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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Retrospective dietary and smoking data were gathered by interview of 292 white male patients with lung cancer and 801 control patients with nonrespiratory, nonneoplastic diseases at Roswell Park Memorial Institute, Buffalo, New York. A computed index of vitamin A intake was used to differentiate lung cancer patients from controls. Lung cancer patients had lower values than did controls. The reduced relative risk (RR) of lung cancer associated with vitamin A was most evident among men who smoked heavily. For them, a dose-response relationship increasing to an RR of 2.4 for low values of the index was observed. Frequency of daily milk drinking was lower among patients with lung cancer. Lower RR was found among the men who smoked heavily and frequently consumed carrots. These findings are consistent with evidence from animal studies on inhibition of tumor incidence by retinoids and with previous findings in prospective and retrospective epidemiologic studies.
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PMID:Vitamin A and lung cancer. 28 15

The cytogenetic control of 17 mouse tumor cell strains from of the collection of the bank of the Centre for Oncology Research of the AMS USSR was made: 4 leukemias (L-5178Y, L-1210, L-1210 resistant to 6-mercaptopurine, P-388), 2 sarcomas (S-180, S-298), 8 carcinomas (Ehrlich ascitic carcinoma, carcinoma 755,6-mercaptopurine resistant carcinoma 755, lung cancer LC-67, cervical cancer CC-2, cervical cancer CC-5, stomach cancer GC-5), 2 melanomas (B16, S91) and 1 plasmocytoma (MOPC 21). A comparison of their cytogenetic features allowed a conclusion to be drawn on the absence of any contamination among 14 strains of this collection. Carcinoma 755, sarcoma 298 and leukemia L-5178Y need some further examination for such inference to be valid.
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PMID:[Cytogenetic characteristics of transplantable mouse tumors]. 29 90

A human lung cancer (OTUK-tumor) was transplanted serially to nude mice, which invariably developed a marked neutrophilia. In order to analyze this phenomenon, in vitro agar culture studies were carried out. A three- to fourfold increase of colony-forming units in culture was observed in the femurs of these nude mice. Moreover, the plasma of nude mice bearing this tumor, as well as the tumor extract, had a significantly higher colony-stimulating activity on mouse bone marrow cells than appropriate controls. This activity had the property to stimulate granulocyte and/or mixed cell type colonies rather than mononuclear cells. This activity was also demonstrated, in a dose-dependent way, on normal human bone marrow cells. These findings indicated that the OTUK-tumor produced human granulopoietic colony-stimulating activity, which may have stimulated granulopoiesis in vivo as well.
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PMID:Demonstration of granulopoietic factor(s) in the plasma of nude mice transplanted with a human lung cancer and in the tumor tissue. 30 Jun 38

Cell-to-cell interaction was investigated in various malignant tumor cells (human ovarial tumor, lung cancer, carcinoma of larynx and hamster melanoma cell) and in human lymphoblastoid cells (T-cell (MOLT-4 cell), thymoma cells and B-cells (Burkitt lymphoma cell)). Live lymphoblastoid cells did not adhere to the cell surfaces of tumor cells nor the lymphoblastoid cells were ingested by tumor cells without immunologic and specific treatment. Tumor cells as well as T-cells and B-cells had receptors to concanavalin A on their surfaces, and they showed marked cell binding of tumor cells and lymphoblastoid cells. Moreover, tumor cells that phagocytized lymphoblasts underwent marked cell destruction within 4 hours of cell binding. The cytolytic mechanism of the target tumor cell was probably related to contact with the lymphoblastoid cells and was increased by ingestive activity, and metabolic disturbance by lymphotoxin in tumor cells.
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PMID:Tumor cell phagocytosis and cytotoxicity of lymphoblastoid cells following concanavalin A treatment. 30 16

This paper briefly reviews some mechanisms of tumor immunity and the principles of cancer immunotherapy. Cellular and humoral immunity can both influence tumor cells. Most of the cells belonging to the immune system can act on neoplastic cells. T cells can kill them, macrophages inhibit their growth, and K cells through their Fc receptor also destroy antibody-coated tumor cells. Cancer patients have usually depressed cellular immune functions. The goal of immunotherapy is to amplify the immune reactions in order to destroy the tumor cells. The modalities of immunotherapy are described. They may become important as adjuvant therapy. Immunotherapy has already been successfully in skin cancers, lung cancer and acute myeloblastic leukemia.
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PMID:Cancer immunotherapy. 30 38

A cell line (KSNY) in vitro, which produces colony-stimulating activity (CSA) for human and mouse marrow cells, has been established. A biopsy was performed on the tumor mass of a lung cancer patient who had developed extensive leucocytosis. A piece of the tumor was transplanted to a nude mouse. The seconarily transplanted mice, in turn, developed extensive leucocytosis. The mouse tumor was then removed and placed in culture bottles. To date, the KSNY cells have been maintained in vitro continuously for 15 months. By the use of a methylcellulose bone-marrow colony-formation technique, a high level of CSA in the supernatant of the tumor cell culture was recognized. Doubling time of the cell line is 46 hr. The modal chromosome number is 52, ranging from 45 to 106.
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PMID:Human lung cancer cell line (KSNY) producing colony-stimulating activity which affects both human and mouse marrow cells. 31 53

Alveolar macrophages obtained from Syrian golden hamsters were tested for their ability to destroy tumor cells. Only macrophages obtained from BCG immune animals rechallenged intratracheally with BCG five days before assay exhibited cytotoxic activity. Maximum destruction of tumor cells occurred after 5 days of incubation. Immunologic activation of macrophages was required to attain cytotoxic alveolar macrophages. Induction of inflammatory lung exudates by a variety of nonspecific irritants did not result in tumor cell destruction by macrophages. These observations may prove useful in designing an approach for immunotherapy of lung cancer.
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PMID:Destruction of tumor cells by BCG-activated alqolar macrophages. 33 Jul 56

Cytotoxicity of lymphocytes against allogeneic target cells of a bronchogenic squamous cell carcinoma was examined by a microcytotoxicity test in lung cancer patients after the various kinds of anticancer treatment. Cytotoxicity in untreated cases at stages I, II, and III was higher than the range of controls, but cytotoxicity in those at stage IV decreased to the range of controls. Tumor resection augmented cytotoxicity in patients at stages II and III, when the assays were carried out 3 weeks after the operation. Local irradiation of tumors augmented cytotoxicity in patients at stages II, III, and IV, when the assays were carried out 1 week after the last irradiation. Immunotherapy with BCG cell-wall skeleton augmented cytotoxicity to a marked degree in patients at stages I, II, III, and IV, when the assays were carried out after 4 months of a continuous treatment. The microcytotoxicity test may be useful for estimating the reactivity of lymphocytes in lung cancer patients in various situations.
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PMID:Effect of anticancer therapy of lymphocyte cytotoxicity in lung cancer patients. 35 39

Lung-carcinoma-reactive antibodies have been previously isolated from tumor tissues and pleural effusions. To explore the immunoglobulin (Ig) content of bronchial secretions, bronchial washings of patients with inflammatory and neoplastic lung diseases were studied with respect to Ig levels and specificity. Expressed as Ig/potassium ratios, statistically significant increases in Ig levels were found in inflammatory diseases and even higher increases in lung carcinomas. The isolation of Ig from bronchial washings was achieved by dissociation of immune complexes at low pH, neutralization and subsequent purification by anion exchange chromatography. The isolated immunoglobulins were tested in indirect immunofluorescence against lung cancer cells of various histologic types in tissue cultures and fresh suspensions. Positive cytoplasmic fluorescence was obtained with cells of adeno carcinomas and squamous-cell carcinomas of the lung but not with cells of normal lung. The accessibility of bronchial washings makes the investigation of their lung-cancer-reactive immunoglobulins relatively easy and raises the possibility of its eventual conversion into a screening test.
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PMID:Reactive antibodies in the bronchial washings of lung cancer patients. 36 81

In view of the discouraging results that have been obtained so far with the use of cytotoxic chemotherapy as an adjunct to surgery, a double-blind placebo-controlled evaluation of the adjuvant use of levamisole was conducted in 211 resectable lung cancer patients, following these patients for 2 years after their operation. Levamisole (or the placebo) was given for 3 days every 2 weeks and the dose level ranged 1.1--3.8 mg/kg per day (a fixed dose of 3 x 50 mg was given to all patients). It appeared that recurrences and carcinomatous deaths had occurred significantly less often in patients who had received a high dose (i.e., 2.1--3,8 mg/kg: patients weighing 70 kg or less) but not in the patients who received a lower dose. Patients who had more advanced cancers at the time of surgery seemed to have profited more from the treatment, but the results did not seem to depend upon the histologic type of the tumor or on the immune status of the patients as estimated from the skin test reactivity at the start. There was also suggestive evidence that levamisole may be more effective in preventing hematogenous dissemination than in inhibiting recurrences in the lung or the mediastinal tissues. Levamisole, if dosed adequately, appears to be a very suitable adjuvant treatment in resectable lung cancer patients as judged from its efficacy and its lack of troublesome side-effects.
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PMID:Adjuvant therapy with levamisole in resectable lung cancer. 37 36


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