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

Monoclonal antibodies were generated with spleen cells from nude mice bearing human tumors. Three grafted tumors were selected because of their difference in metastatic ability in nude mice. Two were non-metastasizing carcinomas and one a highly metastasizing adenocarcinoma of the lung (Bur-tumor). Two normal nude mice were used as controls. Culture supernatants were screened by immunoperoxidase using frozen sections from both the immunizing human tumor and normal human tonsil to detect unexpected monoclonal antibodies. Two kinds of monoclonal antibodies were obtained. The first were directed against miscellaneous membrane and/or cytoplasmic antigens expressed by normal cells (e.g. normal tonsillar epithelium). Most of these antibodies corresponded to auto-antibodies and their frequency did not appear to be influenced by the fact that the mice were with or without grafted human tumors. The second type of antibodies were directed against tumor-associated antigen and generated only by fusing splenocytes from nude mice bearing the metastasizing lung adenocarcinoma. On frozen sections Bur-1-anti-tumor antibody stained all but one lung carcinoma. Occasional carcinomas originating from other organs such as pancreas and breast were also labelled. On the other hand, more than half of the cases of so-called "malignant histiocytosis" (Ki-1 lymphoma) seemed to express this epithelial antigen. Some normal cells in the lung, pancreas (acini), and kidney (distal tubules) also bound Bur-1 antibody. These results suggested that Bur-1 antibody could be related to some antibodies already described, directed against epithelial membrane antigens. When Bur-tumor was analysed by immunoblotting with Bur-1 antibody a positive reaction was obtained with material migrating in the kD-45kD molecular-weight region.
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PMID:Production of monoclonal antibodies using spleen cells from nude mice bearing human tumors. 304 26

This paper describes two rat monoclonal antibodies (MAbs) (1A6 and 2H7, both IgG2a) directed against a human adenocarcinoma of the lung (A549). Enzyme-linked immunosorbent assay (ELISA) and immunocytochemistry (Avidin-Biotin-complex method) as the screening of the hybridoma cells revealed that 1A6 and 2H7 MAb mainly reacted with adenocarcinoma of the lung, breast and pancreas, and 2H7 MAb also recognized large cell carcinoma, epithelia of the lung, trachea, tongue or small cell carcinoma of the lung. The antigen molecules recognized by 1A6 MAb was not detected by immunoprecipitation but the molecular size of the antigen by 2H7 was ca. 40Kd. The antibody-producing heterohybridoma cells could be transplanted into peritoneal cavities of nude mice to form ascites. We found these monoclonals useful for immunohistodiagnosis of surgical specimens from patients with lung cancer. Furthermore, we utilized 125I-labeled 2H7 MAb, aiming at localizing A549 tumor mass transplanted into nude mice subcutaneously. This antibody clearly localized the tumor mass. It is suggested that they may be useful as both diagnostic and therapeutic agents.
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PMID:Production and characterization of rat monoclonal antibodies with an apparent specificity for certain lung cancers and their potential clinical application. 313 62

Since the preliminary analyses of the glycolipids of small cell carcinomas of the lung showed an increase of GM2 ganglioside, we generated new murine monoclonal antibodies directed to GM2 to identify the molecular species of the glycolipid. The monoclonal antibodies MK2-34 and MK1-16 (both IgM), which specifically detect N-glycolyl GM2 and N-acetyl GM2, respectively, were generated by immunizing mice with liposomes containing monophosphoryl lipid A, trehalose dimycolate, and the antigenic ganglioside. Among the glycolipid preparations extracted from the cancer tissues of 39 patients with lung cancer, a significant amount of N-acetyl GM2 was detected with MK1-16 antibody in 70% of the squamous cell carcinoma cases, 50% of the lung adenocarcinoma cases, 33% of the large cell carcinoma cases, and 100% of the cases of small cell carcinoma of the lung. On the other hand, N-glycolyl GM2 which was defined by the monoclonal MK2-34 was not found in any of the glycolipid fractions prepared from the lung cancer tissues examined in this study. Immunohistochemical studies of the lung cancer tissues with the MK1-16 antibody showed that the N-acetyl GM2 was present not only in small cell carcinoma tissues as one of the antigens related to tumors of neuroectodermal origin, but also in the squamous cell carcinoma and adenocarcinoma of the lung with a comparable frequency. The appearance of the N-acetyl GM2 antigen correlated well with the degree of differentiation of the cancer cells in patients with squamous cell carcinoma and adenocarcinoma of the lung.
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PMID:Generation of two murine monoclonal antibodies that can discriminate N-glycolyl and N-acetyl neuraminic acid residues of GM2 gangliosides. 316 61

An anti-Purkinje cell antibody was found in the serum and CSF of a man with adenocarcinoma of the lung and paraneoplastic cerebellar degeneration (PCD). This antibody differed from the autoantibodies found in patients with gynecologic cancer and PCD in that it produced a different pattern of Purkinje cell cytoplasmic staining, did not react with PCD antigens in Purkinje cell Western blots, and the antigen had a different species distribution. Unlike the antinuclear antibody found in patients with PCD and small-cell lung carcinoma, the antigen was restricted to the cytoplasm of Purkinje cells. If autoantibodies are important in the pathogenesis of PCD, this case illustrates that they can recognize different antigenic epitopes in the nervous system, but cause similar clinicopathologic syndromes.
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PMID:A variant of the anti-Purkinje cell antibody in a patient with paraneoplastic cerebellar degeneration. 329 Jul

Eighty-nine primary lung carcinomas and 23 metastatic lung tumors were immunohistochemically studied for the expression of pulmonary surfactant apoproteins, by using monoclonal (PE-10) and polyclonal antibodies. Surfactant apoprotein was demonstrated in the cytoplasm and/or nuclear inclusion bodies of only primary lung adenocarcinomas (36 of 75 cases), not in any other histologic type of primary lung carcinoma or in metastatic lung tumors. In primary lung adenocarcinoma, although typical type II pneumocyte type adenocarcinoma was not included in the current series, the majority of surfactant apoprotein-positive single cell type tumors were of the Clara cell type, with a single bronchial surface epithelial cell type, according to the light microscopic subclassification of adenocarcinoma cells. The Clara cell type adenocarcinomas could at times be distinguished only with difficulty from adenocarcinoma of type II pneumocyte type. Normal and hyperplastic type II pneumocytes were of course positive for surfactant apoprotein in the cytoplasm. However, none of the positive cells could definitely be identified as Clara cells in non-neoplastic lungs. The findings obtained in this study indicate that surfactant apoprotein is a good marker to distinguish adenocarcinoma of the lung from other histologic types of lung cancer and from neoplasms metastatic to the lung, and that type II pneumocytes and Clara cells, non-neoplastic and neoplastic, are morphologically and functionally closely related and might belong to the same cell lineage.
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PMID:Immunohistochemical localization of pulmonary surfactant apoproteins in various lung tumors. Special reference to nonmucus producing lung adenocarcinomas. 333 20

The profiles of prostanoid biosynthesis from endogenous arachidonic acid in 16 established cell lines derived from 4 histological classes of human carcinomas were determined by capillary gas chromatography-mass spectrometry. Detectable quantities of prostanoids were isolated from the culture medium of cell lines representative of the different histological classes of human tumors: colorectal adenocarcinomas (one of three cell lines); ovarian adenocarcinomas (one of three cell lines); prostate adenocarcinomas (zero of two cell lines); non-small cell carcinomas of the lung (four of five cell lines); and small cell carcinomas of the lung (zero of three cell lines). Prostaglandins E2 and F2 alpha were the only prostanoids synthesized in detectable quantities. Prostaglandin E2 biosynthesis (mean +/- SD), pmol/10(6) cells, n = 4) in cell lines exhibiting positive prostaglandin H synthase activity was: LoVo (colorectal adenocarcinoma, 0.4 +/- 0.1); A2780 (ovarian adenocarcinoma, 1.3 +/- 0.3); NCI-H322 (bronchioloalveolar cell carcinoma, 8.4 +/- 3.1); NCI-H358 (bronchioloalveolar cell carcinoma, 7.8 +/- 2.4); EKVX (adenocarcinoma of the lung, 21.3 +/- 5.5); and A427 (large cell undifferentiated carcinoma of the lung, 12.6 +/- 2.8). Prostaglandin F2 alpha production (pmol/10(6) cells +/- SD) was: LoVo (0.3 +/- 0.1); NCI-H322 (0.6 +/- 0.2); NCI-H358 (0.4 +/- 0.1); EKVX (1.8 +/- 0.4); and A427 (11.1 +/- 3.1). These findings suggest that within certain limitations cultured tumor cells provide simplified experimental systems for determination of prostaglandin biosynthetic characteristics of human tumors and that prostanoid biosynthesis may be particularly characteristic of certain non-small cell carcinomas of the lung.
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PMID:Profiles of prostaglandin biosynthesis in sixteen established cell lines derived from human lung, colon, prostate, and ovarian tumors. 340 18

We have described a patient who had a clinical picture of CREST syndrome and pulmonary interstitial fibrosis, and in whom adenocarcinoma of the lung developed over a four-year period. Despite absence in the literature of the association of lung carcinoma in patients with CREST syndrome, our case is an example of pulmonary fibrosis complicated by lung cancer without any evidence of other risk factors. We believe this to be the first report of such an association. Clinicians, therefore, must be aware that pulmonary interstitial fibrosis in patients with the CREST syndrome may represent a risk for lung cancer.
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PMID:CREST syndrome: a variant of progressive systemic sclerosis, associated with interstitial pulmonary fibrosis and malignancy. 342 Apr 53

Review of the histology of 219 lung cancers initially diagnosed at Lutheran General Hospital, Park Ridge, Illinois, in 1963-1967 and 1974-1976, confirms the increasing incidence of adenocarcinoma. This is due to an increase of adenocarcinoma in men. In women, the incidence of adenocarcinoma was higher than squamous carcinoma in the earliest period (44% adeno, 18% squamous). The percentage of women with lung cancer has also significantly increased from 19% to 31%, which increases the overall incidence of adenocarcinoma of the lung. As the number of women with lung carcinoma has increased, there has been no change in the percentage of adenocarcinoma in women.
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PMID:Increasing incidence of adenocarcinoma of the lung. 626 19

Incidence rates by income level were computed for squamous cell carcinomas of the gum and mouth, larynx, and esophagus and for squamous cell carcinoma, small cell carcinoma, and adenocarcinoma of the lung in white males and females aged 35--64 years, with the use of data for the nine geographic areas of the Third National Cancer Survey and the 1970 U.S. census. Within sex, age, and geographic area groups, patterns of cancer incidence by income level were analyzed by use of a nonparametric statistical method. Higher rates for males than for females were found for every histologic type studied, and the ratio of male-to-female rates increased with age (especially for squamous cell carcinomas of the larynx and lung). A strong inverse relation to income level was found for all of the histologic types studied in males and for squamous cell carcinomas of the gum and mouth and esophagus and small cell carcinoma of the lung in females. These findings are discussed with reference to patterns of smoking and alcohol use by sex and social class.
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PMID:Major histologic types of cancers of the gum and mouth, esophagus, larynx, and lung by sex and by income level. 628 90

The tumor cell colony-forming efficiency in soft agarose was evaluated in 190 specimens obtained from patients with either small cell carcinoma of the lung (SCCL) or adenocarcinoma of the lung (ACL). Tumor cell colony formation was observed in 45 out of 53 (84%) specimens containing cytopathologically identifiable SCCL tumor cells obtained from a variety of metastatic sites. Tumor cell colony formation was also observed in 6 out of 10 specimens containing ACL tumor cells. The colony-forming efficiency for these lung cancer specimens ranged from 0.003 to 0.72% per nucleated cell plated and from 0.05 to 1.5% per tumor cell plated. There were no differences in plating efficiency for SCCL and ACL. The tumor cell origin of the cells in the agarose colonies was confirmed by cytologic examination, flow cytometric DNA content analysis, and electron microscopy examination. The 'stem cell' nature was demonstrated by the ability of colonies to form typical SCCL or ACL tumors when inoculated into athymic nude mice. In addition, continuous tumor cell lines were established from several specimens forming tumors in nude mice. These data confirm the tumor cell origin and 'stem cell' nature of lung cancer cell colonies growing in soft agarose. Whether the low colony-forming efficiency represents a property inherent in the tumor cells, or a defect in the culture system, remains to be determined.
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PMID:Demonstration of the stem cell nature of clonogenic tumor cells from lung cancer patients. 629 85


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