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)

Systemic administration of interleukin (IL)-2 to patients with malignant diseases induces peripheral eosinophilia. In the present study, to clarify the mechanism of eosinophilia induced by IL-2, we examined the changes in the number of eosinophils and eosinophil colony-stimulating factor (Eo-CSF) activity in the pleural fluids of six patients with malignant pleurisy caused by lung cancer or malignant mesothelioma during and after intrapleural administration of IL-2. Results showed that intrapleural administration of IL-2 induced marked eosinophilia in the pleural fluid and moderate eosinophilia in the peripheral blood, and that during IL-2 administration, marked Eo-CSF activity appeared in the pleural fluid before increase in the number of eosinophils, but that this activity did not appear in the peripheral blood. This Eo-CSF activity was inhibited by a combination of anti-IL-5 antibody, anti-IL-3 antibody, and anti-granulocyte/macrophage colony-stimulating factor (anti-GM-CSF) antibody, but not by each antibody alone. Chemotactic activity for eosinophils was also detected in the pleural fluid during IL-2 treatment. These results suggest that eosinophilia in the pleural fluid induced by IL-2 injection into the pleural cavity of patients with malignant pleurisy is due to the Eo-CSF activities of various components, including IL-5, IL-3, and GM-CSF, and chemotactic factors for eosinophils induced locally in the pleural cavity by IL-2.
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PMID:Eosinophil colony-stimulating factor induced by administration of interleukin-2 into the pleural cavity of patients with malignant pleurisy. 220 37

We examined frozen sections of frontal cortex, medulla, and dorsal root ganglia from a patient with small-cell lung cancer and paraneoplastic encephalomyelitis, involving the medulla and dorsal root ganglia, with a panel of antibodies reactive for IgG, IgM, C3, B cells, T cells, T cell subsets, macrophages, and class I and II (HLA-DR) major histocompatibility complex (MHC) antigens. We detected an antineuronal antibody (anti-Hu) in the serum and CSF of the patient and found deposits of IgG in the periphery of some neurons in dorsal root ganglia. The infiltrates were almost exclusively T cells with a predominance of CD8-positive cells. Neurons did not express class I or II MHC antigens. Satellite cells in the dorsal root ganglia from the patient and controls were HLA-DR-positive. These data indicate that CD8-positive T cells predominate in the inflammatory infiltrates of paraneoplastic encephalomyelitis. IgG deposits may be relevant in the damage of the sensory neurons.
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PMID:Immunohistochemical analysis of the immune reaction in the nervous system in paraneoplastic encephalomyelitis. 223 46

The major hematopoietic growth factors have been produced through recombinant DNA technology and have entered initial clinical trials; results of these trials will be reviewed here. Granulocyte colony-stimulating factor (G-CSF) has been tested in patients with bladder cancer and small-cell carcinoma of the lung. In these studies, G-CSF ameliorated the leukopenia associated with combination chemotherapy, reduced the incidence of mucositis in the bladder cancer patients, and nearly eliminated the occurrence of serious infections in the lung cancer patients. Trials involving another factor, granulocyte macrophage colony-stimulating factor (GM-CSF), have resulted in a marked increase in white blood cell (WBC) counts in patients with myelodysplastic syndromes, and has accelerated the appearance of leukocytes and platelets after autologous bone marrow transplants. GM-CSF can also increase the WBC counts in acquired immunodeficiency syndrome patients treated with zidovudine. Both G-CSF and GM-CSF may produce multilineage effects in certain clinical settings and dose ranges. Finally, interleukin-1 (IL-1) and IL-3, which commit very early stem cells to a myeloid pathway, may be used in combination with G-CSF or GM-CSF to produce a synergistic response to various clinical situations.
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PMID:Status of colony-stimulating factors in cancer and AIDS. 240 93

We administered recombinant human granulocyte colony-stimulating factor (rhG-CSF) to four patients with myelodysplastic syndrome (MDS) and three patients with non-MDS (two malignant lymphoma and one lung cancer) as a part of a phase II trial and analyzed the effects of rhG-CSF on the neoplastic cells of MDS by performing sequential chromosome analyses on the bone marrow cells. A greater than 3-fold increase in neutrophil count was observed in the MDS patients after rhG-CSF infusions, whereas the number of blasts in the bone marrow did not increase and none of them progressed into the leukemic phase. After rhG-CSF treatment, the bone marrow cells obtained from patients without MDS did not show any particular chromosome abnormalities such as chromosomal breakage. On the contrary, two of the four MDS patients with acquired chromosome abnormalities showed a change in the frequency of marrow cells with clonal abnormalities after rhG-CSF treatment; the proportion of metaphase cells with additional numerical chromosome abnormalities decreased in these two MDS patients. After discontinuation of the treatment, the constitution of marrow cells with chromosome changes reverted to that before treatment. The remaining two MDS patients did not show any particular chromosome changes after the rhG-CSF treatment, indicating that rhG-CSF may not promote the characteristics of dyshematopoiesis in MDS, and act on cells derived from an MDS clone.
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PMID:Hematologic and cytogenetic findings in myelodysplastic syndromes treated with recombinant human granulocyte colony-stimulating factor. 248 Sep 43

Muramyl dipeptide (MDP) and its synthetic derivatives which comes from the major constituent of bacterial cell wall has various biological activities as host defence mechanisms. One of the synthetic MDP derivatives, MDP-Lys (L 18), muroctasin has potent biological activities with less adverse reactions among various MDP derivatives. Muroctasin has proved to be safe to use clinically as the results of phase I clinical study. We attempted to evaluate its clinical usefulness and safety from the view point of restorative activity in leukopenia that was induced by cancer chemotherapy in patients with malignancies. It is concluded that muroctasin is effective as well as useful on the restorative activities against leukopenia in lung cancer patients after cancer chemotherapy, with the optimal daily dosage of 200 micrograms for six times by subcutaneous injections through phase II and phase III clinical cooperative studies in Japan. Supposed mode of action of muroctasin for granulocytosis may be the results of CSF production due to stimulation of macrophage by muroctasin. This first clinical success of restoration of leukopenia in patients with cancer receiving cancer chemotherapy by MDP derivative, muroctasin, might be not only advantageous for cancer chemotherapy and/or radiation therapy but also for preventing infections occurring in compromised host due to neutropenia in cancer patients by means of cytotoxic cancer chemotherapy or irradication.
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PMID:[Muramyl dipeptide derivative and its clinical application]. 259 64

Bacterially synthesized recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) is an agent with therapeutic potential for neutropenic states, but even at doses below the maximal tolerated dose adverse effects occur during short courses of administration. We have recognized a syndrome of hypoxia and hypotension that follows the first but not subsequent doses of rhGM-CSF. Thirteen of 42 patients receiving rhGM-CSF in phase I studies and 4 of 6 patients in a phase II study developed a reaction that occurred after the first dose of 24 of 78 cycles of rhGM-CSF therapy. The reaction was characterized by flushing (16 of 24), tachycardia (16 of 24), hypotension (14 of 24), musculoskeletal pain (13 of 24), dyspnea (12 of 24), nausea and vomiting (11 of 24), rigors (5 of 24), involuntary leg spasms (3 of 24), and syncope (3 of 24). The reaction did not occur after any of more than 600 second and subsequent consecutive rhGM-CSF doses. Oxygen saturation decreased during first-dose reactions by 8% +/- 4% as compared with 3% +/- 1% on first days without reactions (P less than .001) and 2% +/- 1% on subsequent days (P less than .001). Pulmonary dysfunction was characterized by hypoxemia (59 +/- 9 mm Hg, mean +/- SD) that was fully correctable with supplementary oxygen, decreased single-breath carbon monoxide diffusion capacity, and increased alveolar-arterial oxygen gradients (25 +/- 6 to 60 +/- 4 mm Hg, mean +/- SD), but no significant abnormalities on chest roentgenogram or lung perfusion scan. Factors predisposing to reactions were rhGM-CSF dose greater than or equal to 3 micrograms/kg (P less than .01), intravenous (IV) rather than subcutaneous (SC) administration (P less than .05), occurrence of a reaction after the first dose of a previous cycle of rhGM-CSF therapy (P less than .01), and for patients receiving 15 micrograms/kg/d by SC bolus, the presence of lung cancer (P less than .05). Administration of 15 micrograms/kg/d rhGM-CSF by 24-hour SC infusion rather than SC bolus resulted in a delayed onset of reaction from 30 +/- 8 minutes to 240 +/- 190 minutes (mean +/- SD, P less than .001), and a slower rate of initial transient decrease in neutrophil levels and a more prolonged duration of transient leukopenia. The time of onset of reactions correlated with the rate of rise of rhGM-CSF levels.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Characterization of the clinical effects after the first dose of bacterially synthesized recombinant human granulocyte-macrophage colony-stimulating factor. 268 97

We investigated the interaction between GM-CSF and its receptor on human granulocytes and on several human tumor cell lines. Specific high-affinity binding for GM-CSF was characterized by Scatchard plot analysis. The specific radioactivity of the 125I-labeled derivative of rH. GM-CSF was determined by self-displacement analysis and calculated to be 30 microCi/micrograms. The maximum concentration of binding sites (B max) in granulocytes was 40 fmol/mg protein (2,200 molecules GM-CSF bound/cell) and the dissociation constant (KD) was 0.42 nM. No binding sites for GM-CSF were found in two lung cancer cell lines, SCLC-16HV and NCI-N417 or in the urinary bladder carcinoma cell line 5637, whereas the promyelocytic leukemia cell line HL60 was positive for GM-CSF binding. Time course experiments showed maximum binding of GM-CSF in granulocytes after an incubation period of 60 min and a decrease in binding after an incubation period of 2 h. In parallel, we found a maximum biological signal when granulocytes were preincubated for 90 min with GM-CSF, and a decrease after an incubation time of 120 min. Preincubation of the cells with rH. GM-CSF induced an enhancement of the production of activated oxygen species by the cells in response to PMA.
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PMID:Granulocyte-macrophage colony-stimulating factor binding sites and oxidative metabolism in human granulocytes. 268 55

In 121 proven cases of intracranial metastases, lung cancer was as high as 48 per cent. Multiple lesions were noted (67.8%) in almost every type of organ source. Brain parenchyma (80.3%), predominantly supratentorium was the major site of metastases. The minority was observed in leptomeninge, cranial bone and subgaleal tissue. Subarachnoid seeding tumors along CSF pathways spread mainly from pineal neoplasms; a few cases from lung and choriocarcinoma. Extensive brain edema occurred in metastases from almost every type of primary organ source. Calcification exhibited 5.8 per cent and their origins were lung and breast. Bleeding tumors were noted in 10.7 per cent mainly from choriocarcinoma, a few from lung and GI. Hyperdense tumors occurred in 86.8 per cent on noncontrast scans. Almost all tumors (95.2%) showed contrast enhancement, predominantly ring-shaped lesions. Their organ sources were GI, lung and breast. A few patterns of enhancement were homogeneous and heterogeneous. Non-enhanced lesion were noted in 4.8 per cent mainly due to the high density of calcium and blood inside the tumors. Apart from seeding, calcified and bleeding tumors, the CT findings were not specific for various types of metastases.
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PMID:CT findings of brain metastases. 279 20

Creatine kinase (CK) and its BB isoenzyme (CK-BB) were measured in CSF in 65 evaluable patients suspected of CNS metastases secondary to small-cell lung cancer (SCLC). In addition, CSF and plasma levels of beta-2-microglobulin (beta-2-m) were measured in a group of 73 evaluable patients. Of the 65 patients analysed for CK-BB, 17 had meningeal carcinomatosis (MC), 26 had parenchymal metastases only, and 22 had no CNS disease. Patients with MC had a significantly higher CK-BB concentration in CSF than did patients belonging to the other two groups (P less than .01). Taking 0.4 U/L (upper limit in patients without CNS disease) as a cut-off point, 15 patients (88%) with MC had elevated CSF concentrations of CK-BB. Patients without CNS metastases had no CSF levels exceeding this value, whereas five patients with multiple CNS metastases did. Receiver operating characteristic (ROC) analysis suggests that CK-BB may be useful in distinguishing MC among patients suspected of having CNS metastases, and CK-BB appears superior to total CK, CSF protein, and CSF lactic dehydrogenase (LDH). In 12 patients with MC at autopsy, CK-BB was, with the above cut-off point, elevated in six patients with a false negative cytology. Of the 73 patients examined for beta-2-m, 18 had MC, 30 had parenchymatous metastases only, and 25 patients had no CNS metastases. The CSF concentrations in the three groups were not significantly different. The median concentrations in the groups were 133 nmol/L, 125 nmol/L, and 107 nmol/L, respectively. The ratios between beta-2-m in CSF and plasma were also not significantly different between the three groups. Thus, the data on CK-BB are promising, and further studies are warranted to see if the usefulness of CK-BB can be more firmly established. By contrast, beta-2-m has no role as a marker of CNS disease secondary to SCLC.
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PMID:Creatine kinase BB and beta-2-microglobulin as markers of CNS metastases in patients with small-cell lung cancer. 299 99

The most examined tumor markers in lung cancer patients are CEA, hormonal peptides, and some neurogenic enzymes in small cell carcinoma. Calcitonin, ACTH, ADH, CEA, neurophysin, oxytocin, beta-endorphin, neuron-specific enolase, and CK BB are elevated in serum specimens in 25-75% of cases of small cell carcinoma. The level of these markers is related to the stage of the disease in groups of patients; elevated pretreatment levels decrease with tumor regression. Marker levels are not valid in defining the tumor load and the presence of disease in the individual patient. It has not yet been documented that the markers can be used for clinical decisions on antineoplastic therapy. A recent development is the finding that measurement of CSF and plasma concentrations of ADH, calcitonin, CK BB, bombesin, and neuron-specific enolase may contribute in the diagnosis of CNS metastases including meningeal carcinomatosis.
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PMID:Tumor markers in patients with lung cancer. 300 40


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