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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The establishment of a new glioma cell line, DBTRG-05MG, in a modified RPMI 1640 medium is described. The cells were derived from an adult female with glioblastoma multiforme who had been treated with local brain irradiation and multidrug chemotherapy; the tumor showed substantial change in histologic appearance compared to the original biopsy 13 mo. previously. The line has been successfully cryopreserved and passaged up to 20 times. The karyotype of the cells demonstrated it as a hypotetraploid line; the DNA index of 1.9 confirmed the karyotype analyses. By immunocytochemical analysis, the cell line reacted with polyclonal antibodies to vimentin, S100, and neuron specific enolase, reflecting its primitive neuroectodermal character. Positive immunostaining for epidermal growth factor receptor correlated with the excess of chromosome 7 seen in the karyotype. The cell line reacted negatively to antibodies against platelet-derived growth factor and its receptor, neuronal cell adhesion molecule, and glial fibrillary acidic protein. By flow cytometry, the cells were major histocompatibility class I antigen positive and class I antigen negative. Growth kinetic studies demonstrated an approximate population doubling time of 34 to 41 h and a colony forming efficiency of 71.4%. Western blot analysis showed the presence of low levels of normal-sized retinoblastoma protein. When compared to the patient's lymphocyte DNA, no loss of heterozygosity of the p53 tumor suppressor gene was observed in the DBTRG-05MG cell line DNA.
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PMID:Characterization of a continuous human glioma cell line DBTRG-05MG: growth kinetics, karyotype, receptor expression, and tumor suppressor gene analyses. 133 Oct 21

Forty patients with malignant supratentorial gliomas received iterative intraarterial (IA) infusions of ACNU, 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea at a dose of 150 mg repeated every 6 weeks. Group A consisted of eighteen patients previously treated with surgery, radiation therapy (RT) and sometimes chemotherapy, who received IA ACNU at tumor recurrence. Group B consisted of twenty two patients who received IA ACNU in the postoperative pre-RT period. In group A, 8/18 patients (44%) had an objective response, including 6/12 anaplastic astrocytomas (AA) and 2/6 glioblastoma multiforme (GBM), while 10/18 patients (56%) did not respond. Median survival time was 6 months for GBM and 12 months for AA. In group B, 6/22 patients (27%) had an objective response (4/18 GBM and 2/4 AA) and 16/22 patients (73%) did not respond. Nine patients had such an extensive tumor after one or two courses of IA ACNU that RT was cancelled. Median survival time was 8 months for GBM and 8 months for AA. Three patients (8%) had ophthalmologic toxicity on the infused side. There was no case of leukoencephalopathy.
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PMID:Treatment of malignant gliomas with surgery, intraarterial chemotherapy with ACNU and radiation therapy. 133 43

We have developed an in vivo method of measuring the blood-brain transfer constant (K) of iopamidol and the cerebral plasma volume (Vp) in brain tumors using a clinical X-ray CT scanner. In patient studies, Isovue 300 (iopamidol) was injected at a dosage of 1 ml/kg patient body weight. Serial CT scans of the tumor site and arterial blood samples from a radial artery were taken up to 48 min after injection. The leakage of iopamidol into the brain through the blood-brain barrier was modelled as an exchange process between two compartments, the intravascular plasma space and the tissue interstitial space. Using this model and the concentration measurements in blood plasma and tissue, quantitative estimates of K and Vp in brain tumors were obtained. In addition, distribution of the estimated values of K and Vp in tumors were displayed as false colour functional images overlaid on the conventional CT scan. In a study of twelve patients with anaplastic astrocytoma (n = 3), glioblastoma multiforme (n = 4) or metastases (n = 5) the mean K and Vp values in tumor were found to be 0.0273 +/- 0.0060 ml/min/g and 0.068 +/- 0.11 ml/g respectively. These values were significantly higher than those in grey or white matter in the contralateral 'normal' hemisphere (p less than 0.05). The functional images showed variations in K and Vp within the tumor which were difficult to perceive in the original contrast enhanced CT scans.
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PMID:In vivo CT measurement of blood-brain transfer constant of iopamidol in human brain tumors. 133 51

In experiments to identify molecules that might be important in the pathogenesis of glioblastoma multiforme, the most common malignant brain tumor, we found that annexin II (Lipocortin 2, p36), a likely second messenger in several different mitogenic pathways, was highly expressed in tumor tissue of glioblastoma multiforme (9 of 9) and highly anaplastic astrocytoma (2 of 6), but not in astrocytomas of lower pathological grade (0 of 6). We also detected high levels of annexin II expression in fetal brain during the period when radial glia proliferate, although annexin II expression was not detected in normal adult brain. These data demonstrate that annexin II expression is developmentally regulated in the human central nervous system and suggest that the early progenitor radial glia share important characteristics with highly malignant glial tumors.
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PMID:Developmental regulation of annexin II (Lipocortin 2) in human brain and expression in high grade glioma. 133 84

Between July 1983 and December 1990, 39 patients with pathologically documented glioblastoma multiforme were treated with radiotherapy after biopsy (5 patients) or resection (34 patients). There were 30 males and 9 females ranging in age from 9 to 68 years (median 52). All but one of the 39 patients were treated with 10 MV photons. Whole brain irradiation was delivered through lateral parallel opposed fields for the first 40 Gy, followed by reduced portals to boost the tumor bearing area. The range of tumor dose was 58 to 70 Gy, with a median dose of 64 Gy (33 patients). Treatment was executed at 2 Gy per fraction, 5 days per week for all patients except 2 who received 1.8 Gy per fraction. Eight patients underwent reoperation at least once after radiotherapy due to suspicion of recurrence of the disease. No patients were lost to follow-up: 35 patients had died and 4 were still alive. The median survival time was 11.8 months. The 1- and 2-year survival rates were 49% and 12% respectively. A prognostic factor analysis shows that treatment response and the pre-irradiation Karnofsky status were statistically significant variables influencing survival. The median survival was 28.7 months for patients with complete response, compared with 9.8 months for those with partial response or stable disease (p = 0.002). The median survivals were 13.5 and 9.0 months in high (> or = 70%) and low Karnofsky performance scale (p = 0.04). Smaller tumors, a larger extent of resection, reoperation and younger age were favorable factors with borderline significance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postoperative radiotherapy for glioblastoma multiforme. 133 21

The human brain tumor, astrocytoma, typically progresses through three histopathologically defined stages with the passage of time: one premalignant stage, low-grade astrocytoma; and two malignant stages, anaplastic astrocytoma and glioblastoma multiforme. We correlated the results of a sequence analysis of the tumor suppressor gene, p53, and a restriction fragment length polymorphism analysis of chromosomes 17 and 10 in 45 patients with cerebral astrocytomas at different stages. To detect p53 mutations in tumor DNA, we analyzed polymerase chain reaction products corresponding to every p53-coding exon for single-strand conformation polymorphisms and confirmed the mutations by sequencing. Loss of heterozygosity (LOH) was determined by Southern transfer analysis of somatic and tumor DNA from these same patients using polymorphic markers for various loci on chromosomes 10 and 17. p53 mutations were found in 7 of 25 glioblastomas (28%), in 5 of 14 anaplastic astrocytomas (36%) but in 0 of 6 low-grade astrocytomas. p53 mutations were found in 62% of patients with LOH on chromosome 17p. These results indicated that p53 inactivation is a common genetic event in astrocytoma progression that may signal the transition from benign to malignant tumor stages. LOH on chromosome 10 was found in 61% of glioblastomas, in 23% of anaplastic astrocytomas, but in 0% of low-grade astrocytomas. LOH on chromosome 10 and p53 mutation were found together only in patients with glioblastoma multiforme (22%), suggesting that these genetic changes may accumulate during astrocytoma progression.
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PMID:p53 mutation and loss of heterozygosity on chromosomes 17 and 10 during human astrocytoma progression. 134 55

Thirty-one new RFLP systems corresponding to 24 loci have been identified from a chromosome 10-specific cosmid library. Twelve of the markers on the proximal long arm (cen-q11.2) of this chromosome, including four RFLP systems for the RET locus, will be especially useful in efforts to identify the gene responsible for multiple endocrine neoplasia type 2A (MEN2A). The new panel of markers also may contribute to fine-scale mapping of tumor suppressor genes associated with glioblastoma multiforme or renal cell carcinoma, because allelic deletions in these tumors have implied the presence of a tumor suppressor gene(s) on chromosome 10.
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PMID:Thirty-one new RFLP systems detected by twenty-four DNA markers on human chromosome 10. 134 81

Significant advances have recently been made in a number of areas concerning central nervous system (CNS) neoplasia. Particularly salient are the following: (1) gene amplification is related to increasing grade of human glioma malignancy and occurs in approximately 40% of the most common and most malignant variety of glioma, glioblastoma multiforme (GBM), (2) by far the most commonly amplified gene in glioblastomas is the epidermal growth factor receptor (EGFR) gene, which is amplified in about one third of GBMs, (3) a small percentage of GBMs amplify N-myc or the novel sequence gli, (4) the EGFR gene is rearranged in at least half of gliomas in which it is amplified, and (5) EGFR gene rearrangement results in external domain deletions that yield truncated EGF receptors. Antibodies specific for the mutant EGF receptor fusion junction have been successfully produced and provide stimulating new potential avenues for tumor imaging and therapy. For pediatric CNS neoplasms, only medulloblastoma has been investigated in adequate numbers; a small percentage exhibit amplification of either the N-myc or c-myc genes.
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PMID:Amplified cellular oncogenes in neoplasms of the human central nervous system. 137 22

Human CG is composed of two subunits, alpha and beta. In addition to its eutopic synthesis in normal and malignant trophoblasts, the hormone is produced ectopically by a variety of tumor cell lines of nonplacental origin. Regulation of the alpha CG gene in trophoblasts appears to differ from that in nontrophoblasts. To determine whether these differences are reflected in the chromatin structure at the alpha CG locus, DNase I-hypersensitive sites within this domain were mapped in human tumor cell lines that differentially express the gene. Two hypersensitive sites were detected in DNA from cell lines that produce the alpha-subunit. The latter includes trophoblastic (JAr and JEG-3 choriocarcinoma) and nontrophoblastic (HeLa cervical carcinoma and ChaGo bronchogenic carcinoma) tumor cell lines. The most prominent site (HS 1) was located approximately 100 base pairs upstream from the transcription start site. In trophoblasts, accessibility of HS 1 increased substantially upon induction of the gene by cAMP, likely reflecting alterations in DNA-protein interactions at the cAMP response element and/or tissue-specific enhancer. In nontrophoblasts, where alpha-subunit synthesis is enhanced by sodium butyrate but not by cAMP, neither butyrate nor cAMP altered the accessibility of HS 1. The HS 2 is comprised of multiple sites with weak to moderate DNase sensitivity located downstream at +1600 to +4000 in cell lines that produce alpha-subunit. Cell lines that do not express the alpha CG gene possess a distinct hypersensitive site (HS 3) within the first intron at about +600; these include 3A-Sub-E (SV40 transformed placenta), CBT (glioblastoma multiforme), and CaSki (cervical carcinoma). Cleavage by DNase at HS 1 and HS 2 is not evident in nuclei from cell lines that do not produce alpha-subunit. These results suggest that HS 1 and HS 3 are characteristic of active and inactive states of the alpha CG gene, respectively, and that the accessibility of HS 1 generally correlates with the level of expression.
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PMID:Deoxyribonuclease-hypersensitive sites in the glycoprotein hormone alpha-subunit gene from trophoblastic and nontrophoblastic human tumor cell lines: correlation with expression and effect of chemical inducers. 137 9

The origin of the vascular hyperplasia seen in glioblastoma multiforme is a matter of debate. To test the predominant hypothesis that these glomeruloid structures are of endothelial origin the following study was undertaken. Seven glioblastomas containing prominent glomeruloid vascular structures were stained with Ulex europaeus agglutinin I (UEA-1) and with antibodies against factor VIII/related antigen (fVIII/RAg), glial fibrillary acidic protein (GFAP), S-100 protein, muscle specific alpha-actin (MSA) and smooth muscle specific alpha-actin (SMSA). The GFAP and S-100 antibodies stained the neoplastic glial component of each tumor but did not bind to vascular cells. Endothelial cells lining the lumina of normal vessels and the lumina of glomeruloid vascular structures stained positively with both UEA-1 and fVIII/RAg antibody. No other cells were found to be stained by UEA-1 or by fVIII/RAg antibody. Smooth muscle cells of the normal vasculature stained positively exclusively with anti-MSA and anti-SMSA antibodies. The same pattern of positive actin antibody staining was seen in the majority of cells forming the glomeruloid structures; however, the cells lining the vascular lumina did not bind the MSA and SMSA antibodies. These data strongly suggest that the vascular proliferation resulting in glomeruloid structures is due in large measure to smooth muscle hyperplasia.
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PMID:Vascular smooth muscle hyperplasia underlies the formation of glomeruloid vascular structures of glioblastoma multiforme. 138 13


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