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

The morphology and occurrence of tubuloreticular and undulating membraneous structures (TRS and UMS) associated with the endoplasmic reticulum were examined under normal and pathologic conditions. It was concluded that TRS and UMS are cytoplasmic inclusions of similar type but of different organization. The occurrence of UMS in a human cell line derived from a carcinoma of the lung and in a transplantable chicken hepatoma derived from an MC-29 virus-induced liver tumour is described.
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PMID:Undulating membraneous structures associated with the endoplasmic reticulum in tumour cells. 18 16

The Madison lung (M109) tumor cell line, initiated from a "spontaneous", anaplastic murine lung carcinoma, has been propagated continuously in vitro for more than 300 cell generations. Cytogenetic analysis revealed a mouse karyotype with a mode of 78 chromosomes (2n = 40). Three distinct marker chromosomes were identified by trypsin-giemsa banding. The cells piled up in culture and had a short generation time and high plating efficiency. Electron microscopy revealed highly undifferentiated cells with little rough endoplasmic reticulum, an abundance of free polysomes, the presence of few and often odd-shaped mitochondria, lipid bodies and phagocytic vacuoles. Virus particles of the C-type were found frequently. The subcutaneous transplantation of M109 cultured cells at a relatively low cell inoculum produced highly metastatic tumors in syngeneic BALG/c mice.
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PMID:Establishment and characterization of a cell line derived from a spontaneous murine lung carcinoma (M109). 19 26

One hundred human primary lung carcinomas were studied by light and electron microscopy and by light microscopic histochemistry to demonstrate mucosubstances. The tumors were classified histogenetically and were grouped into three major categories depending on their cell of origin: 1) tumors from basal and/or mucous cells; 2) tumors from neurosecretory cells; and 3) tumors from Clara cells. Most carcinomas (88%) arose from basal and/or mucous cells. These were subdivided into epidermoid carcinomas (21%), combined epidermoid and adenocarcinomas (46%), and adenocarcinomas (21%). The criteria for epidermoid differentiation included the presence of tonofilament bundles, poorly developed endoplasmic reticulum and Golgi apparatus, and well-developed desmosomes. The criteria for adeno differentiation included well-developed endoplasmic reticulum and Golgi apparatus, poorly developed desmosomes, the presence of extracellular and/or intracellular alveoli, and/or other evidence of cellular secretion such as secretory granules. In adenocarcinomas with extracellular alveoli, typical junctional complexes were also present at the luminal aspect where the cell apexes bordered the alveolus. With these criteria, combined epidermoid and adenocarcinomas were the most common type of lung carcinoma. We anticipate that the new data will clarify categories such as small cell anaplastic carcinoma and large cell carcinoma of the World Health Organization classification. In addition, the histogenetic classification of lung tumors may be of value in the future in studies of risk factors, prognosis, prevention, and treatment of lung cancer.
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PMID:The respiratory epithelium. V. Histogenesis of lung carcinomas in the human. 21 Feb 96

We have investigated the growth-factor-like activity of a approximately 200-kDa, IP 8.3, cytoplasmic glycoprotein, the expression of which appears to be restricted to normal and malignant human mesothelium. This substance stimulated the growth of human mesothelioma cell cultures at greater rates than did foetal calf serum, but it failed to induce proliferation of lung carcinoma cell cultures. In addition, we have tried to trace the biosynthetic pathway of this mitogenic factor in normal human mesothelial cells by means of immuno-electron microscopy with a polyclonal antibody directed against this molecule. Positive immunogold labelling was found in the lumina of the cisternae of the endoplasmic reticulum, to a lesser extent on the outer surface of the plasma membrane, and also in structures corresponding to the coated pits. These ultrastructural findings are consistent with the hypothesis of the glycosylation of the newly synthesized protein in the endoplasmic reticulum and the subsequent uptake of the secreted molecule, which accumulates in the coated pits before internalization. The results suggest that this mitogenic glycoprotein could play a role in an autocrine growth control mechanism influencing mesothelial cell proliferation.
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PMID:Mitogenic effects of a mesothelial cell growth factor: evidence for a potential autocrine regulation of normal and malignant mesothelial cell proliferation. 157 Dec 79

To investigate the nature of various endocrine cells immunoreactive for human chorionic gonadotropin (hCG alpha) in the lung, immunoelectron microscopic study was performed on fibrotic adult lungs and endocrine neoplasms of the lung. The mode of localization of hCG alpha and the size profile of hCG alpha granules were different among endocrine cells under various proliferative conditions. The population of hCG alpha granules in the grouped type of endocrine cells was more variable with a shift to smaller size (mean area: 1.395 x 10(-2) microns 2, mean maximum diameter: 149.8 nm), than that in solitary ones (1.493 x 10(-2) microns 2, 155.4 nm). Tumorlet endocrine cells had larger hCG alpha granules (1.800 x 10(-2) microns 2, 171.3 nm) without change of SD of size parameters. In carcinoid tumors, the size profile of hCG alpha granules was considerably different from that in the three types described above. Moreover, hCG alpha granules were significantly smaller in size in carcinoid tumors without lymph node metastasis (2.295 x 10(-2) microns 2, 189.8 nm) than those in malignant carcinoid tumors with metastasis (3.368 x 10(-2) microns 2, 230.5 nm). The population of hCG alpha granules in atypical endocrine tumor was the parallel shift to a larger scale (6.251 x 10(-2) microns 2, 307.5 nm) from that of malignant carcinoids and the distribution pattern was different from that in benign carcinoids. In small cell carcinoma of the lung, hCG alpha immunoreaction was preferentially present in perinuclear space and dilated rough endoplasmic reticulum. The mode of localization of hCG alpha and the size profile of hCG alpha granules, representing specific features of intracellular processing of hCG alpha, may be closely related with some qualitative changes in the neoplastic process of pulmonary endocrine cells.
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PMID:Human chorionic gonadotropin alpha-subunit in endocrine cells of fibrotic and neoplastic lung. Its mode of localization and the size profile of granules. 215 84

Oncofetal aspects of ACTH and pro-opiomelanocortin (POMC)-derived peptides were studied immunohistochemically at the light and electron microscopic level in human fetal pituitary glands, pituitary adenomas, and small-cell carcinoma of the lung. ACTH, beta-endorphin, and gamma-MSH were localized in the same cells of both fetal and adult pituitary, as well as in the above-mentioned neoplastic tissues. However, alpha-MSH was observed only in the early fetal pituitary, its concentration decreasing with advancing gestational age. The adult pituitary contained only a few alpha-MSH-positive cells. By immunoelectron microscopy, ACTH in the adult pituitary was localized exclusively in the secretory granules. In fetal pituitary at 9 weeks' gestation, ACTH was localized in the perinuclear spaces (PNS), cisternae of rough endoplasmic reticulum (RER), Golgi saccules, and secretory granules. The staining pattern of ACTH in these organelles varied from cell to cell. In fetal pituitaries of greater gestational ages, ACTH was localized in secretory granules. The pituitary adenomas mimicked the staining characteristics of the adult pituitary, i.e., negative or only very occasional alpha-MSH staining and localization of ACTH in the secretory granules. The ectopic ACTH-producing tumors showed a staining pattern similar to that of the early fetal pituitary, i.e., positive staining for alpha-MSH and the presence of ACTH in PNS and cisternae of RER.
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PMID:Light and electron microscopic localization of ACTH and pro-opiomelanocortin-derived peptides in human developmental and neoplastic cells. 608 43

Superoxide dismutase (SOD) activity, plasma caeruloplasmin activity and the level of whole tissue and subcellular lipoperoxides have been determined in normal and neoplastic tissues from control and tumour-bearing mice, measurements being made nine, twelve and fifteen days after the inoculation of Lewis lung carcinoma cells. SOD activity of host liver and lung tissues did not vary significantly from those of the control animals. Blood SOD activity of the tumoured animals was markedly elevated on the ninth and twelfth days after inoculation, decreasing to control levels on the fifteenth day. Tumor SOD diminished from activity on the ninth day which was greater than that for control lung to a level significantly lower than that for control lung on the twelfth and fifteenth days after inoculation. The presence of a tumor did not appear to affect plasma caeruloplasmin oxidase levels. The lipoperoxide level of hepatic tissue rose significantly as the tumour progressed. In the lung tissue the lipoperoxides decreased from a level four times higher on the ninth day to one not significantly different from that of the controls. Tumour lipoperoxides were about twice the level of hepatic tissue and of the order of ten-fold greater than those of lung. The level of lipoperoxide in the plasma of tumoured mice did not differ markedly from that of control mice. Assays of lipoperoxide in subcellular fractions of liver, lung and tumour tissue revealed that the elevated lipoperoxide was principally synthesized in the endoplasmic reticulum.
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PMID:Superoxide dismutase activity, caeruloplasmin activity and lipoperoxide levels in tumour and host tissues of mice bearing the Lewis lung carcinoma. 688 27

Cytotoxic T lymphocytes (CTL) recognize antigenic peptides bound to major histocompatibility complex class I antigens on the cell surface of virus-infected cells. It is believed that the majority of peptides originate from cytoplasmic degradation of proteins assumed to be mediated by the "20S" proteasome. Cytosolic peptides are then translocated, presumably by transporters associated with antigen processing (TAP-1 and -2), into the lumen of the endoplasmic reticulum (ER) where binding and formation of the ternary complex between heavy chain, beta2-microglobulin (beta 2m) and peptide occurs. In this study, we have analyzed and compared the phenotype of two mutant cell lines, the thymoma cell line RMA-S and a small lung carcinoma cell line CMT.64, in order to address the mechanism that underlies the antigen processing deficiency of CMT.64 cells. Unlike RMA-S cells, vesicular stomatitis virus (VSV)-infected CMT.64 cells are not recognized by specific CTL. Interferon gamma (IFN-gamma) treatment of CMT.64 cells restores the ability of these cells to process and present VSV in the context of Kb. We show that although CMT.64 cells express a low level of beta 2m, the recognition of VSV-specific CTL is not restored by increasing the amount of beta 2m synthesized in CMT.64 cells. In addition, we find that CMT.64 cells express moderate levels of Kb heavy chain molecules, but most of it is unstable and rapidly degraded in the absence of IFN-gamma treatment. We infer that the antigen processing deficiency does not lie at the level of beta 2m or Kb production. We find also that the mRNAs for both TAP-1 and -2 are present in RMA and RMA-S cells but are absent in uninduced CMT.64 cells. Upon IFN-gamma induction, both mRNAs are highly expressed in CMT-64 cells. In addition, we find that the low molecular mass polypeptides 2 and 7, and additional components of the proteasome are induced by IFN-gamma in CMT-64 cells. Finally, introduction of the rat TAP-1 gene in CMT.64 cells restores CTL recognition of VSV-infected cells. These results indicate that a TAP-1 homodimer may translocate peptides in the ER and explain partially the CMT.64 defect and the RMA-S phenotype. These findings link a dysfunction in the transport and/or generation of antigenic peptides to the capacity of tumor cells to evade immunosurveillance and provide a unique model system to dissect this phenomenon.
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PMID:Comparison of cell lines deficient in antigen presentation reveals a functional role for TAP-1 alone in antigen processing. 793 Oct 74

The NSP gene was recently shown to constitute the prototype of a novel gene family, to be selectively transcribed in neural and endocrine cells, and to encode three overlapping proteins, NSP-A, NSP-B, and NSP-C. These proteins were collectively designated reticulons, because they were found to be anchored to membranes of the endoplasmic reticulum through their common carboxy-terminal regions. The goal of the present study was to determine whether the reticulons might be used as markers for neuroendocrine differentiation in human lung tumors. Therefore, the tissue distribution of the NSP-A protein was studied and expression in human lung tumors was evaluated. Immunohistochemical analysis of normal tissues with monoclonal antibodies specifically recognizing the NSP-A protein indicated that NSP-A exhibits a distinct neuroendocrine distribution pattern since it was found to be expressed in a variety of cells with an established neuroendocrine phenotype but not in cells lacking such features. Results with specimens of a wide variety of primary human tumors provided further support for this claim. Immunohistochemical analysis of primary lung carcinomas revealed that NSP-A was readily detectable in small cell lung carcinoma (SCLCs) (8 of 12) and carcinoid tumors of the lung (3 of 3) but not in nonneuroendocrine non-SCLCs (0 of 10). In 13 of 27 non-SCLCs expressing the neural cell adhesion molecule and/or neurofilament proteins, however, NSP-A was found to be expressed. Northern blot analysis of human lung carcinoma cell lines revealed expression of NSP-A- and/or NSP-C-encoding mRNAs in all 18 SCLC cell lines that were studied, except one; however, no expression of these mRNAs could be detected in any of the 11 non-SCLC cell lines tested. The NSP transcript encoding NSP-B was found only in SCLC cell line NCI-H82. In conclusion, the results of our studies suggest that, in lung tumor cells, expression of NSP-A and most likely also NSP-C is restricted to cells with a neuroendocrine phenotype.
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PMID:NSP-encoded reticulons are neuroendocrine markers of a novel category in human lung cancer diagnosis. 806 78

Intracellular antigens must be processed before presentation to CD8+ T cells by major histocompatibility complex (MHC) class I molecules. Using a recombinant vaccinia virus (Vac) to transiently express the Kd molecule, we studied the antigen processing efficiency of 26 different human tumor lines. Three cell lines, all human small cell lung carcinoma, consistently failed to process endogenously synthesized proteins for presentation to Kd-restricted, Vac-specific T cells. Pulse-chase experiments showed that MHC class I molecules were not transported by these cell lines from the endoplasmic reticulum to the cell surface. This finding suggested that peptides were not available for binding to nascent MHC molecules in the endoplasmic reticulum. Northern blot analysis of these cells revealed low to nondetectable levels of mRNAs for MHC-encoded proteasome components LMP-7 and LMP-2, as well as the putative peptide transporters TAP-1 and TAP-2. Treatment of cells with interferon gamma enhanced expression of these mRNAs and reversed the observed functional and biochemical deficits. Our findings suggest that downregulation of antigen processing may be one of the strategies used by tumors to escape immune surveillance. Potential therapeutic applications of these findings include enhancing antigen processing at the level of the transcription of MHC-encoded proteasome and transporter genes.
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PMID:Identification of human cancers deficient in antigen processing. 842 5


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