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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The temporal activities of suppressor T lymphocytes (Ts) and cytotoxic T lymphocytes (CTL) were investigated in a syngeneic murine malignant glioma (a methylcholanthrene-induced ependymoblastoma of C57BL/6 mouse origin, 203-glioma). After the s.c. tumor inoculation, it was suggested that both Ts and CTL were generated with target specificity against 203-glioma cells, because neither Ts nor CTL activity were seen against syngeneic EL 4 (benzpyrene-induced thymoma), allogeneic P815 (methylcholanthrene-induced mastocytoma of DBA/2 mouse origin) or YAC-1 (Moloney leukemia-induced T-cell lymphoma of A/Sn mouse origin), but only against 203-glioma. It was found that the generation of Ts preceded that of CTL and that the turnover was faster; furthermore, Ts were generated in the thymus and spleen, while CTL were distributed in regional lymph nodes and spleen. Surface marker analysis revealed that only Lyt-1-.2.3+ T-cells participated in suppressor responses in contrast to both Lyt-1-.2.3+ and Lyt-1+.2.3+ T-cells participating in cytotoxic responses. The effects of adult thymectomy (ATx) on the changes of the immunized T-cell subsets were also investigated. In mice thymectomized 3 weeks previously, the Ts activity was abrogated, whereas the CTL activity increased markedly and Lyt-1+.2.3+ T-cells were not detected. The results suggest that CTL or their precursors bearing Lyt-1+.2.3+ phenotype and Ts bearing Lyt-1-.2.3+ phenotype are short-lived lymphocytes. Accordingly, it is suggested that in tumor-bearing mice short-lived Ts are generated earliest with target specificity and, due to the reciprocal relationships between Ts and CTL activities, may have a modulating influence on CTL; furthermore, ATx may alter the patterns of generation of the precursor T-cells and Ts.
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PMID:Temporal changes of suppressor T lymphocytes and cytotoxic T lymphocytes in syngeneic murine malignant gliomas. 293 88

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

Suppressor T cells in syngeneic tumor-bearing mice that inhibited in vitro generation of tumor antigen-specific cytotoxic T lymphocytes were characterized with respect to the kinetics, the nature and the target specificity, using murine malignant glioma (a methylcholanthrene-induced malignant ependymoblastoma, 203-glioma). Suppressor cell activity was assessed by the inhibition of tumor cell killing activity of cytotoxic T lymphocytes, which were prepared from splenic T enriched lymphocytes of mice immunized with 1 X 10(6) mitomycin C (50 micrograms/ml, 45 minutes)-treated 203-glioma cells twice at an interval of 7 days. It was confirmed that suppressor T cells were generated in 203-glioma-bearing mice, and they were tumor antigen-specific as evidenced by the fact that sensitized splenic T lymphocytes from mice bearing other syngeneic EL4 thymoma or allogeneic P 815 mastocytoma or YAC-1 T cell lymphoma did not exhibit the inhibition of the cytotoxic T lymphocyte activity against 203-glioma cells. Significant suppressor cell activity was detected in spleen cells 1 to 5 days after the subcutaneous inoculation of 203-glioma cells with the peak activity on day 3 and it disappeared as early as on day 7, suggesting strongly that the turn-over of suppressor T cells is very quick. Surface markers of suppressor T cells in 203-glioma-bearing mice were checked on day 3 with the results that the suppressor cell activity was eliminated by the treatment with anti-Lyt-2 monoclonal antibody and complement, indicating that the phenotype of suppressor T cells is Lyt-1-.2.3+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Suppressor mechanism in tumor immunology: characteristics of suppressor T-cells in glioma-bearing mice]. 619 6

Recombinant human interleukin-1 (IL-1) alpha and beta were found to activate a latent cytosolic form of the transcription factor NF kappa B in rat C6 glioma. IL-1 beta was 10 times more potent than IL-1 alpha for this activity and both were inhibited by the IL-1 receptor antagonist. The activation was detectable from 20 min and remained sustained for up to 24 h. The electrophoretic mobility of the activated complex was shown to be different from that of the corresponding complexes in another IL-1-responsive cell line, the murine thymoma line EL4.NOB-1. C6 cells, when transiently transfected with five NF kappa B consensus sequence repeats linked to the reporter gene chloramphenicol acetyltransferase (CAT), demonstrated increased CAT activity in response to IL-1 beta treatment. The activation of NF kappa B in glial cells may thus represent an early step in IL-1 signalling in brain and is likely to have consequences for IL-1-induced gene expression in these cells.
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PMID:Interleukin-1 activates transcription factor NF kappa B in glial cells. 837 49

High affinity "peripheral-type" benzodiazepine binding sites were detected in an interleukin-1 (IL-1) responsive murine thymoma cell line EL4.NOB-1. Exposure of these cells to IL-1 over a period of at least 24 hr resulted in down-regulation of the binding sites. This effect was inhibited by the IL-1 receptor antagonist (IL-1RA) which in these cells inhibits IL-1 binding to the type I IL-1 receptor. Phorbol myristate acetate (PMA), another activator of EL4.NOB-1 cells, had an opposite effect to IL-1 in that it increased binding site expression dramatically suggesting different mechanisms of action for these two effectors. IL-1 produced a similar response in the rat glioma cell line C6 whereas PMA was ineffective. Such modulation of the peripheral-type benzodiazepine receptor may provide an insight into its physiological role and its possible participation in IL-1 actions in different cells.
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PMID:Interleukin-1 and phorbol myristate acetate modulate the peripheral-type benzodiazepine receptor in lymphocytes and glial cells. 839 35

It has been shown that leukemia and glioma cells are sensitive to cannabidiol (CBD)-induced apoptosis, whereas primary monocytes and glia cells are relatively insensitive. In the current study, the cellular events and sensitivity to CBD-induced apoptosis between murine thymocytes and EL-4 thymoma cells were compared. Cannabidiol markedly induced apoptosis in a time- and concentration-related manner in both cells. The efficacy of CBD to induce apoptosis was comparable between the 2 types of T cells, whereas CBD induced apoptosis in thymocytes with a slightly greater potency than in EL4 cells. Time-course analyses revealed CBD-mediated apoptosis occurred earlier in EL-4 cells than that in thymocytes. An increased level of cellular reactive oxygen species (ROS) was detected in both cells with the peak response at 2 h post CBD treatment. Concordantly, CBD triggered a gradual diminishment in the cellular thiols. The presence of N-acetyl-L-cysteine (NAC), a precursor of glutathione, markedly attenuated the induction of apoptosis, and restored the diminished levels of cellular thiols. The results demonstrated that both thymocytes and EL-4 thymoma cells were susceptible to CBD-induced apoptosis and that ROS played a critical role in the apoptosis induction.
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PMID:A comparative study on cannabidiol-induced apoptosis in murine thymocytes and EL-4 thymoma cells. 1838 16

The aim of the study was to verify the possibility of treating patients with poor prognosis early-intermediate Hodgkin's disease with a combined modality therapy consisting of three cycles of ABVD followed by extended field irradiation (EFRT). No patient had bulky mediastinum or had previously been administered chemo- or radiotherapy. At pathological restaging, 40/44 (91%) evaluable patients achieved complete responses (CR). After a ten-year followup, freedom from progression (FFP), relapse-free survival (RFS) and overall survival (OS) were 80%, 83% and 81%, respectively. Of the prognostic factors, univariate analysis showed that only stage III negatively influenced RFS, but not OS. Toxicity was mild except for subclinical mediastinal fibrosis in 32.5% of CR patients. No patient reported reduced fertility. Two cases of second neoplasms were recorded: one ameboid glioma and one thymoma, both occurring within five years after discontinuing chemo-radiotherapy. Our data suggest that three cycles of ABVD preceeding EFRT is an effective treatment for poor prognosis early-intermediate stage Hodgkin's disease; nevertheless, stage III patients and some stage II patients with unfavorable prognostic factors should be treated with a more aggressive approach.
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PMID:Three cycles of ABDV plus extended field radiotherapy in patients with poor prognosis early-intermediate stage Hodgkin's disease. 2154 11

The aim of this review is to evaluate clinical applications of (11)C-acetate positron emission tomography (PET). Acetate is quickly metabolized into acetyl-CoA in human cells. In this form it can either enter into the tricarboxylic acid cycle, thus producing energy, as happens in the myocardium, or participate in cell membrane lipid synthesis, as happens in tumor cells. (11)C-acetate PET was originally employed in cardiology, to study myocardial oxygen metabolism. More recently it has also been used to evaluate myocardial perfusion, as well as in oncology. The first studies of (11)C-acetate focused on its use in prostate cancer. Subsequently, (11)C-acetate was studied in other urological malignancies, as well as renal cell carcinoma and bladder cancer. Well differentiated hepatocellular carcinoma represents an (18)F-fluoro-deoxyglucose ((18)F-FDG) PET pitfall, so many authors have proposed to use (11)C-acetate in addition to (18)F-FDG in studying this tumor. (11)C-acetate PET has also been used in other malignancies, such as brain tumors and lung carcinoma. Some authors reported a few cases in which (11)C-acetate PET incidentally found multiple myeloma or rare tumors, such as thymoma, multicentric angiomyolipoma of the kidney and cerebellopontine angle schwannoma. Lastly, (11)C-acetate PET was also employed in a differential diagnosis case between glioma and encephalitis. The numerous studies on (11)C-acetate have demonstrated that it can be used in cardiology and oncology with no contraindications apart from pregnancy and the necessity of a rapid scan. Despite its limited availability, this tracer can surely be considered to be a promising one, because of its versatility and capacity to even detect non (18)F-FDG-avid neoplasm, such as differentiated lung cancer or hepatocellular carcinoma.
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PMID:The clinical use of PET with (11)C-acetate. 2313 1

This report describes the case of a 49-year-old man who presented to the hospice with severe neuropathic pain, cramps, muscle twitching, generalised sweating, insomnia and anxiety in the context of metastatic thymoma. The symptoms were exquisitely corticosteroid sensitive raising the possibility of an immunogenic aetiology. Morvan's syndrome, a paraneoplastic, immune-mediated syndrome characterised by peripheral nerve hyperexcitability, dysautonomia and central nervous system dysfunction was thus considered. Nerve conduction studies and electromyography were negative as were initial serological assays. Subsequent assays for antibodies to leucine-rich, glioma inactivated one protein and contactin-associated protein-2, recently discovered to be associated with Morvan's syndrome, confirmed the diagnosis. By the time the diagnosis of Morvan's syndrome was reached the patient was too unwell to receive disease-modifying treatments. An awareness of Morvan's syndrome in Palliative and Supportive care is essential to improve the outcome of patients with this devastating syndrome.
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PMID:A complicated case of metastatic thymoma. 2539 17

Morvan's syndrome (MoS) is a rare, complex neurological disorder characterized by neuromyotonia, neuropsychiatric features, dysautonomia and neuropathic pain. The majority of MoS cases have a paraneoplastic aetiology, usually occurring prior to the diagnosis of the underlying tumour and showing improvement following its treatment. The present study reports the case of a 35-year-old Caucasian male patient who was diagnosed with stage IVA thymoma. Thymectomy, lung resection, diaphragmatic pleurectomy and pericardio-phrenectomy were performed 6 months after neoadjuvant chemotherapy. The pathological evaluation revealed a type B2-B3 thymoma with focal squamous differentiation. Two years later, the patient underwent new surgical treatment for a local recurrence of the same histological type, and 4 weeks later, the patient presented with complex neurological symptoms compatible with MoS, including neuromyotonia, neuropsychiatric features, dysautonomia and neuropathic pain. Electromyography was compatible with a diagnosis of neuromyotonia. Brain magnetic resonance imaging scan and tests for serum anti-acetylcholine receptor, anti-striated muscle antibodies and anti-30-kDa titin fragment antibodies were all negative, whereas tests for anti-voltage-gated potassium channel (VGKC)-complex antibodies (333.3 pmol/l), anti-leucine-rich glioma inactivated protein 1 and anti-contactin-associated protein-like 2 antibodies were positive. The patient underwent 3 cycles of intravenous administration of immunoglobulins (0.4 g/kg/day for 5 days every 4 weeks) with little clinical and electrophysiological improvement. We speculated that the late onset of the symptoms in the present patient may have been triggered by an increase in the serum level of anti-VGKC antibody, which was caused by the surgery performed for the treatment of recurrent thymoma. To the best of our knowledge, the present report is the first case of MoS associated with this histological type of thymoma uncommonly occurring upon surgical treatment of recurrent thymoma.
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PMID:Paraneoplastic Morvan's syndrome following surgical treatment of recurrent thymoma: A case report. 2769 47


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