Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CSF beta-glucuronidase, polyamines and carcinoembryonic antigen (CEA) were analyzed in 16 patients with meningeal carcinomatosis from solid tumor in systemic organs, 27 with benign brain lesions, 18 with primary brain tumors, 14 with metastatic brain tumors and 5 with leptomeningeal dissemination of other malignant diseases. Beta-glucuronidase levels in all cases of meningeal carcinomatosis, meningeal gliomatosis and meningeal lymphoma were higher than 100 micrograms/dl/hr; on the other hand, levels in all cases of benign brain lesions were below 100 micrograms/dl/hr. Levels of beta-glucuronidase and polyamines were not high in the cases with positive cytology after tumor resection. Polyamine levels were below 0.05 nmol/ml in all cases after resection of the metastatic brain tumor. Cystic fluid of malignant tumors showed high levels of beta-glucuronidase and polyamines. On the other hand, the levels of polyamines in the cystic fluid of benign tumor were low, although the levels of beta-glucuronidase were high. Some cases of meningeal carcinomatosis with high levels of serum CEA did not show high levels of CSF CEA. For metastatic brain tumors, the cases with intraparenchymal tumors, especially with dural attachment showed high levels of beta-glucuronidase and CEA preoperatively, but they returned to normal after surgery. In cases of meningeal carcinomatosis treated by intrathecal chemotherapy with methotrexate (MTX) and cytosine arabinoside (Ara-C), CSF beta-glucuronidase reflected the neurological status better than the cell count decreased rapidly following chemotherapy and beta-glucuronidase was considered as a useful CSF marker in cases of meningeal carcinomatosis to monitor the course of the disease. The same situation was observed in CSF CEA and CEA was also considered as a useful marker when CEA levels in CSF are higher than those in serum.
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PMID:Measurements of CSF biochemical tumor markers in patients with meningeal carcinomatosis and brain tumors. 156 Feb 55

Retrospective evaluation of 120 patients treated for leptomeningeal metastases at the Hadassah Hebrew University Hospital disclosed 3 patients with spontaneous spinal subarachnoid hemorrhage (SAH) occurring in the absence of bleeding tendency. These patients are described in detail. A search of the English literature revealed only 2 additional cases. The primary neoplasm originated in the central nervous system in 4 of these 5 patients; a resection of an intraparenchymal posterior fossa tumor antedated the development of subarachnoid seeding in 3 of the 5 patients; SAH occurred in face of a negative CSF cytology and in the presence of macroscopic subarachnoid deposits that were diagnosed with the aid of neuroimaging techniques. It is suggested that spontaneous spinal SAH in a patient with a history of primary or secondary brain tumor and with no bleeding tendency indicates probable presence of macroscopic leptomeningeal deposits.
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PMID:Spinal subarachnoid hemorrhage associated with leptomeningeal metastases. 156 Feb 63

Macrophage inflammatory protein 1 (MIP 1), initially purified from the conditioned medium of endotoxin-stimulated macrophages, is a low m.w. heparin-binding protein doublet comprising two peptides, MIP 1 alpha and MIP 1 beta. Although native doublet MIP 1 has previously been shown to exert pyrogenic, mitogenic, and proinflammatory effects on other cell types, its actions on its cell of origin, the macrophage, have not been well catalogued. Our study reports several aspects of macrophage function that are modulated by MIP 1. MIP 1 was not directly cytotoxic for WEHI tumor cells, but MIP 1-treated macrophage exhibited enhanced antibody-independent macrophage cytotoxicity for tumor targets. MIP 1 treatment stimulated proliferation of mature tissue macrophages, and this effect was enhanced upon costimulations with either CSF-1 or granulocyte-macrophage-CSF. Thioglycollate-elicited peritoneal exudate macrophages incubated with native doublet MIP 1-secreted bioactive TNF and IL-6, as well as immunoreactive IL-1 alpha, and these effects were enhanced significantly when the cells were costimulated with IFN-gamma. Purified preparations of the recombinantly derived MIP 1 alpha peptide alone stimulated the secretion of TNF, IL-1 alpha, and IL-6 by peritoneal macrophages, but MIP 1 beta did not. In fact, as little as eightfold excess MIP 1 beta blocked TNF-induction by MIP 1 alpha to a significant degree. By contrast to these apparent "macrophage activating" properties of MIP 1, the cytokine failed to trigger the macrophage oxidative burst, or to up-regulate the expression of Ia on the macrophage surface. Taken together, these data reveal that MIP 1 peptides act as autocrine modulators of their cells of origin, and raise the possibility that MIP 1 peptides may play a role in modulating macrophage responses to inflammatory stimuli in vivo.
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PMID:Macrophage inflammatory protein 1 modulates macrophage function. 157 67

Chronically immunosuppressed individuals are susceptible to lymphoreticular tumors. Up to 15% of patients with congenital deficiencies such as ataxia=telangiectasia may develop malignancies, mainly high-grade B cell non=Hodgkin's lymphomas (NHLs). AIDS lymphomas are comprised of NHLs including Burkitt's lymphoma (BL) and primary cerebral lymphomas (PCLs). Almost 3% of all AIDS patients (2824 of 97,258 cases) developed NHL. Epstein-Barr virus (EBV) as a co-factor in AIDS lymphomagenesis has been studied: in 12 cases of 24 AIDS lymphomas EBV by DNA in situ hybridization was found. In an analysis of 6 primary cerebral lymphomas, .5 were positive for EBV DNA by Southern blotting. In Burkitt's lymphoma the characteristic genetic alteration affects the c-myc oncogene. In 1/3 of BL p53 mutations were found but none in the 43 NHLs suggesting that p53 mutations and c-myc activation act synergistically in the pathogenesis of these tumors. Cytotoxic agents dideoxyinosine, dideoxycytosine, and zidovudine may cause secondary neoplasia. 8 of 55 AIDS patients under zidovudine treatment developed high-grade lymphoma 23.8 months subsequently; recently doses were reduced. PCL was found in 21 of 90 patients. A 5.2 months survival was associated with combined treatment with cyclophosphamide, Oncovin (vincristine), methotrexate, etoposide, and cytosine arabinoside compared with 11.3 months with chemotherapy. Colony-stimulating factors (CSFs) alleviate drug-induced myelotoxicity and zidovudine-induced neutropenia, however, l8 of 11 patients receiving granulocyte-macrophage CSF developed hematological toxicity. Interleukine-2 produced by T-helper cells enhancing tumor cells cytotoxicity has been used in AIDS-associated cryptosporidial diarrhea and in 4 patients with AIDS lymphoma with modest response, but its stimulation of the HIV-infected substrate may increase viral proliferation.
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PMID:AIDS lymphomas. 161 63

A case of malignant meningioma metastasizing through the cerebrospinal pathway is presented. The primary tumor was a parasagittal malignant meningioma invading into the brain. The tumor seeded to the cerebellopontine angle cistern and thoracic spine after multiple operations. Although this type of tumor borders the CSF, metastasis through the cerebrospinal pathway is rare, and only 18 such cases have been reported (2, 3, 10, 12).
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PMID:Malignant meningioma metastasizing through the cerebrospinal pathway. 162 2

Intravoxel incoherent motion MRI was used to assess six intracranial, extraaxial cysts and tumors including two epidermoids, two cystic acoustic schwannomas, and two arachnoid cysts. A maximum gradient strength of 0.7 g/cm was used simultaneously along all axes (maximum gradient beta value: 445 s/mm2) and comparisons were made with an external water phantom. In epidermoid tumors the apparent diffusion coefficient (ADC) was similar to that of normal brain, thus indicating their solid nature. In acoustic schwannomas an ADC similar to the external water phantom indicated cystic components, whereas an ADC similar to brain was found in the solid portions of the tumor. The ADC of arachnoid cysts was similar to that of the water phantom, indicating their fluid nature. Due to macroscopic CSF flow, cisternal CSF showed high ADC, which enabled epidermoid tumors to be highlighted.
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PMID:Intravoxel incoherent motion (IVIM) MRI in intracranial, extraaxial tumors and cysts. 162 6

Mycosis fungoides (MF) is a malignant T-cell lymphoma that primarily involves the skin, but may, in its advanced stages, metastasize to internal organs. From autopsy series, CNS involvement of MF can be seen in 14% of patients. We describe the CT and MR findings in three patients with CNS metastases. The images showed various manifestations of CNS MF, including parenchymal homogeneously intensely enhancing masses and ependymal enhancement. The CSF and biopsy results were eventually diagnostic in all three cases. One patient was treated prior to pathologic diagnosis, the other two were treated after diagnosis. The tumor improved following treatment in two patients. Although the imaging findings of CNS MF are nonspecific, they can be the first evidence of the disease.
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PMID:CNS mycosis fungoides: CT and MR findings. 162 8

Inversion recovery (IR) sequences with an inversion time (TI) designed to markedly reduce or null the signal from CSF (TI of approximately 2,100 ms at 1.0 T) and a very long echo time (TE) of 240 ms were used to image the brain of two normal adult volunteers, one 34-year-old man with an intrinsic tumor, and one 3-month-old infant with an infarct. Using these very heavily T2-weighted pulse sequences, adult gray and white matter showed similar signal intensity in many areas of the brain, but normal white matter in regions of the centrum semiovale, posterior internal capsule, parietopontile tract, occipitothalamic radiation, and brain stem showed a much higher signal intensity than surrounding gray or white matter. The infant displayed a low signal intensity in myelinated regions in the internal capsule and occipitothalamic radiation and a high signal in unmyelinated white matter. In many of the images there were strong similarities to the distribution of high signal within white matter seen with pulsed gradient spin echo sequences (TE 130 ms) designed to demonstrate effects due to anisotropic diffusion. Arguments are advanced to support the view that the high signal intensity in white matter tracts is due to one or more long T2 components that may be associated with unmyelinated or sparsely myelinated fibres within white matter. The resemblance to diffusion weighted images may reflect the fact that both employ long TEs and both produce a low signal from CSF. If myelin possessed a different susceptibility from axoplasm so that magnetic field gradients were generated around nerve fibres when their orientation was not parallel to B0, diffusion of water might then produce the observed dependence on fibre direction. The high signal regions in white matter are a potential source of confusion in image interpretation, and measurements of T2 in white matter need to be made with these regional variations in mind. The concept of normal appearing white matter also needs to be applied with a knowledge of these differences. The IR sequences used in this study provide a very high T2 dependence with a low signal from CSF and may be useful for detecting disease in the CNS of adults and children.
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PMID:High signal regions in normal white matter shown by heavily T2-weighted CSF nulled IR sequences. 162 5

Hodgkin's disease (HD) is a neoplastic disease that is characterized by unbalanced and/or unregulated cytokine production. Information accumulated in our own and other laboratories indicates that the cytokines interleukin-1 (IL-1), IL-5, IL-9, tumor necrosis factor-alpha (TNF-alpha), granulocyte colony-stimulating factor (G-CSF), macrophage CSF (M-CSF), and transforming growth factor-beta (TGF-beta) are secreted by Hodgkin's and Reed-Sternberg (H-RS) cells. These and perhaps additional cytokines are likely to be responsible for the unique histopathologic and clinical alterations seen in patients with HD. In this study, we confirmed that IL-6 is produced by cultured H-RS cells as well as by H-RS cells in tissues. By using an enzyme-linked immunosorbent assay, we found that approximately 2 to 10 ng/ml of IL-6 was secreted by cultured H-RS cells (10(6) cells/ml). In tissues, we were able to immunolocalize IL-6 in the cytoplasm in 10 to 30% of H-RS cells by using rabbit polyclonal and mouse monoclonal anti-IL-6 antibodies. There was no correlation among the IL-6 staining intensity, number of H-RS cells stained, and the degree of plasma cell infiltration. However, in 3 of 17 cases studied, a large number (60%) of H-RS cells were positive for IL-6, and in these patients, abundant plasma cells were present. In one patient, the involved lymph node also showed histologic features similar to those of Castleman's disease. In this patient, we noted abundant IL-6 expression not only in H-RS cells, but also in most reactive histiocytes. The cultured H-RS cells did not express functional receptors for IL-6, and exogenously added IL-6 did not induce proliferation of these cells. We also conducted studies with specific anti-IL-4 antibodies, which did not show IL-4 production by H-RS cells in both cultures and tissues. In tissues, only rare IL-4 positive lymphoid cells or dendritic cells were identified. Thus, the study demonstrated that adequate amounts of IL-6 are required for an abundant plasma cell reaction, and that an additional source of IL-6 from histiocytes is essential for the formation of Castleman's disease-like changes in lymph nodes involved by HD. Furthermore, IL-4 is not likely to be responsible for the T-lymphocyte reaction in tissues, by a mechanism distinct from that in T-cell-rich B-cell lymphomas.
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PMID:Interleukin-6, but not interleukin-4, is expressed by Reed-Sternberg cells in Hodgkin's disease with or without histologic features of Castleman's disease. 163 58

A series of initial radiobiologic investigations have been performed using three animal models. The baboon model proved to be a valuable technique to assess the in vivo radiobiologic response of single-fraction irradiation doses delivered to the primate brain stem. Multimodality neurodiagnostic testing, including CT, MR imaging, xenon-enhanced CT, evoked potential studies, and analysis of CSF myelin basic protein levels, all of which eventually were correlated with neuropathologic examination, enabled detection of lesions produced with high-dose (150 Gy) radiosurgery as early as 6 weeks. Within the first 6 months after radiosurgery, lower doses (20 Gy, 50 Gy) did not result in clinically or neurodiagnostically detectable lesions. The rat arteriovenous fistula model permits analysis of the delayed histopathologic effects of radiosurgery on an experimentally created fistula designed to mimic an AVM. The rat C6 glioma model is designed to evaluate the effect of radiosurgery in an infiltrative tumor that simulates a human malignant brain tumor. These studies are intended eventually to increase our knowledge about the safety and efficacy of radiosurgery in both the normal and tumor-implanted brains. We believe that such fundamental studies ultimately will improve our ability to reach the goals of radiosurgery: to destroy the target and spare the surrounding brain. Eventually, it may become feasible to achieve these goals by combining radiosurgical technique with both radiation sensitizers (for the treated volume) and brain protectors.
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PMID:Radiobiologic models for radiosurgery. 163 53


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