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)

A fraction showing tumour-associated antigenic properties has been isolated from pleural effusions of patients with squamous-cell carcinoma of the lung. Purification of the material was accomplished by ion-exchange and affinity chromatography, and by immunoabsorbents. The antigenic activity was monitored by its inhibitory capacity in a specific complement-dependent cytotoxic system. The final fraction has a mol. wt. of approximately 1.7 X 10(5), as judged by gel filtration on Sephadex G200, and the main component appears to be a glycoprotein with N-acetyl-D-glucosamine groups. The most purified antigen preparation exhibited a highly selective capacity to inhibit in the cytotoxic assay and to bind, when labelled with 125I, to 2 specific antisera. The active fractions isolated from pleural effusions fully crossreacted with fractions prepared from squamous-cell carcinoma extracts. CEA and bacterial antigens were not detected in the material, and the presence of alpha-fetoprotein, HLA and blood-group antigens may be ruled out on account of their respective molecular weights.
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PMID:A tumour-associated antigen from the pleural effusion of patients with squamous-cell carcinoma of lung. 67 26

The concept of genetic factors playing a role in the pathogenesis of lung cancer has gained increased attention. The present study was undertaken to reexamine the question of HLA antigen association with carcinoma of the lung. In a study of 90 patients, a significant association occurred between HLA-DR7 and resistance to lung cancer, after accounting for smoking status and sex. HLA class I antigens were also implicated. These results suggest that major histocompatibility complex loci affect carcinoma of the lung.
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PMID:HLA antigens influence resistance to lung carcinoma. 191 91

In view of the evidence for an autoimmune pathogenesis of the Lambert-Eaton myasthenic syndrome, we have sought associations with IgG heavy chain allotypes (Gm) and HLA antigens in 30 patients, of whom 20 had evidence of lung carcinoma (histologically proven small ("oat") cell type in 17). A highly significant overall increase in frequency of Glm(2) (chi 2 = 10.95; p less than 0.001; n = 30) and of HLA-B8 (chi 2 = 19.07; p less than 0.001; n = 23) was observed. These two factors apparently occurred independently of each other. The Glm(2) frequency in 36 non-myasthenic small cell carcinoma cases was the same as in a control panel (n = 167). We conclude that Glm(2) and HLA-B8 both associate with increased susceptibility to the Lambert-Eaton myasthenic syndrome, and suggest that Glm(2) may be in linkage disequilibrium with a limited number of VH genes coding for antibodies to restricted antigenic determinants at the nerve terminals, which may be shared by the carcinoma cells.
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PMID:Increased frequency of IgG heavy chain marker Glm(2) and of HLA-B8 in Lambert-Eaton myasthenic syndrome with and without associated lung carcinoma. 299 7

Recent reports have described the expression of myeloid cell surface antigens on cells of small cell carcinoma of the lung (SCCL). In order to confirm and extend these findings, we have examined by cytofluorography a large panel of well-characterized cell lines derived from SCCL tumors for the expression of several myeloid cell-associated antigens, some of which were not examined in previous reports. In addition, we have studied the expression of Classes I and II HLA antigens on these SCCL cell lines. Finally, we examined the effect of gamma-interferon on the expression of several cell surface markers and on proliferation of SCCL cells. We have found that several SCCL cell lines expressed a Mr 55,000 polypeptide antigen, My23, previously found only on monocytes and monocytic leukemia cells. In addition, the cell lines studied expressed another antigen, defined by monoclonal antibody AML-1-99, which is associated with monocytes and hematopoietic stem cells. We confirmed previous studies that the Leu-7 antigenic determinant is expressed on SCCL cells but observed only minimal or absent binding of monoclonal antibody OKM1 to most cell lines. Class I HLA antigens were present on eight of nine lines examined while Class II HLA was expressed on three of nine lines. Gamma-Interferon decreased the proliferative rate of all lines examined. However, this lymphokine was capable of inducing Class I HLA on several lines. The effect of gamma-interferon on other cell surface antigens was variable. These studies confirm that some myeloid cell-associated antigens are expressed on cultured SCCL lines and, additionally, show that their expression can be modulated by immune interferon. Determining the significance of finding myeloid cell-associated antigens on SCCL cells will require further study.
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PMID:Expression of myeloid and major histocompatibility antigens on small cell carcinoma of the lung cell lines analyzed by cytofluorography: modulation by gamma-interferon. 300 87

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

Cinnamic acid, a naturally occurring aromatic fatty acid of low toxicity, has a long history of human exposure. We now show that cinnamic acid induces cytostasis and a reversal of malignant properties of human tumor cells in vitro. The concentration causing a 50% reduction of cell proliferation (IC50) ranged from 1 to 4.5 mM in glioblastoma, melanoma, prostate and lung carcinoma cells. Using melanoma cells as a model, we found that cinnamic acid induces cell differentiation as evidenced by morphological changes and increased melanin production. Moreover, treated cells had reduced invasive capacity associated with modulation of expression of genes implicated in tumor metastasis (collagenase type IV, and tissue inhibitor metalloproteinase 2) and immunogenicity (HLA-A3, class-I major histocompatibility antigen). Further molecular analysis indicated that the anti-tumor activity of cinnamic acid may be due in part to the inhibition of protein isoprenylation known to block mitogenic signal transduction. The results presented here identify cinnamic acid as a new member of the aromatic fatty acid class of differentiation-inducers with potential use in cancer intervention.
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PMID:Cinnamic acid: a natural product with potential use in cancer intervention. 762 77

The reactivity of a mAb (M16) raised against a small cell lung carcinoma line is described. M16 identifies a surface antigen expressed on cells of neuroectodermal origin following activation, as well as neoplastic transformation. M16 antigen expression is increased on retinoblastoma and neuroblastoma cell lines upon 'in vitro' stimulation and it is induced 'in vivo' on glial cells activated following brain injury. Furthermore, glial tumors show levels of M16 molecule expression increasing with the degree of malignancy, and in a retinoblastoma cell line, the expression of M16 was inversely related to the level of HLA-Class I and N-CAM antigens. The M16 antigen may represent a marker of both activation and neoplastic progression for neuroectodermal cells.
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PMID:Biochemical characterization and membrane expression of an antigen shared by activated and neoplastic cells of neuroectodermal origin. 770 33

MHC-I binding peptides and beta 2 microglobulin (beta 2-m) can upregulate the MHC-I heavy chain expression on certain peptide transporter mutant cells. We have further studied this with normal cells and non-mutant cell lines. No MHC-I upregulation was seen with normal, resting or activated T cells. On mouse cell lines P815 and B16, both peptides and human beta 2-m gave an additive upregulation response. With the human small cell lung carcinoma H82, an optimal HLA.A2 binding peptide (GILGFVFTL) gave an upregulation response, whereas beta 2-m alone or in combination with this peptide had no effect. However, beta 2-m potentiated the response of H82 cells to a slightly longer peptide. Using mutant RMA-S cells, it was found that both Brefeldin A (BFA) and chloroquine, but not leupeptin, inhibited MHC-I upregulation response to both peptide and beta 2-m. In contrast to chloroquine, BFA also gave a reduction of background membrane MHC-I expression, presumably due to a block in Golgi transport. Human beta 2-m, which binds to RMA-S cells, and which is known to internalize into endosomes, did not reappear on the cell surface. When Db on RMA-S cells was upregulated by human beta 2-m, the sensitivity of these cells to Db restricted CTL cells increased. Even if beta 2-m did not upregulate the overall MHC-I expression on normal cells, it may still quantitatively increase the expression of optimally presented peptides and endosomal recycling many be important in this process.
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PMID:Regulation of MHC class I membrane expression by beta 2-microglobulin. 821 Oct 1

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

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


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