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Query: UMLS:C0684249 (lung carcinoma)
23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cultured human melanoma, lung carcinoma, and colon carcinoma cells were isotope labeled and incubated with a combination of effector cells and mouse monoclonal antibodies to tumor-associated cell surface antigens. The former were derived from the peritoneal cavity of mice or from peripheral blood of healthy human subjects. Monoclonal antibodies MG-21, 96.5, and L6, which are IgG3, IgG2a, and IgG2a, respectively, were all cytolytic when added in the presence of mouse effector cells to target cells expressing the relevant antigens. MG-21 and L6 were cytolytic also with human effector cells, while monoclonal antibody 96.5 was not. The effector cells attached to plastic surfaces, stained with neutral red, were peroxidase positive and mediated their effect over a 24- to 72-h time period as compared to the 4 h generally sufficient for antibody-dependent cellular cytotoxicity by natural killer cells. In tests on human effector cells with a fluorescence-activated cell sorter, they stained with antibody LCM-3C10 to the CD14 antigen, as well as with antimonocyte antibody 61D3. The cytolytic effect of human effector cells and antitumor antibody was not abolished by incubation with antibodies FC2 or 60.3 to CD16 and CD18, respectively, known to interfere with the antibody-dependent cellular cytotoxicity activity and natural killing of natural killer cells. This suggests, together with the other findings, that the effector cells were macrophages.
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PMID:Antibody-mediated killing of human tumor cells by attached effector cells. 333 25

Mice were given i.v. injections of various tumor cell lines and, beginning 24 h later exposed for 3 weeks to 70% oxygen. Hyperoxia reduced the number of lung colonies derived from MT-7 cells (originally a mammary carcinoma) and of the lung-tumor derived cell lines 498 and Line-1 early passage. Lung colonies derived from Line-1 late passage, lines M109, B16-F10 and Lewis lung carcinoma were oxygen resistant. Lung metastases following i.m. injection of MT-7 cells were oxygen-sensitive and metastases derived from B16-F10 cells or Lewis lung carcinoma were oxygen resistant. Pre-exposure of mice for 48 h to 100% oxygen enhanced colony formation for all cell lines examined whereas exposure to 100% oxygen after i.v. injection only curtailed the growth of the cell lines previously shown to be sensitive to 70% oxygen. There was no correlation between oxygen sensitivity or resistance and the levels of total glutathione or activities of superoxide dismutase (SOD), glutathione reductase or peroxidase or glucose 6-phosphate dehydrogenase in the cell lines. However, upon injection in mice a resistant cell line increased its anti-oxidant defense mechanisms while growing in vivo whereas a sensitive cell line failed to show such adaptation.
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PMID:Effects of hyperoxia on growth of experimental lung metastasis. 334 81

Lectin binding was assessed in subcutaneous tissues of 9 primary tumors of liver and lung metastasizing variants of murine Lewis lung carcinoma (LLC) and their metastases, using the avidin-biotin peroxidase technique. Dolichos bifloris agglutinin, concanavalin A, Ricinis communis agglutinin, and wheat germ agglutinin bound to equal numbers of primary and metastatic tumor cells, indicating that the carbohydrate moieties detected by them were not associated with metastatic potential. However, with peanut agglutinin (PNA), soybean agglutinin (SBA), and Ulex europaeus agglutinin I (UEA-I), the majority of primary tumor cells had the phenotype PNA-, SBA-, UEA-; metastatic tumor cells to the liver had the phenotype PNA+, SBA+, UEA-1-, and metastases to lung had the phenotype PNA+, SBA+, UEA-1+. Thus, LLC tumor cells that were PNA+ SBA+ had metastatic potential, but with no organ-specific preference. However, those that were UEA-I- or UEA-I+ preferentially metastasized to the liver and lung, respectively, implying that selective metastasis was associated with differences in the carbohydrate composition of metastatic tumor cells.
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PMID:Lectin binding by liver and lung metastasizing variants of the murine Lewis lung carcinoma. 339 99

Thirty monoclonal antibodies from eight laboratories exchanged after the First Workshop on Monoclonal Antibodies to Human Melanoma held in March 1981 at NIH were tested in an antibody-binding radioimmunoassay using a panel of 28 different cell lines. This panel included 12 melanomas, three neuroblastomas, four gliomas, one retinoblastoma, four colon carcinomas, one lung carcinoma, one cervical carcinoma, one endometrial carcinoma, and one breast carcinoma. The reactivity pattern of the 30 monoclonal antibodies tested showed that none of them were directed against antigens strictly restricted to melanoma, but that several of them recognize antigenic structures preferentially expressed on melanoma cells. A large number of antibodies were found to crossreact with gliomas and neuroblastomas. Thus, they seem to recognize neuroectoderm associated differentiation antigens. Four monoclonal antibodies produced in our laboratory were further studied for the immunohistological localization of melanoma associated antigens on fresh tumor material. In a three-layer biotin-avidin-peroxidase system each antibody showed a different staining pattern with the tumor cells, suggesting that they were directed against different antigens.
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PMID:Reactivity spectrum of 30 monoclonal antimelanoma antibodies to a panel of 28 melanoma and control cell lines. 620 35

This report describes a patient with small-cell carcinoma of the lung associated with blindness. The serum of this patient was tested for immunoreactivity with retinal sections because there was no evidence of tumor metastasis to the central nervous system and because neuroendocrine cells of the lung share common antigens with retinal neurons. The immunoglobulins in the sera from this patient, from two other patients with small-cell carcinoma, from two patients with multiple sclerosis and from three controls were reacted with 8 micrometers thick sections of retina. Dog, cat and human retinal sections were used. Antihuman immunoglobulins that were conjugated to horseradish peroxidase were used as the second antibody to identify the cells which bound the patients' immunoglobulins. A high titer (1:500) antibody level against retinal ganglion cells was found in the patient with small-cell carcinoma and blindness; the antibody reaction was similar with retina from the three species. The large ganglion cells bound the immunoglobulins of the patients with small-cell carcinoma and blindness while the immunoglobulins from the control and multiple sclerosis subjects did not bind these cells selectively at high dilutions. It remains to be shown whether these antibodies have an etiologic significance in the development of blindness.
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PMID:Occurrence of anti-retinal ganglion cell antibodies in patients with small cell carcinoma of the lung. 628 90

Using a specific antiserum, it was possible to demonstrate (with the Ouchterlony-test, immunofluorescence and peroxidase-antiperoxidase reaction) that the epidermal thiolprotease inhibitor was present in all the squamous epithelia tested by us, e.g. oesophagus, vagina and portio. Immunological methods further showed that epidermoid carcinoma of the skin, squamoepithelial carcinomas of the portion and oesophagus, and squamoepithelial carcinoma of the lung contained an immunoreactive protein reminiscent of the epidermal protease. The immunoreactive protein typical of squamous epithelium was also visible in part of the anaplastic lung carcinomas, which means that the determination of the inhibitor may be of significance in the classification of lung tumors.
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PMID:[Demonstration of an epidermal SH-protease inhibitor in normal epithelium and in some human neoplasms--an immunological study (author's transl)]. 678 89

An unlabelled antibody peroxidase-antiperoxidase method for the detection of IgG, IgM, complement (C3 and Clq), fibrinogen and albumin was applied to routinely processed paraffin sections of lung from 27 cases. The results in 11 cases were compared with those obtained by immunofluorescence using frozen sections. Tissue was obtained from surgical specimens of cases with interstitial pneumonia comprising 10 of the usual type (UIP) and three of the desquamative type (DIP). Tissue was also obtained from the specimens of cases with sarcoidosis (two cases) and granulomatous inflammation of unknown cause (one case). There were 11 control cases, nine with primary carcinoma of the lung and two with metastatic tumours of the lung. Immunoglobulins of various types and complement were seen in diseased lung tissue. Although most of these deposits were probably due to a non-immunological mechanism there was evidence of the possible implication of immune complexes in three cases of UIP and in the interstitial pneumonia present in the two cases of sarcoidosis. The immunoperoxidase technique is a more sensitive method than immunofluorescence and has the additional advantage of the easy identification of the precise sites of the various deposits.
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PMID:Immunohistological study of human lungs by immunoperoxidase technique. 704 Apr 81

The bcl-2 gene product (bcl-2 protein, BCLP) prevents apoptotic cell death. Via a 14;18 chromosomal translocation, BCLP is overexpressed in most follicular lymphomas as well as some other non-Hodgkin's lymphomas, and it has also been documented in other nonlymphomatous malignancies. To address the possible prognostic value of this marker in predefined subsets of non-small cell lung carcinoma (NSCLC), the authors studied 126 T1N0M0 cases seen between the years 1986 to 1991 at our institution. Patients were treated by lobectomy (105 cases) or wedge excision (21 cases) with negative margins; neuroendocrine carcinomas of all grades were specifically excluded. The mean follow-up period was 39 months. Immunostaining for BCLP was done using a monoclonal antibody (clone no. 124; DAKO, Carpinteria, CA), and the avidin-biotin-peroxidase complex (ABC) technique. The study cases included 73 adenocarcinomas (ACs) as well as 40 squamous cell (SCC), five adenosquamous (ASC), and eight large cell/poorly differentiated (LCC) carcinomas. As assessed with the Kaplan-Meier method, overall survival was 64% at 5 years (66% AC vs 59% SC). BCLP was detected in 47 of 126 cases (37%) including 32 AC (44%), 10 SCC 925%), two ASC (40%), and three LCC (38%). No significant difference in 5-year survival was noted in a comparison of all cases with BCLP expression (63%) and those without (59%). There was, however, a significant difference in the survival of grade 1 BCLP(+) cases, when compared with grade 2 or 3 BCLP(+) cases (P = .01). A nonstatistically significant trend toward increased survival was observed in BCLP(+) SCC cases (66% 5-year survival in BCLP[+] vs 45% in BCLP[-] [P = .11]). Proportional hazards analysis failed to disclose significant independent risk factors. These data suggest that bcl-2 protein immunoreactivity has limited prognostic value in the pathological evaluation of NSCLC.
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PMID:Expression of bcl-2 protein in stage T1N0M0 non-small cell lung carcinoma. 759 Jun 97

We studied the effect of lentinan, a fungal polysaccharide immunomodulator, on mouse peritoneal macrophages. The i.p. treatment of mice with 10 mg/kg lentinan affected the number, plastic-adherence, and endogen peroxidase activity of peritoneal cells. The cytotoxicity of lentinan-stimulated peritoneal macrophages was determined against several murine and human metastatic tumor targets: Lewis lung carcinoma (LLT) and two human melanomas, and was found to be significantly higher than that of the macrophages from control animals. However, the highly metastatic variant of LLT (LLT-HH) was resistant to the cytolytic effect of resident and lentinan-activated macrophages as well, indicating that the stimulation for cytotoxicity depends not only on the functional activity of the effector but also on the sensitivity of the target.
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PMID:Effect of lentinan on macrophage cytotoxicity against metastatic tumor cells. 842 9

Cryosections of normal adult lung (n = 7) and pulmonary epithelial tumors, including squamous (n = 8), adeno (n = 8), bronchioloalveolar (n = 5), and large cell (n = 4) carcinomas (SCC, ACC, BAC, LCC), carcinoids (Cd, n = 7), and neuroendocrine carcinomas (NEC) of variable grades (n = 14) were immunostained by the avidin-biotin peroxidase (ABC) method with monoclonal antibodies to the alpha1-6 and alpha(v) and the beta1-4 integrin subunits. Normal adult alveolar septae showed variably intense immunoreactivity for alpha1,3,6 and beta1, whereas reactions for alpha5 and alpha(v) were weaker and uneven; the remaining integrin subunits were not detected. Bronchial and bronchiolar epithelium showed variably intense staining for alpha2.3,6,v and beta1,4. Reactions were often, though not invariably, basally polarized. SCC, ADC, and LCC showed variably intense reactions for alpha2.3,6,v and beta1,4. BAC were strongly and uniformly stained for alpha1.3 and beta1. In Cd, alpha1,2,3,v and beta1 reactions were noted, whereas in NEC, weak alpha1,3 and beta1 staining was detected with only traces of alpha6 and alpha(v). We conclude that alveolar epithelial cells do not express the hemidesmosome-associated, laminin-binding integrin alpha6beta4 of the bronchial epithelium but rather the alpha1beta1 and alpha3beta1, collagen IV, and laminin receptors, respectively. SCC, ADC, and sampled LCC express an integrin repertory qualitatively similar to that of the bronchial epithelium. Distinct from the latter, the integrin repertory of BAC parallels that of the alveolar epithelium by its strong expression of the multipotential alpha1beta1 and alpha3beta1 integrins. NEC tumors do not display the laminin receptors alpha6beta4 and alpha6beta1 shown by SCC and ADC but express instead alpha1beta1, a collagen IV-laminin receptor rarely found in epithelial neoplasms except for BAC. In NEC tumors, integrins, especially alpha2, decrease with dedifferentiation. Notably distinct from epithelial mesotheliomas, the major fibronectin-binding integrin alpha5beta1 was not found in any type of lung carcinoma.
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PMID:Immunolocalization of integrins in the normal lung and in pulmonary carcinomas. 930 25


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