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)

A survey of in vitro cytotoxic effects of camptothecin in human epitheliod sarcoma, colon, breast and ovarian carcinomas, glioblastoma, and neuroblastoma (PNET) cell lines, was done. We chose the MTT assay to measure survival and observed that 24 h exposures to camptothecin caused consistently greater toxicity than 1 h exposures. The LD50 for camptothecin was in the 12.5-25 ng/ml range. There was a 10-fold range of growth rates measured by OD after 5 days exposure and varied expression of MDR1 in these cell lines--none of which could be correlated with tumor sensitivity to drug. The most sensitive cell lines were colon and glioblastoma, and the most resistance were ovarian, breast and epithelioid sarcoma.
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PMID:Camptothecin cytotoxic effects in vitro: dependency on exposure duration and dose. 757 68

Models for hematogenous spread of human cancer to the central nervous system (CNS) were established by injecting human tumor cells into the internal carotid artery of nude rats. With 4 out of 10 cell lines, belonging to four different tumor types, metastases developed in all injected animals. Tumor growth manifested clinically as neurological symptoms which appeared after a median latency ranging from 19-87 days for the different tumors. The H-146 and DMS-273 small cell lung cancers and the LOX melanoma almost exclusively gave meningeal tumors, whereas with FEMX-I melanoma cells bone metastases in the skull dominated. For these tumor types a correlation was found between the capacity for experimental metastasis formation and the s.c. tumorigenicity. In agreement with clinical experience, none of the 2 sarcoma and 2 glioblastoma lines gave CNS metastases. With a modified microsurgical technique, allowing for repeated ipsilateral intracarotid injections, we analyzed the drug concentrations obtained in tumor and surrounding brain tissue after i.v. treatment with doxorubicin. The concentration in the LOX tumor reached therapeutic levels and was approximately 100 x higher than in normal brain tissue, both with and without intraarterial pretreatment with arabinose. In the same model, the tissue concentrations of 9.2.27-abrin immunotoxin 10 min after intracarotid injection were examined. Although the levels were low, a tumor to brain concentration ratio of up to 9 was achieved. The data demonstrate that clinically relevant tumor models can be established with the techniques described, and these models may successfully be used to evaluate the pharmacokinetics and effect of intravenous or intraarterial therapy.
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PMID:Nude rat models for human tumor metastasis to CNS. Procedures for intracarotid delivery of cancer cells and drugs. 769 16

Interphase cytogenetics, i.e., in situ hybridization using probes to chromosome-specific DNA, enables histological identification of cells bearing numerical chromosome aberrations and cytogenetic analysis of composite tumors. We studied routinely processed tissues from seven glioblastomas and three gliosarcomas using biotinylated probes to pericentromeric alpha-satellite sequences on chromosomes 10, 17 and X. By applying various pretreatment protocols, an evaluable compromise between morphology and signal intensity was obtained in most cases. Compared to vascular cells with normal chromosomal counts, a significant subpopulation of glioblastoma cells showed monosomy 10 (four of five cases), monosomy 17 (one of seven cases) and loss of one X chromosome (one of seven cases). All monosomy 10 cases comprised additional areas where two copies of chromosome 10 were retained. Among the gliosarcomas, both the glioma and the sarcoma portion showed monosomy 10 in one case and monosomy 17 in another case. In contrast, in the third case of gliosarcoma, monosomy 10 was found only in the glioma portion, whereas a gain of chromosome X was observed in the sarcoma portion. We conclude that: (1) numerical chromosome aberrations can be detected in routinely processed brain tumor biopsy specimens using interphase cytogenetics, making retrospective studies feasible; (2) glioblastomas show intratumoral cytogenetic heterogeneity with formation of monoclonal cell clusters; and (3) sarcoma and glioma elements in gliosarcomas may exhibit the same or different numerical chromosome aberrations, suggesting various histogenetic pathways of the sarcoma-like portion.
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PMID:Interphase cytogenetics of glioblastoma and gliosarcoma. 784 70

Previously, we identified an amplified gene in a stomach cancer cell line, KATO-III, and designated it K-sam. This gene was later found to be identical with a gene for a receptor tyrosine kinase, bek/FGFR2. One of the characteristics of the K-sam gene is structural diversity of its transcripts; K-sam complementary DNA (cDNA) cloned from human brain (K-sam-I) has a completely different sequence at the third extracellular immunoglobulin-like domain as compared to that of the K-sam cDNA derived from KATO-III cells (K-sam-II). Recent study has revealed that this difference signifies a differential ligand affinity; the receptor encoded by the K-sam-I cDNA has a high affinity for basic fibroblast growth factor (bFGF), while the K-sam-II cDNA corresponds to a receptor with the high affinity for keratinocyte growth factor (KGF). Reverse transcription-polymerase chain reaction and RNA blot analysis showed that the K-sam-II-type transcript was present in carcinoma cell lines but not in any of the sarcoma cell lines examined. The K-sam-I-type transcript was expressed in both carcinoma and sarcoma cell lines. Furthermore, KGF enhanced the DNA synthesis of the esophageal cancer cells, TE-1, in a dose-dependent manner, while the effect of bFGF was not substantial. In contrast, the glioblastoma cell line, A-172, that expressed the bFGF receptor showed a mitogenic response to bFGF but not to KGF. These data suggest that KGF is a growth factor used preferentially in cancer cells, and this preference is based on the presence of the K-sam-II-type receptor in carcinoma cells but not in sarcoma cells due to alternative splicing.
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PMID:Preferential expression of the third immunoglobulin-like domain of K-sam product provides keratinocyte growth factor-dependent growth in carcinoma cell lines. 827 90

A case of gliosarcoma with a large cyst is reported. A 22-year-old female was admitted to our hospital with complaints of blurred vision and headache. Plain skull x-ray films showed a radiolucent area in the right frontal area. Computed tomography (CT) revealed an iso-dense mass in the right frontal lobe with a large cyst. After administration of contrast medium, the solid part and cyst wall were well enhanced and the content of the cyst was slightly enhanced. CT number of the cyst fluid was increased from 64.2 to 83.5 Hounsfield units, after administration of the contrast medium. Axial T1-weighted magnetic resonance image (MRI) revealed an iso-intense mass with marked enhancement by Gd-DTPA in the same area. A large cyst was shown to be located in the dorsal part of the mass. A small round protrusion, 10 mm in diameter, was found on the anterior portion of the mass on this MRI. Right carotid angiogram showed a tumor stain fed by the frontopolar artery. Right frontal lobectomy including the tumor was carried out with a preoperative diagnosis of glioblastoma. The patient received radiation therapy of 60Gy (whole brain 40Gy; focal 20Gy) and chemotherapy postoperatively. Histologically, necrosis, hemorrhage and endothelial hyperplasia were revealed at the tumor lesion. The tumor was composed of proliferation of glial and mesenchymal elements. The glial element appeared as fibrillary astrocytoma and polar spongioblastoma. The mesenchymal element showed sarcoma. As mentioned above, this tumor was diagnosed as gliosarcoma. It was difficult to make a diagnosis of gliosarcoma preoperatively because of the complex findings similar to malignant gliomas in conventional neuroradiological imaging.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of gliosarcoma associated with large cyst]. 832 57

Borocaptate sodium (BSH) and L-boronophenylalanine (L-BPA) are two boron carriers used for boron neutron capture therapy (BNCT) in the treatment of glioblastoma and melanoma, respectively. The suitability of these two compounds was evaluated on the basis of pharmacokinetic studies aiming at characterizing their biodistribution, tumor uptake and tumor selectivity. Boric acid was also used as a reference compound since it is nonselective and relatively freely diffusible. The compounds were investigated in two tumor models, a B16 pigmented melanoma and the RIF1 sarcoma. Mice were sacrificed after different boron doses at various post-injection times and tissue and plasma levels measured using inductively coupled plasma atomic emission spectroscopy (ICP-AES). The proposed minimum effective tumor boron concentration of 15 ppm was achieved in both tumor models for the three compounds tested, although only for L-BPA in the melanoma was this achieved when tumor-plasma ratios were above 1. In the RIF1 model, maximum tumor concentrations of 44 and 31 ppm B were reached after administration of 50 micrograms B/g body weight for boric acid and BSH, respectively. After administration of 12.5 micrograms B/g of L-BPA, maximum concentrations of 15 and 21 ppm were found in the RIF1 and B16 models, respectively. Tumor-plasma ratios (TPR) for BSH remained close to or below unity at all times studied in both tumors. Brain levels of BSH were very low, however, leading to tumor-brain ratios markedly greater than 1 at all times. L-BPA and boric acid showed TPR values above unity in both tumor models, reaching 3.2 in B16.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selectivity of boron carriers for boron neutron capture therapy: pharmacological studies with borocaptate sodium, L-boronophenylalanine and boric acid in murine tumors. 832 32

An IgM human monoclonal antibody (HuMAb) SK1 was generated from mesenteric nodal lymphocytes of a colon cancer patient that were fused with a human B-lymphoblastoid cell line SHFP-1. The reactivities of HuMAb SK1 to various human cell lines were screened by cell enzyme linked immunosorbent assay and immunocytochemical staining. The HuMAb SK1 reacted strongly with all 11 human carcinoma cell lines that were tested and had no detectable binding with noncarcinoma cell lines of the following origins: fibroblast; fetal lung; melanoma; soft tissue sarcoma; neuroblastoma; and glioblastoma. Carcinoma preferred reactivity of HuMAb SK1 was further confirmed by immunoperoxidase staining of a large number of frozen tissues, both malignant and benign. The antigen SK1 (AgSK1) in human carcinoma detected by immunoperoxidase staining was also identified biochemically as a sialoglycoprotein that migrated at M(r) 42,000 with an isoelectric point (pI) of approximately 5.9. A preferential staining by HuMAb SK1 was seen among colorectal, gastric, pancreatic, and lung cancers. Competitive inhibition study in solid-phase immunoassay suggested that the HuMAb SK1 did not cross-react with other antibodies specific for CEA, CA 19-9, and TAG 72. The AgSK1 appears to be a novel carcinoma associated antigen which may be a useful tumor marker in cancer diagnosis and treatment.
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PMID:AgSK1, a novel carcinoma associated antigen. 843 57

The presence of connective tissue elements in gliomas necessitates in every case a thorough analysis of the character and derivation of such elements to allow the formulation of an appropriate diagnosis. Four cases are presented in this paper. In cases 1 and 2 (anaplastic astrocytomas in two children, 9 and 4 years old, respectively) all the neoplastic elements were astrocytes and their ability to produce or indirectly promote the production of reticulin and collagen fibers accounted for the presence of such elements in close association with the tumor cells. The term "gliofibroma" has been coined for such tumors, but "desmoplastic astrocytoma", (low grade or anaplastic) or in highly malignant cases "desmoplastic glioblastoma", as the case may be, also seem to be appropriate terms for such neoplasms. In contrast, cases 3 and 4 represented composite tumors in adults (66 and 58 years old, respectively) and the neoplasms of these patients consisted of glioblastoma and sarcoma, the latter component demonstrably being of vascular origin. This is the type of tumor usually referred to as gliosarcoma or "Feigin tumor". Although some apparent similarities between the two groups may exist at times, the histogenesis of the latter group's sarcomatous or sarcoma-like portions is different from that of the first group and, therefore, warrants separate diagnostic terms and placement in brain tumor classification.
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PMID:Gliofibromas (including malignant forms), and gliosarcomas: a comparative study and review of the literature. 848 May 9

The major cytotoxic component of hemin was identified as metal free protoporphyrin IX in an epithelioid sarcoma cell line (VA-ES-BJ) and a glioblastoma cell line (U-373 MG) by exposing the cell lines to the iron chelator deferoxamine, tin-protoporphyrin IX, and protoporphyrin IX. The contribution of lipid peroxidation and free radical generation to toxicity was examined using DL-buthionine-[S,R]-sulfoximine (BSO), and 21-aminosteroid (lazaroid, U74500A). Hemin caused significantly greater toxicity in VA-ES-BJ than in U-373 MG. While exogenous PpIX was more toxic than hemin in both cell lines, this toxicity was not due to iron depletion following intracellular heme formation since ferric citrate did not reverse PpIX toxicity. Pre-treatment with BSO enhanced hemin toxicity in the VA-ES-BJ cell line but not in U-373 MG, suggesting different modes of toxicity in the two cell lines. Exposure to lazaroid protected only VA-ES-BJ from protoporphyrin-induced toxicity implicating a specific sensitivity to lipid peroxidation and/or free radical generation by this cell line. These characteristics of the VA-ES-BJ cell line distinguish it from the glioblastoma and emphasize its utility for exploring cytotoxic effects of hemin and its precursors.
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PMID:Hemin toxicity in a human epithelioid sarcoma cell line. 857 85

The purpose of this study is to evaluate the radiation sensitivity of human soft tissue sarcoma cell lines in vitro and to compare with that of human breast carcinoma and glioblastoma cell lines. The intrinsic radiation sensitivity parameters of seven human soft tissue sarcomas and eight breast carcinoma cell lines were investigated in vitro by clonogenic assays for single-dose irradiation under aerobic conditions on cells in exponential phase of growth. The results for sarcoma cell lines showed that the mean surviving fraction at 2 Gy (SF2) was 0.39 (SD +/- 0.09) with a range of 0.24 to 0.53, and the average mean inactivation dose (MID) was 1.92 (SD +/- 0.35) range from 1.36 Gy to 2.49 Gy. These values were not different from that of breast cell lines examined concurrently and using the same experimental methods (mean SF2 0.38, SD +/- 0.09; MID 1.9 Gy, SD +/- 0.37). However radiobiological parameters of nine karyotyped human malignant glioma cell lines determined earlier in this laboratory were significantly higher (mean SF2 0.50 +/- 0.14; mean MID 2.61 +/- 0.60). In conclusion, the data presented here do not support the view that cells of sarcomas show unusual radiation resistance. To the extent that the in vitro determined cellular radiation sensitivity reflects the tumor response in vivo, the success rate for radiation applied against sarcoma and breast carcinoma of comparable size could be similar.
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PMID:Comparison between the in vitro intrinsic radiation sensitivity of human soft tissue sarcoma and breast cancer cell lines. 862 1


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