et al., J. Biol. Chem., 270: 16775-16780, 1995). The cell killing was hIL-13- and hIL-4-specific, indicating that a common binding site for the two cytokines is present in several solid tumor cell lines. Herein, we report that an array of established glioma cell lines is killed by very low concentrations of hIL-13-PE38QQR, often reaching <1 ng/ml (<20 pM). Glioma cells express up to 30,000 molecules of IL-13 receptor/cell which has intermediate affinity toward hIL-13. hIL-13-PE38QQR is more active (up to 3 logs difference in cytotoxic activities) than are the corresponding chimeric toxins containing hIL-4 or hIL-6. The cytotoxic action of hIL-13-PE38QQR is blocked by an excess of hIL-13 on all cell lines studied, and it is not neutralized by hIL-4 on some of these cells. Our results show that human brain cancers richly express receptors for IL-13. Furthermore, the interaction detected previously between receptors for IL-13 and IL-4 on solid tumors cell lines is of a qualitatively different character in U-251 MG and U-373 MG glioma cells. The receptor for IL-13 may represent a new marker of brain cancers and an attractive target for anticancer therapies.
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PMID:Human glioma cells overexpress receptors for interleukin 13 and are extremely sensitive to a novel chimeric protein composed of interleukin 13 and pseudomonas exotoxin. 981 19

The chromosomal region 10q23-24 is frequently deleted in a number of tumour types, including prostate adenocarcinoma and glioma. A candidate tumour-suppressor gene at 10q23.3, designated PTENor MMAC1, with putative actin-binding and tyrosine phosphatase domains has recently been described. Mutations in PTEN have been identified in cell lines derived from gliomas, melanomas and prostate tumours and from a number of tumour specimens derived from glial, breast, endometrial and kidney tissue. Germline mutations in PTEN appear to be responsible for Cowden disease. We identified five PTEN mutations in 37 primary prostatic tumours analysed and found that 70% of tumours showed loss or alteration of at least one PTEN allele, supporting the evidence for PTEN involvement in prostate tumour progression. We raised antisera to a peptide from PTEN and showed that reactivity occurs in numerous small cytoplasmic organelles and that the protein is commonly expressed in a variety of cell types. Northern blot analysis revealed multiple RNA species; some arise as a result of alternative polyadenylation sites, but others may be due to alternative splicing.
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PMID:Mutation and expression analysis of the putative prostate tumour-suppressor gene PTEN. 982 69

The kinetics of an indium-111 labeled bleomycin complex (111In-BLMC) after rapid intravenous injection in patients with brain tumors was quantified by using compartmental and non-compartmental models. The models were applied to data obtained from 10 glioma, one meningioma, and one adenocarcinoma brain metastasis patients. Blood and urine samples from all the patients and tumor samples from three patients were collected. The mean transit time of 111In-BLMC in the plasma pool was 14 +/- 7 min without and 1.8 +/- 0.6 h when accounting for recirculation, and 13 +/- 4 h in the total body pool. The mean plasma clearance of 111In-BLMC was 0.3 +/- 0.1 m/blood/min and the mean half-life in urine was 3.5 +/- 0.6 h. The mean transfer coefficients for the open three-compartmental model were: excretion from plasma = 0.02 +/- 0.01, from depot to plasma = (12 +/- 9)*10(-4), from plasma to depot = 0.01 +/- 0.01, from tumor to plasma = 0.39 +/- 0.19 and from plasma to tumor = 1.11 +/- 0.57, all in units minute-1. The mean turnover time from the tumor was 4.5 +/- 2.7 min and from the depot 20 +/- 8 h. It is concluded that both compartmental and non-compartmental models are sufficient to describe the kinetics of indium-111 labeled bleomycin complex. The non-compartmental model is more practical and to some extent more efficient in describing the in vivo behaviors of 111In-BLMC than the compartmental model. The compartmental model used provides estimates of both extraction and excretion from the plasma and tumor.
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PMID:Kinetics of 111In-labeled bleomycin in patients with brain tumors: compartmental vs. non-compartmental models. 997 68

The aliphatic dicarboxylic acid surprisingly afforded potent cytotoxicity and in vivo antineoplastic activity. The agents were active against the growth of a variety of leukemias, lymphomas, and suspended HeLa uterine carcinoma. Suppression of growth of cell lines derived from human solid cancers, e.g. SW-480 colon adenocarcinoma, lung MB- 9812, glioma HS-683, and rat osteosarcoma UMR-106 was observed. A mode of action study in L1210 lymphoid leukemia demonstrated that DNA and RNA syntheses were inhibited at multiple sites including ribonucleoside reductase, purine de novo synthesis at PRPP-amidotransferase and IMP dehydrogenase and nucleic acid kinases. These studies could not exclude the possibility that the agents also interacted with the DNA molecule itself interfering with the utilization of the template.
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PMID:Cytotoxicity and mode of action of aliphatic dicarboxylic acids in L1210 lymphocytic leukemia cells. 1022 44

We established a protocol for the non-isotopic in situ detection of adhesion molecule CD44 messenger RNA (mRNA) in archival formalin-fixed paraffin-embedded sections of human surgical materials. Four brain tumor samples with different histopathologies (a metastatic adenocarcinoma, a metastatic squamous carcinoma, a glioblastoma and a craniopharyngioma) were thus studied using a 157 nt digoxigenin-labeled RNA probe complementary to the common mRNA region to all the CD44 isoforms. The CD44 transcript was detected in the cytoplasm of glioma and such epithelial tumor cells as metastatic carcinoma and craniopharyngioma. A competitive hybridization study confirmed the specificity of the CD44 probe. The optimization of critical conditions are also discussed. This protocol should therefore be useful in making an accurate evaluation of mRNA localization and may also facilitate the successful completion of extensive retrospective studies on a large number of archival samples.
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PMID:Non-isotopic in situ hybridization of CD44 transcript in formalin-fixed paraffin-embedded sections. 1023 50

Turcot's syndrome is characterized clinically by the occurrence of primary brain tumor and colorectal tumor and has in previous reports been shown to be associated with germline mutations in the genes APC, hMLH1, and hPMS2. Here we describe three patients with Turcot's syndrome, each having colorectal adenocarcinoma and malignant glioma. All the colorectal and brain tumors from these patients showed replication errors in most of the microsatellite loci investigated. Search for underlying germline mutations in the nucleotide mismatch repair genes revealed three different hMSH2 mutations. All colorectal tumors showed a frameshift in the A(10) tract in the coding sequence of the transforming growth factor beta type II receptor (TGFBRII) gene, but no such change was detected in any of the brain tumors. Frameshift mutation in the BAX gene was found in one colon carcinoma and mutations in insulin-like growth factor type II receptor (IGFIIR) gene in one glioma. Our data have broadened the possible mutation spectrum of patients with Turcot's syndrome. The difference in the mutation spectrum of TGFBRII, BAX, and IGFIIR between brain and colorectal tumors in these individuals suggests that the mutator phenotype may target different pathogenic pathways in the oncogenic process of the two organs.
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PMID:Germline hMSH2 and differential somatic mutations in patients with Turcot's syndrome. 1033 89


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