Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of HLA-DR antigens and Fc IgG receptors as well as C3 complement component, was studied on patients with the primary lung carcinoma and in the control group of nonsmokers and smokers. Macrophages were isolated by broncho-alveolar lavage using bronchofiberoscope. The study was carried out before the treatment, within its course and during remission. The percentage of macrophages with HLA-DR antigens and Fc IgG receptors and C3 complement was observed to diminish before the treatment, after chemo- and radiotherapy as compared to the control. In the course of alpha interferon-treatment and at remission, the expression of HLA-DR antigens on macrophages increased in relation to the remaining groups of patients (p less than or equal to 0.05). The expression of Fc IgG receptors and C3 complement revealed no statistically significant differences. As the findings show the expression of HLA-DR antigens is modulated by interferon and has a tendency to increase in the course of convalescence. On the other hand, the expression of RFc IgG and RC3 complement shows great stabilization in the primary lung carcinoma and undergoes no changes either in the course of treatment or remission.
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PMID:Study on the expression of HLA-DR antigens, Fc IgG receptors and C3 complement component on lung macrophages in the primary lung carcinoma. 215 44

Using a panel of monoclonal antibodies, cells from lymph node biopsies have been examined in three patients with small cell carcinoma presenting with cervical lymphadenopathy. Two patients had small (oat) cell carcinoma of the lung; in the third patient, a primary tumor was not found. Two lymph node biopsies showed typical small (oat) cell carcinoma, and one was an intermediate cell variant; in the last, lung biopsy showed small (oat) cell carcinoma. Electron microscopy demonstrated desmosomes in all three tumors. In each case, lymph node cell suspensions were examined by indirect immunofluorescence with the use of a panel of monoclonal antibodies to antigens usually associated with lymphoid or myeloid cells. In two of the three cases malignant cells were positive with the lymphoid marker BA-2; in two cases malignant cells were positive with OK1a1, a marker for the Ia-like antigen (HLA-DR); and in one case malignant cells were positive with My-1. Caution is needed in the interpretation of cell surface marker studies in the differential diagnosis of small round cell tumors.
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PMID:Hematopoietic cell surface markers on metastatic small cell carcinoma detected with monoclonal antibodies. 299 66

The reactivity of 74 lung-derived monoclonal antibodies (MAbs) provided by the Third International Workshop on Lung Tumor Antigens and of 41 non-lung-derived commercially available MAbs against sections of 15 lung tumors of various histologic types was investigated by immunohistochemistry. Three MAbs with specificity for human neural-cell adhesion molecule (H-NCAM) and 3 MAbs with specificity for small-cell lung carcinoma (SCLC) were able to distinguish between neuro-endocrine (NE) and non-NE tumors. Fifteen MAbs stained non-small-cell carcinomas (NSCLC) but not SCLC. Neuron-specific enolase (NSE) stained all NE tumors but also some of the non-NE tumors. Two MAbs showed specificity for mesotheliomas. Carcino-embryonic MAb strongly stained all SCLC and NSCLC. Among MAbs with lymphoid-cell specificities, Leu 7 (CD57) stained SCLC, but not NSCLC. LN2 (CD45R), LN3 (HLA-DR), Leu 22 (CD43) and BLA 36 reacted with NSCLC and were non-reactive with SCLC. Some of the lung-derived MAbs showed immune staining of lymphoma and melanoma.
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PMID:Reactivity of lung tumors with lung-derived and non-lung-derived monoclonal antibodies. 751 26

The frequencies of HLA class I and II antigens and TNF-beta polymorphism in lung cancer patients were investigated in two areas with different immunogenetic backgrounds, in Okinawa and in mainland Japan (Honshu). In Okinawa frequencies of HLA-Cw3 in squamous cell lung carcinoma patients were higher and those of HLA-DR, both in all lung cancer and in adeno lung carcinoma patients, were lower compared to those of normal controls. Among serologic HLA-DR4-positive individuals, no difference of DRB1*04 gene allele frequency was shown between patients and controls. In Honshu no statistically significant difference of HLA-class I and II alleles frequencies was found; however, the frequency of TNF-beta 10.5-kb homozygote in lung cancer patients was lower than that of controls. For 2-year survival, there was no difference between DR4-positive and -negative individuals and also between each TNF-beta type in Okinawa. In contrast, Honshu patients with 10.5-kb homozygote showed an improved 5-year survival ratio compared to those with heterozygote. We postulate that different immunogenetic backgrounds or environments might have caused the varying HLA or TNF-beta association in the predisposition to or prognosis of lung cancer.
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PMID:HLA and tumor necrosis factor beta gene polymorphisms in Okinawa lung cancer patients: comparative study with mainland Japan lung cancer patients. 759 76

Work from our laboratory indicates that HLA class II induction by IFN- gamma in the retinoblastoma (RB) protein-defective breast carcinoma line MDA-468-S4 (S4) requires reconstitution of functional RB. To determine whether RB is required for HLA class 11 expression in multiple tumor types, the RB-defective non-small cell lung carcinoma line H2009 and its RB-reconstituted subclones were examined for class II inducibility. Surface HLA-DR (DR) was not inducible by IFN-gamma in H2009. However, unlike the RB-reconstituted subclones of S4, DR surface expression was not detected in the H2009 RB-positive subclones. IFN-gamma induction of CIITA, a major regulator of class II transcription, suggested that H2009 retained at least part of the IFN-gamma signaling pathway leading to class II expression. Examination of class II mRNA indicated that IFN-gamma induction of RB was rescued in the RB-positive subclones of H2009, confirming the requirement for RB for HLA class II inducibility and revealing that RB is required for inducibility in developmentally distinct tumor types. However, DRA inducibility was not rescued in the H2009 RB-positive subclones, which explained the lack of surface DR induction in the RB-positive H2009 subclones. DPA and DPB were also only weakly inducible in the RB-reconstituted H2009 subclones, compared with the previously described, S4 RB-positive subclones. Finally, data reported here indicates that RB's ability to inhibit IFN-gamma-induced apoptosis is not a viable explanation for why RB expression rescues DRB inducibility in H2009.
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PMID:Apoptosis-independent retinoblastoma protein rescue of HLA class II messenger RNA IFN-gamma inducibility in non-small cell lung carcinoma cells. Lack of surface class II expression associated with a specific defect in HLA-DRA induction. 878 10

Several immunologic parameters have been reported to correlate with the clinicopathologic status of lung cancer patients. However, these studies were based on relatively small numbers of patients and often yielded conflicting results. We prospectively studied cellular immunologic parameters related to age, gender, and stage in lung cancer patients. We obtained pretreatment peripheral blood samples from 287 lung cancer patients. Lymphocyte subsets (percentage of lymphocytes positive for CD3, CD4, CD8, HLA-DR, or representing FcgammaR IIIa-positive T cells), natural killer (NK) cell activity, and lymphoblastogenesis (LB) after stimulation by phytohemagglutinin (PHA) were evaluated. Significant decline was seen in older patients in percentages of cells positive for CD3 or CD4, in the CD4/CD8 ratio and in LB. The percentage of FcgR IIIa-positive T cells increased with age. LB as well as CD4 positivity were significantly greater in women than in men. NK cell activity showed the greatest cytotoxic responses in stage IIIA, with significantly less response in stage IV than in IIIA. Node-negative patients showed higher reactivities for LB and lower positivity for HLA-DR than node-positive patients. Patients with no distant metastases had a higher level of NK cell activity than patients with distant metastases. Immune parameters are variously related to age, gender, and the stage in lung cancer patients, some may prove to be useful predictors of survival.
Lung Cancer 2000 May
PMID:Cellular immunologic parameters related to age, gender, and stage in lung cancer patients. 1071 31

We obtained a lytic CD4 T-cell clone that recognized an antigen presented by HLA-DRB1*1101 on the tumor cells of a melanoma patient who enjoyed an unusually favorable clinical evolution. The antigen appeared to be shared between several melanoma cell lines. To identify the encoding gene, we used a new method, based on the cotransfection into human embryonal kidney cell line 293 of a cDNA library from the tumor together with a cDNA clone encoding the class II transactivator, which induces the expression of HLA class II molecules. The product of the gene coding for the antigenic peptide is EphA3, a member of the Eph family of tyrosine kinase receptors, which mediate the repulsion of neural cells by cells carrying the ligand Ephrins on their surface. EphA3 is expressed at a high level in the retina and fetal brain, at a lower level in several normal tissues, and not at all in hematopoietic cells, the only cells that constitutively express HLA class II molecules. It is overexpressed in several types of tumors, including melanoma, lung carcinoma, and sarcoma. On the basis of this pattern of expression, EphA3 may be a source of tumor-specific antigens recognized on tumor cells that express HLA class II molecules. Anti-EphA3 T cells may have participated in a tumor rejection response in the patient, because the cells of metastases collected several years later than the metastasis used to characterize the antigen had lost expression of HLA-DR or EphA3, therefore escaping recognition by these lymphocytes.
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PMID:Identification of a tumor-specific shared antigen derived from an Eph receptor and presented to CD4 T cells on HLA class II molecules. 1098 98

In the present report, we have investigated TRAIL/APO2 ligand (APO2L) expression, regulation, and function in human lung carcinoma tumor-infiltrating lymphocytes. Using a panel of non-small cell lung carcinoma cell lines, we first showed that most of them expressed TRAIL-R1/DR4, TRAIL-R2/DR5, but not TRAIL-R3/DcR1 and TRAIL-R4/DcR2, and were susceptible to APO2L/TRAIL-induced cell death. Two APO2L/TRAIL-sensitive tumor cell lines (MHC class I(+)/II(+) or I(+)/II(-)) were selected and specific CD4(+) HLA-DR- or CD8(+) HLA-A2-restricted CTL clones were respectively isolated from autologous tumor-infiltrating lymphocytes. Interestingly, although the established T cell clones did not constitutively express detectable levels of APO2L/TRAIL, engagement of their TCR via activation with specific tumor cells selectively induced profound APO2L/TRAIL expression on the CD4(+), but not on the CD8(+), CTL clones. Furthermore, as opposed to the CD8(+) CTL clone which mainly used granule exocytosis pathway, the CD4(+) CTL clone lysed the specific target via both perforin/granzymes and APO2L/TRAIL-mediated mechanisms. The latter cytotoxicity correlated with APO2L/TRAIL expression and was significantly enhanced in the presence of IFN-alpha. More interestingly, in vivo studies performed in SCID/nonobese diabetic mice transplanted with autologous tumor and transferred with the specific CD4(+) CTL clone in combination with IFN-alpha resulted in an important APO2L/TRAIL-mediated tumor growth inhibition, which was prohibited by soluble TRAIL-R2. Our findings suggest that APO2L/TRAIL, specifically induced by autologous tumor and up-regulated by IFN-alpha, may be a key mediator of tumor-specific CD4(+) CTL-mediated cell death and point to a potent role of this T cell subset in tumor growth control.
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PMID:Tumor-infiltrating CD4+ T lymphocytes express APO2 ligand (APO2L)/TRAIL upon specific stimulation with autologous lung carcinoma cells: role of IFN-alpha on APO2L/TRAIL expression and -mediated cytotoxicity. 1209 84

Immunologic prognostic factors in lung cancer have not been fully clarified. We report the results of a prospective study undertaken to clarify the correlation between various cellular immunologic parameters and the survival of lung cancer patients. A total of 287 lung cancer patients were enrolled in this study. Representative in vitro cellular immune activities including lymphoblastogenesis and natural killer cell activities, in addition to the percentage of main lymphocyte subsets (CD3, CD4, CD8, HLA-DR, and Fc gamma R III on T cells) in the peripheral blood were evaluated before the initiation of therapy. The immune factors that influence the prognosis were analyzed by the log rank test and a multivariate analysis using the Cox proportional hazards model. Univariate analysis of the survival curves revealed a significant difference with regard to disease stage (P<0.0001), age (P=0.007), gender (P=0.0037), and HLA-DR (%) (P=0.048), when all the non-small cell lung cancer (NSCLC) patients (n=257) were analyzed together. This analysis, based on the histologic type, revealed that HLA-DR (%) was a significant predictor of survival in squamous cell carcinoma (P=0.0013) and small cell carcinoma (P=0.0025). A decreased CD4/CD8 ratio in small cell carcinoma (P=0.0062) and male gender in adenocarcinoma (P=0.0086) were factors associated with a worse prognosis. Multivariate analysis identified a significant correlation between survival and disease stage (P<0.0001) and gender (P=0.0243) in adenocarcinoma, disease stage (P<0.0001), age (P=0.0436) and HLA-DR (%) (P=0.0142) in squamous cell carcinoma, and HLA-DR (%) (P=0.0212) and CD4/CD8 (P=0.0112) in small cell carcinoma, suggesting independent prognostic significance. A variety of immunologic indices have prognostic significance for the different types of lung cancer. Among these, the HLA-DR (%) in the peripheral blood is the most reliable factor for squamous cell carcinoma and small cell carcinoma.
Lung Cancer 2002 Aug
PMID:Immunologic parameters as significant prognostic factors in lung cancer. 1214 Jan 39

Cytotoxic CD8+ T cells have been suggested to be key players in the pathogenesis of chronic obstructive pulmonary disease (COPD). We wanted to investigate the phenotype of lung tissue T lymphocytes (LTL) and tumour-infiltrating T lymphocytes (TIL) in smokers with peripheral non-small cell lung carcinoma (NSCLC) with moderate/severe versus mild COPD. Lung tissue and tumour samples were obtained from patients with moderate/severe stage of COPD (n = 10) and from patients with mild stage of COPD (n = 7) at lung resection for a solitary peripheral NSCLC, processed and analysed by flow cytometry. The flow-cytometric results showed that lung tissue T cells, regardless of the severity of COPD, were mostly of the activated phenotype, expressed the CXCR3 chemokine receptor characteristic of type 1 T cells, and did neither significantly differ in the expression of activation markers (CD69, CD25 and HLA-DR), differentiation markers (CD27 and CD28) and chemokine receptors (CXCR3 and CCR4) between the selected groups, nor showed any significant correlation with lung function measured as forced expiratory volume in 1 s (FEV1) or TLCO. Compared with LTL, a significantly greater proportion of TIL expressed the activation markers CD69 and CD25, but a lower proportion showed a fully differentiated CD27- 28- phenotype. We conclude that lung LTL patterns are similar in NSCLC patients with moderate/severe or mild stages of COPD, and are not significantly related to lung function. LTL and TIL possess different phenotype characteristics. The majority of tumour tissue T cells are activated, but it seems that their process of differentiation is incomplete.
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PMID:Lung tissue and tumour-infiltrating T lymphocytes in patients with non-small cell lung carcinoma and chronic obstructive pulmonary disease (COPD): moderate/severe versus mild stage of COPD. 1794 7


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