Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been observed that neopterin, a specific marker of macrophage activation, increases during cancer immunotherapy with IL-2, and this effect is mediated by interferons produced by IL-2-stimulated lymphocytes. Moreover, our previous studies have shown that neopterin rise during IL-2 immunotherapy is associated with an enhanced release of soluble IL-2 receptor (SIL-2R), which may suppress IL-2-dependent immune functions. This finding would suggest that neopterin increase may be related to the generation of suppressive events, which occur during IL-2 immunotherapy. On the basis of the documented modulatory effect of IL-3 on macrophage functions, we have evaluated the influence of IL-3 on neopterin secretion during IL-2 immunotherapy. The study was performed in advanced lung cancer patients. We have investigated 9 immunotherapeutic courses consisting of IL-2 (6M IU/day s.c. for 5 days/week for 3 weeks) plus IL-3 (1 microgram/(kg x day) i.v. for 14 days, starting 7 days before IL-2). The results were compared to those found during 18 courses with IL-2 alone. Mean neopterin levels increased significantly during IL-2 alone, but not in response to IL-3 plus IL-2. SIL-2R rise was significantly higher during IL-2 than during IL-3 plus IL-2. Mean numbers of NK cells and activated lymphocytes increased significantly in both groups of patients, but were significantly lower at the end of the treatment in patients receiving IL-2 alone than in those treated with IL-3 plus IL-2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of macrophage response to interleukin-2 immunotherapy by interleukin-3 in cancer patients. 129 6

The levels and activities of endogenous IL-6 in malignant pleural effusions due to lung cancer before and during daily intrapleural instillations of recombinant IL-2 were examined by enzyme immunoassay and bioassay using an IL-6-dependent murine hybridoma cell line MH60.BSF2. Before therapy, malignant pleural effusions contained various levels of IL-6. Daily intrapleural instillation of recombinant IL-2 for treatment of malignant pleurisy resulted in significant augmentation of the levels and activities of IL-6 in the pleural effusions. On fractionation of the pleural effusion by chromatography, one major peak of material with a mol. wt of 24 kD showed IL-6 activity. In contrast, no significant level of tumour necrosis factor-alpha or IL-1 beta was detectable in pleural effusions before or during local IL-2 therapy. These data suggest that IL-2 is an important regulatory factor of secondary IL-6 production.
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PMID:IL-6 in malignant pleural effusions and its augmentation by intrapleural instillation of IL-2. 131 27

The stimulatory effect of IL-2 on cortisol rise represents an undesirable biological event during IL-2 cancer immunotherapy. At present, no cytokine has been proven to be able to counteract IL-2-induced cortisol increase. This study was carried out to evaluate the influence of IL-3 on IL-2 stimulation of cortisol secretion. Five lung cancer patients were investigated after IL-2 (3 x 10(6) IU s.c.), after IL-3 (1 mcg/kg b.w. i.v.) and after IL-3 plus IL-2, by administering IL-3 two hours before IL-2 injection. IL-2 significantly stimulated cortisol secretion. IL-3 alone had no effect on cortisol levels. The pretreatment with IL-3 completely neutralizes IL-2-induced cortisol release. These preliminary results would suggest that IL-3 may be associated with IL-2 during cancer immunotherapy to modulate the effect of IL-2 on the endocrine system.
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PMID:Inhibitory effect of interleukin-3 on interleukin-2-induced cortisol release in the immunotherapy of cancer. 133 54

We examined the effect of fibrin coagulation on tumor cytotoxicity mediated by human lymphokine (IL-2)-activated killer (LAK) cells. LAK cells were induced from peripheral blood mononuclear cells (MNC) by culture with recombinant IL-2 for 4 or 5 days, and LAK cell-mediated cytotoxicity against tumor cells was assessed by 51Cr release assay in the presence or absence of plasma from normal subjects and lung cancer patients. Plasma did not affect the phase of induction of LAK activity by IL-2, but dose-dependently inhibited the effector phase of LAK cell-mediated cytotoxicity against Daudi cells. Similar inhibition of LAK cell-mediated cytotoxicity was observed on pretreatment of Daudi cells and human lung cancer cell lines with human fibrinogen plus thrombin. A parallel relationship was found between the amount of fibrinogen in plasma of lung cancer patients and inhibition of LAK cytotoxicity. This inhibition was reduced by addition of anticoagulants (heparin or argatroban). These findings suggest that fibrin coagulation on tumor cells protects them from LAK cell-mediated tumor cytotoxicity in malignant lesions and that a combination of an anticoagulant drug and IL-2/LAK therapy may be effective for treatment of lung cancer patients.
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PMID:Inhibition by fibrin coagulation of lung cancer cell destruction by human interleukin-2-activated killer cells. 145 61

We established a method of in vitro immunization of human lymphocytes against human cancer cells and efficiently obtained human-human hybridomas producing cancer-specific antibodies using the in vitro immunized lymphocytes. Human lymphocytes were cocultured with human lung cancer cell line A549 for four days in medium containing various immunoactive reagents. In vitro immunization was effectively caused by the addition of OK-432 or muramyl peptides, IL-2, and IL-6, to the coculture of A549 cells and lymphocytes. Although specific antibodies of both IgM and IgG classes were produced by this method, the ratio of IgG to IgM was greater than or equal to 2. The efficiencies of in vitro immunization fluctuated about threefold in lymphocytes derived from several donors. The in vitro immunized lymphocytes were fused with human fusion partner A4H12 cells. Hybridomas producing specific antibodies reactive to A549 cells were efficiently obtained by sequential cell fusion. The efficiency of acquisition of hybridomas producing specific antibodies with the in vitro immunized lymphocytes was about 10-fold higher than that with lymphocytes spontaneously immunized in bodies of lung cancer patients.
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PMID:In vitro immunization of human lymphocytes with human lung cancer cell line A549. 157 23

Thirty patients with hepatocellular carcinoma who underwent hepatic resection during the recent 2 years in our department were randomized. We derived LAK cells from the autologous spleen removed during operation. The cultivation of LAK cells were done with IL-2. Adriamycin 20mg/body was injected into hepatic artery via subcutaneous implanted reservoir on the 8th postoperative day. In group A, 1.0-7.6 x 10(9) LAK cells were injected i.a on day, 10, 14, and 21 after operation. IL-2 of 5 x 10(5) JU were also injected i.a. during 3 weeks. Group B patients were treated only by adriamycin. High fever was seen in all patients belonged to group A. Twelve patients in each group were evaluable. Recurrence rate 8.3% in group A was significantly lower than 50% in group B. In experimental study, accumulation of 111In-oxine labelled LAK cells in mouse 3LL lung cancer was augmented in splenectomized ones. Adopted immunotherapy by spleen LAK-cells may be effective and safe treatment to preventing recurrence of hepatocellular carcinoma after hepatectomy.
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PMID:[Adopted immunochemotherapy using IL-2 and spleen LAK cell--randomized study]. 165 91

By using thymocytes of mice as target cells in bioassay, IL-2 production activity was investigated in 24 lung cancer patients, 24 noncancerous pulmonary lesions as well as 20 normal individuals. Fourteen cancer patients were reexamined after the first course of chemotherapy. This research demonstrated that: 1. PBL capable of IL-2 production in lung cancer patients were rare in comparison with benign disease or normal control. 2. IL-2 activity was markedly enhanced by chemotherapy. It is suggested that IL-2 is a good indicator for estimating the efficacy of treatment of lung cancer.
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PMID:[A study of IL-2 activity on lung cancer]. 166 44

Chemoimmunotherapy with anticancer drugs and immunoregulatory drugs and cytokines is a logical combination of 2 forms of therapy that have different mechanisms of action and no overlapping toxicity. Generally, anticancer drugs show rapidly the strong suppressive effect on tumor growth but also on host hemato-immunological functions. On the other hand, immunotherapy demonstrate the potential of restoring the hemato-immunological dysfunction of chemotherapy as well as the gradual antitumor effect through activating host defense mechanisms against cancer, indicating that these therapeutic modalities are complementary. On these biological rationale of chemoimmunotherapy mentioned above, we have demonstrated that immunostimulant, Nocardia-CWS is capable of producing tumoricidal macrophages being different from anticancer drugs in cytotoxic mechanism against cancer, and also that macrophage tumoricidal activity is significantly suppressed by exposure to anticancer drug, mitomycin C. Another beneficial activity of immunostimulant showed in our previous studies is a capability of production of colony stimulating activities. In a cooperative study with lung cancer patients it has been shown that recovery of leucopenia after chemotherapy is accelerated by administration of immunostimulant, MDP-Lys. Recently, immunomodulatory lymphokine, IL-2, has been clinically used for induction of activated killer lymphocytes (LAK cells) with tumoricidal activity. According to our studies, however, anticancer drug, when administered to cancer patients or added directly to culture of lymphocytes with IL-2 for LAK induction, shows significant suppressive effect on LAK induction. Considering these experimental and clinical studies, it can be concluded that immunotherapy, when employed as adjuvant after chemotherapy, play the important roles not only in eradication of tumor cells being escaped from chemotherapy but also in prevention of infections complication by activating host defense mechanisms common to cancer and infection.
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PMID:[Bases on timing of combined modality of chemotherapy and immunotherapy]. 169 53

Cellular infiltrates of bronchoalveolar lavage (BAL) and pleural effusion from patients with tuberculosis (TB) and lung cancer were characterized for the presence of different T cell subsets by phenotypic analysis. The specificity of the T cells for mycobacterial antigens was then compared for the two disease compartments. The composition of T cell subsets within the BAL, in contrast to pleural effusion cells (PEC), revealed evidence of sequestration of CD8+ cells. BAL T cells were found to be a predominantly CD29+ DR+ memory population of activated cells. Although polyclonal populations of BAL T cells proliferated poorly to Mycobacterium tuberculosis antigens, mycobacterial antigen-reactive monoclonal T cell populations could be derived from the alveolar compartment. Two clones were shown to recognize the 65-kD heat shock protein of mycobacteria, and one of these clones recognized a conserved sequence of the molecule. Several BAL-derived clones, responding to a mycobacterial soluble extract, did not, however, recognize purified mycobacterial antigens, previously identified as highly stimulatory for PEC-derived T cells. T cell clones, derived from PEC of two TB patients, responded to the 38-kD and 71-kD, as well as the 65-kD mycobacterial antigens. Examination of the activation requirements of BAL-derived T cell clones, specific for mycobacterial antigens, revealed that exogenous IL-2 was necessary for the T cells to sustain proliferation. This was in contrast to the mycobacterial antigen-reactive T cells cloned from PEC. These results suggest that T cell populations with distinct antigen specificities and activation requirements are present in BAL and PEC.
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PMID:Antigenic specificity and subset analysis of T cells isolated from the bronchoalveolar lavage and pleural effusion of patients with lung disease. 173 92

The concomitant induction of immunosuppressive events, at least in part mediated by macrophages, would represent one of the mechanisms responsible for the lower activity of IL-2 in vivo than in vitro. Since macrophages have recently appeared to be under neuroendocrine control, the present study was carried out to evaluate the effect of the pineal neurohormone MLT on IL-2-induced macrophage activation during cancer immunotherapy, by determining serum levels of neopterin, which is a specific marker of macrophage activity. The study included 21 advanced cancer patients (lung cancer: 12; renal cancer: 9), 10 of whom received IL-2 subcutaneous therapy alone (1.8 x 10(6) IU/m2 twice daily), or IL-2 plus MLT (10 mg/day orally at 8.00 P.M.). Neopterin levels increased in all patients during IL-2 immunotherapy, but neopterin mean peak was significantly higher in patients treated with IL-2 alone than in those who received IL-2 plus MLT. This preliminary study would suggest the possible use of neurohormones to modulate host antitumor immune response during cancer immunotherapy with IL-2.
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PMID:Modulation of interleukin-2-induced macrophage activation in cancer patients by the pineal hormone melatonin. 180 63


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