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)

The purpose of these studies was to determine whether blood monocytes of patients with different stages of colorectal carcinoma could be activated by various immunomodulators to become tumor cytolytic. Monocytes obtained from 12 colorectal carcinoma patients and 8 normal donors were incubated in vitro with free or liposome-encapsulated agents. The cytotoxic properties of the monocytes were determined subsequent to interaction with radioactively labeled allogeneic colon carcinoma cells, melanoma cells, glioblastoma cells, and allogeneic nontumorigenic skin cells. Blood monocytes from normal donors and all colorectal carcinoma patients were activated in vitro to become tumoricidal by immunomodulators in free form or entrapped within liposomes; i.e., the monocytes recognized and lysed tumorigenic cells but not nontumorigenic cells. The tumoricidal activity of monocytes was observed in blood monocytes obtained from patients even after multiple doses of radiotherapy and chemotherapy, and that fact suggests that the in vivo activation of macrophages may be feasible.
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PMID:Activation of tumoricidal properties in peripheral blood monocytes of patients with colorectal carcinoma. 300 May 91

Pituitary carcinoma is defined as a malignant pituitary tumour associated with blood- or lymph-borne metastases. Cushing's disease is frequently present in patients with this condition. After adrenalectomy for Cushing's disease, a 37-year-old man developed Nelson's syndrome resulting from a pituitary carcinoma with metastases to the spinal cord, cauda equina, heart, liver, and pancreas. The primary tumour and its metastases showed immunocytochemical staining for ACTH, beta-lipotrophin, and variably for beta-endorphin and alpha-melanocyte stimulating hormone (alpha-MSH). A coincidental glioblastoma was also present. Nine cases of Cushing's disease associated with pituitary carcinoma, including the present patient, are documented in the literature. The case reported is only the second in which immunohistochemical staining of the primary pituitary tumour and its metastases was performed, and the first in which ACTH-related peptides, in addition to ACTH itself, were demonstrated in the carcinoma cells.
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PMID:Pituitary pro-opiomelanocortin-cell carcinoma occurring in conjunction with a glioblastoma in a patient with Cushing's disease and subsequent Nelson's syndrome. 302 76

In this article the authors deal with the morphology of primary tumors of the central nervous system and its coverings. The discussion includes astrocytoma variants/glioblastoma, ependymoma and its variants, subependymoma, choroid plexus papilloma and carcinoma, embryonal CNS tumors, neuronal neoplasms, meningioma, dural hemangiopericytoma (angioblastic mengioma), and hemangioblastoma.
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PMID:Central nervous system tumors. 303 Jun 12

A human X human hybridoma, CLNH11, derived from a lymphocyte of a patient with cervical carcinoma, produces a human monoclonal antibody of gamma 1 and kappa isotypes (CLN-IgG). Immunoperoxidase staining showed that CLN-IgG reacted with frozen tissue sections of human malignant tumors (cervical carcinoma, gall bladder carcinoma, glioblastoma), but not with their normal counterparts. Enzyme-linked immunosorbant assay also demonstrated that CLN-IgG reacted with various human tumor cell lines, but not with non-tumorigenic cells such as some fibroblasts, peripheral blood lymphocytes and red blood cells. Indirect and direct immunofluorescence staining indicated that the tumor antigens recognized by CLN-IgG were located in restricted areas close to the cell surface and exposed on the outer surface of the cell membrane. A protein antigen of Mr 226,000 was purified to homogeneity by affinity chromatography with CLN-IgG from the plasma membrane fraction of A549 lung tumor cell line. The antigen consisted of alpha (Mr 60,000) and beta subunit (Mr 53,000) which were linked by disulfide bond(s) (TA60K/53K). The TA60K/53k antigens were expressed commonly in other tumor cell lines originated from histologically different tissues.
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PMID:Identification of a malignant cell associated antigen recognized by a human monoclonal antibody. 304 15

The production of platelet-derived growth factor like (PDGF-like) material by glioblastomas may be involved in the conversion of normal cells to tumor cells. In an investigation of this problem, we have examined some of the properties of the platelet-derived growth factor B-chain mRNA (c-sis mRNA) by a sensitive and quantitative RNA-RNA solution hybridization method. In 5 out of 8 human glioblastoma cell lines, c-sis mRNA was present, and in the line with the highest level, there were approximately 4-10 molecules per cell. The half-lives of the c-sis mRNA in two glioblastoma cell lines were 2.6 and 3.4 h, while in human umbilical vein endothelial (HUVE) and bladder carcinoma (T24) cells they were 1.6 and 2.5 h, respectively. Inhibiting protein synthesis produced no significant alteration of the c-sis mRNA half-lives in the glioblastoma or HUVE cells. The A-U-rich sequence at the 3' end of the c-sis mRNA therefore does not appear to affect the mRNA stability in the presence of cycloheximide as it does in other transcripts. The similarity of the c-sis mRNA half-lives in normal and tumor cells suggests that regulation of stability of c-sis mRNA is not a major factor in tumorigenesis in the glioblastoma cell lines examined.
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PMID:Expression and stability of c-sis mRNA in human glioblastoma cells. 305 84

A review of the development of regional chemotherapy by perfusion is presented. Techniques have been developed for most regions of the body. Early response rates ranged from 48% for glioblastoma and 55% with carcinoma to 67% with soft tissue sarcoma and 84% with melanoma. By 1984, 1325 patients had been perfused 1509 times. The best responses have occurred with melanoma and soft tissue sarcoma of the limbs. Thus, at 10 years, the cumulative overall survival for Stage I melanoma of the limbs, combining regional perfusion and conservative excisional surgery, was 77%. The best results occurred in female patients with upper-limb disease (83%), and the poorest results were in male patients with lower-limb disease (53%). The overall 10-year survival for regional melanoma was 41%, ranging from 23% for in-transit metastases to 51% for patients with positive regional nodes treated by perfusion and regional lymph node dissection. The 10-year survival for perfusion and limb-sparing excision for soft tissue sarcoma was 65%. Advantages and complications are presented and discussed. Questions and plans for the future are reviewed.
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PMID:Lucy Wortham James lecture. Regional perfusion. Current sophistication, what next? 308 Feb 16

The cell surface receptor for the mitogenic peptide epidermal growth factor (EGF) is involved in control of normal cell growth and may play a role in the genesis of human neoplasia such as squamous carcinoma and glioblastoma. Soft-agar growth and focus-formation experiments with NIH 3T3 mouse fibroblasts transfected with an expression plasmid demonstrated the ligand-dependent transforming potential of the human EGF receptor without structural alterations. Activation of overexpressed normal receptor alone appears to be sufficient for transformation of NIH 3T3 cells in vitro.
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PMID:Ligand activation of overexpressed epidermal growth factor receptors transforms NIH 3T3 mouse fibroblasts. 325 24

Transforming growth factor-beta 1 has been shown to suppress the urokinase activity in the glioblastoma cell line T-MG1 and the carcinoma cell line T-CAR1. The molecular mechanisms behind the decrease in the proteolyic activity is shown to be at least partly due to increased synthesis of plasminogen activator inhibitor type-1 and not by decreased synthesis of urokinase.
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PMID:Transforming growth factor-beta 1 is a potent inducer of plasminogen activator inhibitor type-1 in human glioblastoma and carcinoma cell lines. 326 61

The propagation efficiencies, growth patterns, histological appearances, and roentgenographic demonstration of tumors derived from six continuous human pulmonary tumor cell lines implanted intrathoracically (i.t.) and intrabronchially (i.b.) were compared with the conventional s.c. implantation method at three different tumor cell inocula (N = 184, i.b.; N = 185, i.t.; N = 180, s.c.). A tumor-related mortality of 100% was noted when the six different human lung tumor cell lines, including A549 adenocarcinoma, NCI-H125 adenosquamous carcinoma, NCI-H460 large cell undifferentiated carcinoma, NCI-H69 small cell carcinoma, and NCI-H358 and NCI-H322 bronchioloalveolar cell carcinomas, were implanted i.b. at a 1.0 x 10(6) tumor cell inoculum. A similar (92%) tumor-related mortality was observed when these same lung tumor cell lines were implanted i.t. at a 1.0 x 10(6) tumor cell inoculum (P greater than 0.10), whereas minimal (5%) tumor-related mortality was noted when cells from the six different cell lines were implanted s.c. (P less than 0.001). In addition, a dose-dependent, tumor-related mortality was noted for either i.t. or i.b. implantation when lower (1.0 x 10(5) or 1.0 x 10(4] tumor cell inocula were employed. Histological characteristics and growth patterns of tumors propagated employing the three implantation techniques were closely comparable for all three propagation methods and, in all instances, histological appearances of the tumors were representative of the current tumor cell lines from which they were derived. Approximately 30% of the lung tumors propagated i.t. grew in the chest wall and/or in the lung parenchyma as well as in the pleural space. In contrast, tumors propagated i.b. grew predominantly in the lung parenchyma. When five nonpulmonary human tumor cell lines (including U251 glioblastoma, LOX amelamontic melanoma, HT-29 colon adenocarcinoma, OVCAR 3 ovarian adenocarcinoma, and adriamycin-resistant MCF-7 breast adenocarcinoma) were propagated i.b. or i.t., there was considerable site-specific variability in tumor-related mortality depending on the tumor type. These data demonstrate that both the i.b. and i.t. models should be useful for the in vivo propagation and study of certain human pulmonary and nonpulmonary carcinomas as well as being advantageous for future studies of cancer biology and developmental therapeutics.
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PMID:Comparison of intrapulmonary, percutaneous intrathoracic, and subcutaneous models for the propagation of human pulmonary and nonpulmonary cancer cell lines in athymic nude mice. 335 44

We studied two autopsy cases of primary pituitary carcinoma. Case-1. A 45 year old female was admitted on Oct. 4 1978, with a complaint of right homonymous hemianopsia. And diagnosis was pituitary adenoma. Partial removal of pituitary tumor was performed on Oct. 23 1978. She died on Dec. 5 1978 due to bleeding of gastrointestinal tract. Autopsy disclosed a pituitary carcinoma invading the left hypothalamus, mamillary body, optic and V cranial nerves, and mid brain as well as sphenoid bone. No extracranial metastasis was noted. Case-2. A 44 year old female with a history of acromegaly for 6 years was admitted with a complaint of headache on May 8 1976. She was diagnosed as having pituitary adenoma. The subtotal removal of pituitary tumor was performed on May 21 1976 and followed by 4500 rad irradiation. At this time, pathological diagnosis was eosinophilic adenoma. Seven years later, she complained of progressive right hearing disturbance, dysarthria and ataxic gait 1983. The second subtotal removal of pituitary tumor was performed with a diagnosis of recurrence of pituitary adenoma on Oct. 7 1983. After the operation, she complicated sepsis and died on Jan. 14 1984. An autopsy disclosed a pituitary carcinoma from residual pituitary gland, continuously extending to the subarachnoid space of the pons, and invading right cerebello-pontine angle and cerebellum. The histological examination revealed pituitary carcinoma with high pleomorphism and glioblastoma multiform-like feature were within the tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two autopsy cases of primary pituitary carcinoma]. 341 67


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