Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The culture medium of certain strains of Clostridium botulinum type C contains two separable ADP-ribosyltransferases. Besides the ADP-ribosylation of actin due to botulinum C2 I toxin, a second microbial enzyme causes the mono-ADP-ribosylation of a eukaryotic protein with a molecular mass of about 20 kDa found in platelets, neuroblastoma X glioma hybrid cells, S49 lymphoma cells, chick embryo fibroblasts and sperm. The eukaryotic substrate is inactivated by heating and trypsin treatment. In contrast, the novel ADP-ribosyltransferase, which can be separated by DEAE-Sephadex chromatography, is largely resistant in the short term to trypsin digestion.
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PMID:Clostridium botulinum type C produces a novel ADP-ribosyltransferase distinct from botulinum C2 toxin. 310 Mar 33

A 53-year-old woman was treated for and cured of low grade malignant lymphoma, localized to the neck, by irradiation and chemotherapy. One year later she developed signs of damage to the spinal cord with slight paraparesis of the lower extremities, which remained stationary for seven years. Then, new and rapidly progressive central and peripheral neurological symptoms developed. About one year later the patient died. At autopsy a malignant glioma of the right temporal lobe and radiation damage to the spinal cord were found. Lymphocytic infiltrations in the peripheral nerves and muscles of the lower extremities were also seen. A severe neurogenic atrophy was present but no relapse of malignant lymphoma was found. Depressed immune defense is suggested to be the cause of the pathological changes of the nervous system in this case. The inflammation of the peripheral nerves might be due to activation of a latent virus infection.
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PMID:Late nervous system disorders in cured malignant lymphoma: a clinical and neuropathological study. 320 83

Using a 4-h 51Cr release assay, we observed that thymocytes from Fischer strain rats incubated with recombinant human interleukin-2 (rhIL-2) developed cytotoxicity to YAC-1 lymphoma, 9L-glioma, and B-16 melanoma cells (effector/target ratio = 25/1). Induction of the lymphokine-activated killer (LAK) cells was as follows: (1) when 5 x 10(6)/ml thymocytes were cultured with various concentrations of rhIL-2 (50, 125, 250, 500, or 1,000 units/ml) for 4 days, no cell proliferation was observed at any concentration. However, the LAK cells showed significant cytotoxicity toward all tumor cells at more than 50 units/ml. (2) When 5 x 10(6)/ml thymocytes were cultured for 1 to 6 days with 250 units/ml of rhIL-2, the harvested cell count decreased markedly after the 2nd day. The cytotoxicity of all the tumor cells became significant after the 2nd day, with peak activity on the 4th day. In rat splenocytes, on the other hand, the LAK cells could not be identified because rat splenocytes developed nonspecific cytotoxicity in medium containing fetal calf serum without adding rhIL-2.
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PMID:Induction of lymphokine-activated killer cells from rat thymocytes using recombinant human interleukin-2. 326 Aug 19

Eight cases of AIL-type T-cell malignant lymphoma are reported. The clinical symptoms are the same as those described in AIL: fever, malaise, weight loss, skin rashes, polyadenopathy, and splenomegaly. However, some differences can be noted: the absence of hepatomegaly in all cases but one, the absence of polyclonal hypergammapathy in all cases but one, and predominance in females. The lymph node modifications comprise diffuse infiltrations of lymphoid cells with irregular nuclei and pale cytoplasm, associated with a large number of immunoblasts and plasma cells. Some eosinophilic granulocytes and epithelioid cells can be seen. Hyperplasia of the vessels and remnants of follicles, sometimes with proliferation of follicular dendritic cells, are prominent features. The immunolabelling study demonstrates the presence of an important T-cell population all expressing a high predominance of CD 4 phenotype. These findings are in accordance with those published in Europe and in contrast with those of some of the Japanese cases, particularly the first patients published by Shimoyama et al. The differential diagnosis with AIL is based on the presence of clusters of mainly large cells with a pale cytoplasm, on the loss of expression of one T cell marker, as in 3 cases of our series, and on the presence of a high percentage of lymphoid cells engaged in the mitotic cycle as demonstrated with the Ki 67 monoclonal antibody. However, to draw a clear cut difference between AIL-type T-cell lymphoma and AIL considered as a prelymphomatous dysimmune lymphadenopathy, only the demonstration of cytogenetic abnormalities, as in one of our cases or of rearrangement of the genes coding for beta and/or gamma chain of the antigen receptor of T-cell are valuable criteria. The follow-up of our series is not long enough to appreciate the prognosis. Three patients died, one from a glioma. All the other cases, treated with polychemotherapy show total remission with an evolution of 10 to 39 months.
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PMID:Angio-immunoblastic lymphadenopathy (AIL) or T-cell malignant lymphoma of AIL-type. A histopathological, immunohistochemical and ultrastructural study of 8 cases. 326 11

Normal pressure hydrocephalus is frequently emphasised as a cause of reversible dementia, but is seldom encountered. Over a 2 year period, 5 patients presented with cognitive decline, and gait disturbance, with or without incontinence. CT head examination revealed hydrocephalus. Although none had symptoms of raised intracranial pressure on initial presentation, there were clinical or CT signs of raised intracranial pressure in 4 of the 5. Underlying pathologies were meningeal lymphocytic lymphoma, idiopathic meningeal fibrosis, periaqueductal glioma, basilar aneurysm and basilar invagination. All patients responded to the insertion of a shunt. Over the same period, only 1 patient was shunted for idiopathic normal pressure hydrocephalus, without improvement. We challenge the concept of idiopathic normal pressure hydrocephalus as a cause of cognitive deterioration.
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PMID:Dementia, gait disturbance, incontinence and hydrocephalus. 326 84

The derivation of an IgG1k monoclonal antibody (HSAN 1.2) recognizing a cell membrane determinant on human neuroblastoma cells is reported. The determinant was found on all 17 cultured human neuroblastoma cells that were tested, but the density of the antigen varied widely on different cell lines. The antibody also bound to fresh and cultured Wilm's tumor cells, retinoblastoma cells, and one of two Ewing's sarcoma cell lines tested, it did not bind to mouse neuroblastoma cells, normal fibroblasts, blood, or bone marrow. Tumor cells that did not stain with HSAN 1.2 included glioma, medulloblastoma, melanoma, rhabdomyosarcoma, mesenchymoma, leukemia, and lymphoma cells. The distribution of the HSAN 1.2 antigen in normal tissues was confined to brain and newborn kidney. As few as 0.1% tumor cells in bone marrow aspirates were detectable by fluorescein-conjugated HSAN 1.2 antibody and flow cytometry. This antibody should be useful for the discrimination of neuroblastoma from other pediatric malignancies, for the detection of tumor cells in metastatic sites such as bone marrow, and for selective removal of neuroblastoma cells from marrow harvested for autologous transplantation.
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PMID:Monoclonal antibody recognizing a human neuroblastoma-associated antigen. 332 7

Beta 2-microglobulin (beta 2-MG) levels were determined in serum, cerebrospinal fluid (CSF), and tumor cyst fluid obtained from patients with a variety of intracranial tumors. In addition, a simultaneous determination of the carcinoembryonic antigen (CEA) was carried out in some patients. The beta 2-MG levels were elevated in 11/101 intracranial tumors, including glioma (4/34), non-glial tumors (1/18), malignant lymphoma (2/18), and metastatic brain tumors (4/31). There were no significant differences in the beta 2-MG levels of serum among the different patient groups. On the other hand, the beta 2-MG levels in CSF were significantly higher in patients with malignant lymphoma and metastatic brain tumors than in those with glioma and non-glial tumors. Fifteen (83.3%) of 18 patients with malignant lymphoma and 6(25.0%) of 24 patients with metastatic brain tumors showed increased the levels of beta 2-MG in CSF. The beta 2-MG levels in the tumor cyst fluid of 11 intracranial tumors exceeded normal serum levels in all but two patients. When the CEA levels in the serum and CSF were measured simultaneously, meaningful differences between malignant lymphoma and metastatic brain tumors were clearly observed. The highest incidence and highest levels of the CEA in serum and CSF were only noted in patients with metastatic brain tumors. Conversely, the serum CEA was slightly raised in 11.8% of malignant lymphoma and the levels of CEA in CSF were within normal range in all these patients. Serial determination of CSF beta 2-MG in patients with malignant lymphoma correlated well with their clinical findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical significance of beta 2-microglobulin and carcinoembryonic antigen in intracranial tumors]. 332 88

A series of 22 cases of primary intercerebral lymphoma are reported. The clinical presentation and natural history were similar to high grade glioma in adults. There was a male to female ratio of 2.7:1, and a mean age at presentation of 63 years (range 47-72 years). Single masses were present in 77%, and the frontal lobe was the most frequently involved (64%). Treatment regimes included varying combinations of surgical resection and cranial irradiation. Sixteen patients have died, twelve due to recurrent or persistent intracerebral disease. The median survival was ten months. Six patients are still alive at 52, 12, 10, 9, 6 and 4 months. Failure to control the intracranial tumours was the main cause of death. Significant debulking of the tumour was the single most important prognostic factor, although a good initial response to steroids was also favourable. No patient developed spinal deposits. Even when there is a good response to radiation and prolonged survival, the quality of life may be poor: in this series only five out of 22 patients (23%) returned to a normal life. Radiation dosage and the indications for spinal treatment are discussed.
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PMID:Primary lymphoma of the central nervous system: experience at Addenbrooke's Hospital, Cambridge. 335 97

We have studied the in vitro antitumor effectiveness of murine lymphokine-activated killer (LAK) cells induced by recombinant IL-2 (rIL-2). LAK cells were generated by placing 5 X 10(7) fresh C 57 BL/6 splenocytes (erythrocytes were lysed osmotically) in 10-cm (diameter) dishes (Falcon) containing 10 ml of complete medium (CM). The CM consisted of RPMI 1640 with 0.1 mM non-essential amino acids, 1 microM sodium pyruvate, 5 X 10(-5)M 2-mercaptoethanol, 50 micrograms/ml gentamicin sulfate, 0.03% glutamine, 10% heat-inactivated fetal calf serum (FCS) and 10 units/ml of rIL-2 (TGP-3, provided by TAKEDA Chemical Industries, Ltd). The dishes were incubated horizontally at 37 degrees C in a 5% CO2 atmosphere for 72-96 hr. The LAK cells were then harvested, washed three times, and resuspended in RPMI 1640 with 5% heat-inactivated FCS for the in vitro cytotoxicity assay. The antitumor cytotoxic activity of LAK cells was estimated in triplicate by 4 hr 51Cr release assays. The cytotoxic activity of LAK cells against syngeneic 203 glioma and normal syngeneic glioblasts was approximately 50% and a few %, respectively. The in vitro cytotoxicity of LAK cells against syngeneic EL-4 thymoma, allogeneic YAC-1 lymphoma and P-815 mastocytoma was 72%, 87% and 43%, respectively. Thus LAK cells have apparent tumor specificity in vitro and are easily generated. Fresh splenocytes of CBA/J mice were markedly lytic for natural killer (NK)-sensitive YAC-1 cells, but not for 203-glioma cells or NK-resistant P-815 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The in vitro antitumor effectiveness of murine lymphokine-activated killer (LAK) cells induced by recombinant IL-2]. 348 67

Over 35 intraaxial lesions in 15 patients suspected of having intracranial tumors were studied with MR before and after injection of Gadolinium-DTPA (Gd-DTPA). Diseases included primary and metastatic brain tumors, plaques of multiple sclerosis, occult arteriovenous malformations, lymphoma, toxoplasmosis, and pituitary adenoma. The precontrast T2-weighted sequence (SE 2000/30, 60) was found to be most sensitive in detecting intraaxial lesions, showing 17 lesions that were not seen on the post-Gd-DTPA T1-weighted sequence (SE 500/30). In one case of multiple sclerosis, several lesions seen on the pre-Gd-DTPA study on T2-weighted images faded after injection of Gd-DTPA (due to T2 shortening). In two patients with large metastatic foci, other small metastatic lesions were seen better after Gd-DTPA on both T1- and T2-weighted sequences. Four other patients with only one focal-enhancing lesion and one patient with multifocal lesions on T1-weighted images actually had a much larger single glioma depicted on pre-Gd-DTPA T2-weighted images. In a patient with AIDS, a ring-enhancing lesion thought to be an abscess proved to be lymphoma. The cryptic arteriovenous malformations enhanced but showed more characteristic findings, such as hemorrhage, on pre-Gd-DTPA studies. Our experience suggests that Gd-DTPA may not improve sensitivity of MR in the detection of intraaxial lesions. However, functional aspects of brain disease, such as the presence of perfusion of a lesion and active breach of the blood-brain barrier, are depicted well with Gd-DTPA and are vital for proper diagnosis in many instances.
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PMID:Gd-DTPA in clinical MR of the brain: 1. Intraaxial lesions. 349 Jul 58


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