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)

An autopsy case of glioblastoma multiforms of the pons with a colon cancer, a rectal carcinoid, a renal adenoma and three gastric leiomyomas in a 81-year-old-woman is reported with a statistical analysis on multiple primary cancers associated with primary brain tumors as reported in the Japan autopsy annuals. Out of 329, 705 autopsy cases from 1975 to 1984 in the Japan autopsy registry, double cancers and triple cancers that included a primary brain tumor amounted to 123 cases (0.037%) and 12 cases (0.0036%), respectively. Other sites for primary cancers were the thyroid (23%), the stomach (15%), the lungs (12%), and the colon (10%) in that order of frequency.
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PMID:[An autopsy case of triple primary cancers consisting of glioblastoma multiforme of the pons, colon cancer and rectal carcinoid--a statistical analysis of cases of brain tumor combined with other primary cancers in Japan autopsy annuals]. 282 42

Colony growth in soft agar was used to identify human tumors that were sensitive to the direct antiproliferative effects of mismatched dsRNA (Ampligen). The results suggest that different human solid malignancies vary significantly in their sensitivity to Ampligen. Tumors with 50% or more of their surgical specimens showing sensitivity included carcinoid, glioblastoma, and carcinomas of the kidney, and lung. Resistant tumors (less than 15% sensitivity) included sarcomas and colo-rectal carcinomas. Overall, 42% of the tumor specimens studied showed a 50% or greater reduction in tumor cell colony formation after a single initial treatment with Ampligen (250 micrograms/ml). Interestingly, one patient's tumor which was de novo sensitive to interferon (IFN), but emerged as IFN-resistant following IFN therapy, remained sensitive to Ampligen. Thus, a clonogenic assay may prove useful in identifying human tumors and individuals for clinical trials with Ampligen, including patients resistant to IFN.
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PMID:Antiproliferative effect of mismatched double-stranded RNA on fresh human tumor cells analyzed in a clonogenic assay. 377 78

Thirteen tumor-derived cell lines of human and nonhuman origin and from various tissues were examined for the presence and density of sigma-1 and sigma-2 receptors. Sigma-1 receptors of a crude membrane fraction were labeled using [3H](+)-pentazocine, and sigma-2 receptors were labeled with [3H]1,3-di-o-tolylguanidine ([3H]DTG); in the presence or absence of dextrallorphan. [3H](+)-Pentazocine-binding sites were heterogeneous. In rodent cell lines (e.g., C6 glioma, N1E-115 neuroblastoma, and NG108-15 neuroblastoma x glioma hybrid), human T47D breast ductal carcinoma, human NCI-H727 lung carcinoid, and human A375 melanoma, [3H](+)-pentazocine bound to high- and low-affinity sites with Kd1 = 0.67-7.0 nM, Bmax1 = 25.5-108 fmol/mg protein, Kd2 = 127-600 nM, and Bmax2 = 942-5431 fmol/mg protein. However, [3H](+)-pentazocine bound to a single site in other cell lines. In human U-138MG glioblastoma, SK-N-SH neuroblastoma, and LNCaP.FGC prostate, Kd = 28-61 nM and Bmax = 975-1196 fmol/mg protein, whereas in ThP-1 leukemia Kd = 146 nM and Bmax = 1411 fmol/mg protein. The sigma-1-like nature of [3H](+)-pentazocine-binding sites was confirmed by competition studies which revealed high affinity for haloperidol and enantioselectivity for (+)-pentazocine over (-)-pentazocine. Interestingly, human MCF-7 breast adenocarcinoma showed little or no specific binding of [3H](+)-pentazocine, suggesting the absence of sigma-1 receptors in this cell line. All cell lines examined expressed a high density of sigma-2 receptors with Kd values for [3H]DTG ranging from 20 to 101 nM and Bmax values of 491 to 7324 fmol/mg protein. Competition studies indicated possible heterogeneity of sigma-2 receptors. While sites labeled by [3H]DTG in all cell lines tested exhibited affinity for haloperidol and preference for (-)-pentazocine over the (+)-enantiomer, human cell lines generally showed 4- to 7-fold lower affinity for haloperidol and approximately 10-fold lower affinity for (-)-pentazocine compared with the rodent cell lines. The high density of sigma-1 and sigma 2-binding sites in these cell lines suggests important cellular functions in cancer, as well as potential diagnostic utility for tumor-imaging agents which target sigma sites. These cell lines may be useful as model systems in which to study the functions of sigma sites in normal tissues, as well as their possible role in tumor biology.
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PMID:Sigma-1 and sigma-2 receptors are expressed in a wide variety of human and rodent tumor cell lines. 781 73

Bombesin/gastrin releasing peptide (BN/GRP) receptors were solubilized and purified from human glioblastoma (U-118) and lung carcinoid cell lines (NCI-H720). The U-118 cells, when extracted with CHAPS/cholesterol hemisuccinate (CHS), bound (125I-Tyr4)BN with high affinity (Kd = 2 nM) to a single class of sites (Bmax = 150 fmol/mg protein). Specific (125I-Tyr4)BN binding was inhibited with high affinity by BN, GRP, GRP14-27, and receptor antagonists such as (D-Phe6)BN6-13methylester(ME) and (D-Phe6)BN6-13 propylamide(PA) (IC50 = 2, 22, 3, 1 and 2 nM, respectively) but not GRP1-16 or BN1-12. The solubilized and cellular receptor bound peptides with similar affinity. The solubilized receptor was purified using (Lys0, Gly1-4, D-Ala5)BN and (Lys3, Gly4,5, D-Tyr6)BN3-13 PA affinity resins. When eluted from the affinity resins by NaCl, the receptor bound (125I-D-Tyr6)BN6-13ME with high affinity. The NCI-H720 BN/GRP receptor was purified 86,000-fold after extraction with CHAPS/CHS and purification using both affinity resins. SDS-PAGE analysis indicated that major 65 and 115 kDa proteins were purified. These data indicate that BN/GRP receptors can be solubilized from human cells and purified using affinity chromatography techniques with retention of ligand binding activity.
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PMID:Solubilization and purification of bombesin/gastrin releasing peptide receptors from human cell lines. 839 Dec 95

Meta-iodobenzylguanidine conjugated to 131I-iodine is an effective agent for the targeted radiotherapy of tumors of neural crest origin which express the noradrenaline transporter (NAT). The therapeutic application of 131I MIBG is presently limited to the treatment of phaeochromocytoma, neuroblastoma, carcinoid and medullary thyroid carcinoma. To determine the feasibility of MIBG targeting for a wider range of tumor types, we employed plasmid-mediated transfer of the NAT gene into a human glioblastoma cell line (UVW) which does not express the NAT gene. This resulted in a 15-fold increase in uptake of MIBG by the host cells. A dose-dependent toxicity of 131I MIBG to the transfectants was demonstrated using three methods: (1) survival of clonogens derived from monolayer culture; (2) survival of clonogens derived from disaggregated multicellular spheroids; and (3) spheroid growth delay. 131I MIBG was twice as toxic to cells in spheroids compared with those in monolayers, consistent with a greater effect of radiation cross-fire (radiological bystander effect) from 131I beta-radiation in the three-dimensional tumor spheroids. The highest concentration of 131I MIBG tested (1 MBq/ml) was nontoxic to UVW control cells or spheroids transfected with the NAT gene in reverse orientation. These findings are encouraging for the development of NAT gene transfer-mediated 131I MIBG therapy.
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PMID:Noradrenaline transporter gene transfer for radiation cell kill by 131I meta-iodobenzylguanidine. 1045 18

A constellation of newly diagnosed benign tumours and glioblastoma is an uncommon occurrence in a single individual. We present a case of a patient with a history of skin lipomas who presented with seizures and was found to have a left frontotemporal multifocal enhancing mass on MRI. Work-up for metastatic disease revealed a benign lung carcinoid tumour, a cervical schwannoma, adrenal masses, a growth hormone-secreting pituitary adenoma, and lastly a glioblastoma following brain biopsy.
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PMID:Simultaneous diagnosis of glioblastoma, cervical schwannoma, adrenal masses and growth hormone-secreting adenoma in a previously healthy patient. 3143 70