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)

Peripheral blood mononuclear cells from 11 glioma patients and 11 healthy control subjects were cultured in medium containing recombinant interleukin-2 for a period of 5 days. The cytotoxicity of these lymphokine-activated killer (LAK) cells was tested on chromium-51-labeled freshly prepared allogeneic glioblastoma cells, and on the cell lines K562 (natural killer cell (NK)-sensitive) and Daudi (NK-resistant). Peripheral blood mononuclear cells from all subjects showed high levels of cytotoxicity against these targets. There was no significant difference between the patients and the control group when LAK cytotoxicity was compared. Thus, although glioma patients are known to have depressed immunological reactivity, the cytotoxic capacity of LAK cells derived from glioma patients is similar to that of LAK cells from healthy control subjects. However, the glioma patients had significantly reduced numbers of mononuclear cells in their peripheral blood, possibly due to steroid treatment. Therefore, the volume of blood required to generate the same number of LAK cells was approximately three times larger from the glioma patients than from control subjects.
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PMID:Comparison of in vitro glioma cell cytotoxicity of LAK cells from glioma patients and healthy subjects. 326 Jun 22

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

Employing serum-free media, human peripheral blood mononuclear cells, and purified recombinant interleukin-2 (IL-2), conditions were observed in which the development of IL-2-driven cytotoxic activity was suppressed. The cytotoxic activity of such IL-2-generated lymphokine activated killing (LAK) was tested against natural killer-resistant cultured tumor cells (Daudi, Raji, and a glioma). LAK generation was inhibited by addition of some normal sera, normal platelets, or some tumor cells. Because recent reports have indicated that transforming growth factor-beta (TGF-beta)-like factors are often secreted by tumors and the acidic alpha granules of platelets and can be present in sera, we tested the effect of purified human TGF-beta on the activation of LAK. Our results indicated that TGF-beta is very suppressive for LAK induction, and can completely prevent both the IL-2-driven proliferation and cytotoxicity at concentrations as low as 5 ng/ml. Titrations of IL-2 and of TGF-beta indicated that the suppression is dose-dependent and can be avoided by employing higher levels of IL-2. It was also found that the suppressive effect of TGF-beta can be overcome by washing suppressed cell populations and further culture in low levels of IL-2. Collectively, these data indicate that TGF-beta can be a potent inhibitor of LAK generation under standard activation conditions, but that this effect is regulated by the relative level of IL-2 and may be overcome and/or reversed in vitro.
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PMID:TGF-beta inhibits the in vitro induction of lymphokine-activated killing activity. 326 Aug 21

In theory, lymphokine-activated killer (LAK) cells offer a potential method to treat cerebral gliomas, especially low-grade gliomas. LAK cells would be administered by repeated injections straight into the cavity of a subtotally removed tumour. However, brain-tumour cyst fluid has been shown to be immunosuppressive in lymphocyte stimulation tests. Therefore we wanted to know whether the fluid would reduce the killing efficacy of LAK cells. Using a standard cytotoxity test based on 51Cr release, we compared in vitro the cytotoxity of LAK cells against K-562 tumour cells in brain-tumour cyst fluid, autologous serum and allogeneic serum. Five patients with cystic glioma and one with cystic meningioma were studied and no inhibition of cytotoxity of LAK cells was observed.
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PMID:Cyst fluid of glioma does not inhibit the killing action of lymphokine-activated killer (LAK) cells in vitro. 339 50

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

The killing of Fischer rat 9L glioma in vitro by lymphokine-activated killer (LAK) cells was studied. LAK cells generated by culturing Fischer spleen cells with recombinant interleukin 2 markedly lysed glioma cells but did not kill syngeneic normal brain tissue in a chromium release microcytotoxicity assay. Susceptibility of glioma to lysis by LAK cells was markedly diminished by pretreating the glioma cells with trypsin or chymotrypsin but was unaffected by pretreatment with neuraminidase, glycosidases, or sodium periodate. These results suggest that LAK cell killing of glioma is probably tumor-selective and that a crucial cell surface determinant on glioma cells responsible for its tumor-selective lysis by LAK is a protein sensitive to trypsin and chymotrypsin.
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PMID:Lymphokine activated killer (LAK) cell-mediated lysis of murine glioma: trypsin-chymotrypsin-sensitive glioma protein is responsible for tumor-selective recognition by LAK cells. 348 96

For the purpose to study reasonable treatment for recurrent gliomas, in vitro immunochemosensitivity tests were performed by using human malignant glioma cell line (ONS-12) and its ACNU-resistant cell line (ONS-12/ACNU), which were established in our laboratory. ONS-12/ACNU cells showed a cross-resistance to Ara-C, but not for cisplatin and methotrexate. The lymphokine-activated killer (LAK) cells induced in vitro from the peripheral blood lymphocytes (PBL) of healthy subjects, showed stronger cytotoxicity to ONS-12/ACNU than ONS-12 cells. From these data, selection of appropriate anti-tumor agents on the in vitro sensitivity tests was a most useful method for the treatment of recurrent gliomas, and the adoptive immunotherapy with LAK cells may be useful for ACNU-resistant gliomas.
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PMID:[Experimental studies on the treatment of recurrent gliomas]. 349 51

We report preliminary results of adoptive immunotherapy in 12 patients with malignant glioma. The patients received both 1.8 to 20 X 10(8) autologous lymphokine activated killer (LAK) cells, and 8 to 16 X 10(4) units of interleukin-2. Objective regression of the tumor was observed in 8 patients. In 4 cases, the size of the tumor was remarkably reduced. No severe side effects were observed. Furthermore, LAK cells and their precursor cells were serologically studied.
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PMID:[Adoptive immunotherapy in patients with malignant glioma]. 349 52

In a Phase I study, recombinant interleukin-2 (IL-2) or autochthohous lymphokine-activated killer (LAK) cells were used to treat nine patients with malignant glioma. One patient received the combination of IL-2 and LAK cells. LAK cells were generated by culturing IL-2 with peripheral blood lymphocytes obtained from brain tumor patients. Escalating doses of LAK cells (10(8)-10(10) or recombinant IL-2 (10(4)-10(6) units) were administered by direct injection into the brain tissue surrounding the cavity left following operative tumor removal. There have been no signs of systemic or neurotoxicity following treatment. The tumor selective killing of the LAK cells used for these treatments was demonstrated by their ability to lyse glioma cells but not normal cells in vitro using a chromium release microcytotoxicity assay.
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PMID:Interleukin-2 or autologous lymphokine-activated killer cell treatment of malignant glioma: phase I trial. 351 79

Nine patients with malignant glioma were treated with the lymphokine interleukin-2 (IL-2) or with lymphokine-activated killer (LAK) cells, and one patient received combination therapy with both LAK cells and IL-2. The LAK cells were generated by culturing recombinant IL-2 with peripheral blood lymphocytes obtained from brain-tumor patients. Escalating doses of LAK cells (10(8) to 10(10] or IL-2 (10(4) to 10(6) U) were administered intraoperatively by direct injection into the brain tissue surrounding the cavity left by debulking the tumor. There were no signs of systemic or neural toxicity following treatment. The selective killing of the tumor by LAK cells used for these treatments was demonstrated by a chromium release microcytotoxicity assay which showed in vitro the ability of the LAK cells to lyse glioma cells but not normal cells.
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PMID:Interleukin-2 and autologous lymphokine-activated killer cells in the treatment of malignant glioma. Preliminary report. 351 50


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