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

Recent studies of murine tumor models and certain human tumor cell lines have provided evidence for intratumor heterogeneity in expression of extracellular matrix receptors and in the elaboration of matrix-degrading enzymes. However, little is known about possible intratumoral heterogeneity in the production of matrix macromolecules. We have, therefore, examined the biosynthesis and secretion of matrix proteins by cells derived from a polyclonal human cell line (JH-17) established from a large cell undifferentiated carcinoma of the lung. For the present studies, we focused on the production of collagens and structural glycoproteins by two phenotypically different aneuploid clones, designated C13 and C22. These clones were distinctive in their inability to grow in soft agar or to form tumors in nude mice and had identical DNA contents. Tumor cells were labeled with [3H]proline and the newly synthesized proteins accumulating in the culture medium were identified using biochemical and immunologic techniques. Clone C13 secreted at least three genetically distinct collagens, including type V procollagen (PC), type IV procollagen, and a type VIII-like collagen. By contrast, the clone C22 synthesized fibronectin, and a single bacterial collagenase-sensitive and pepsin-resistant component consistent with type I trimer. These studies emphasize the potential diversity of matrix proteins synthesized by neoplastic cells and suggest that there is intratumoral heterogeneity in matrix protein biosynthesis in vivo. These studies further suggest that tumor-derived matrix may be altered during tumor progression or cell selection in vivo.
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PMID:Heterogeneity in the production of collagens and fibronectin by morphologically distinct clones of a human tumor cell line: evidence for intratumoral diversity in matrix protein biosynthesis. 282 40

Differential cell adhesion has been proposed to play a role in organ-specific tumor metastasis. To further explore this hypothesis, we have employed a Lewis lung carcinoma cell line and 2 variants that differ in their ability to metastasize to lung and liver. The three cell lines were tested for their ability to adhere to defined extracellular matrix components that had been previously adsorbed to nylon membranes. Our results demonstrate that the parental cell line adheres preferentially to fibronectin relative to all other adhesion molecules tested. The lung colonizing variant, M27, adheres well to fibronectin and also to type V collagen but adheres poorly to laminin, to types I and VI collagen or to heparan sulfate. In contrast, the liver colonizing H59 cell line was highly adherent to laminin as well as to fibronectin but did not adhere to heparan sulfate or to any of the collagen types tested. These results demonstrate that three related cell lines with differing metastatic specificities have marked differences in their abilities to bind to defined matrix molecules. Such differences may play a role in the preferential localization to specific organ beds in vivo.
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PMID:Lewis lung carcinoma variants with differing metastatic specificities adhere preferentially to different defined extracellular matrix molecules. 336 May 91

Ultrastructural observations using scanning and transmission electron microscopy were made on three murine tumors, line 1 lung carcinoma, fibrosarcoma (FSA) and mammary carcinoma MCa-11, grown in vitro as multicellular tumor spheroids (MTS). The cytology of these MTS revealed the presence of characteristic cellular organelles as well as varying amounts of intracisternal type-A viral particles. In line 1 and FSA, the occurrence of gap junctions in the outer shells of these MTS was correlated with the growth behavior of these spheroids. In FSA, extracellular collagen bundles were identified next to tumor cells and represent synthetic activity by these cells under these conditions. No specific cytological correlations were made with the slow growing MCa-11 spheroid.
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PMID:Cell contacts and surface features of three murine tumors grown as multicellular spheroids. 336 22

Immunohistopathologic and biochemical studies of different collagen types extracted from human scar carcinoma of the lungs have been carried out for definition and evaluation of which types of collagen are involved in the scarring mechanism of such tumors. Tumor homogenates treated with 0.5 M acetic acid and followed by limited proteolysis with pepsin and then by fractional salt precipitation, demonstrated that Type I collagen constitutes the major collagenous component in addition to a significant increase in Type V collagen extracted from human scar carcinoma of the lung. However, when normal membranoalveolar peripheral lung tissues were processed under the same experimental conditions, Type III and IV collagens were relatively higher. Immunohistochemical studies were carried out, and the results confirmed the data above. Furthermore, these studies demonstrated a relative localized increase in Type III collagen in the area surrounding the tumor acini, which suggested that these areas are of active and recent scar formation. This supports the current concept of the scar origin as a desmoplastic reaction of the host tissues toward the neoplastic cell growth.
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PMID:Collagens in scar carcinoma of the lung. 390 70

We tested the ability of serum-free media to support the in vitro growth of human non-small cell lung carcinoma. A medium containing insulin, transferrin, sodium selenite, hydrocortisone, epidermal growth factor, and bovine serum albumin (1 mg/ml) with serum precoating of culture dishes (modified LA medium) supported three previously established cell lines of non-small cell lung cancer and prevented fibroblast proliferation in fresh tumor specimens but did not support long term tumor cell growth from fresh specimens. We added triiodothyronine, sodium pyruvate, and additional glutamine, insulin, and epidermal growth factor to modified LA medium, precoated with fibronectin and collagen instead of serum, and deleted bovine serum albumin, defining a new medium called ACL-3. ACL-3 medium alone supported the short term growth of 10 of 12 cell lines and the soft agarose cloning of 9 of 12 cell lines tested, and ACL-3 supplemented by an optimal concentration of bovine serum albumin (5 mg/ml) supported the long term growth of 10 of 12 cell lines tested. Moreover, we have grown tumor cells for more than 6 months from 11 of 33 (33%) consecutive fresh clinical specimens of human lung adenocarcinoma in ACL-3 with bovine serum albumin. ACL-3 medium provides a defined environment for the study of growth factor requirements of human non-small cell lung cancer and enhances our ability to grow human lung cancer, particularly adenocarcinoma, in vitro.
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PMID:Growth of cell lines and clinical specimens of human non-small cell lung cancer in a serum-free defined medium. 394 Jun 44

Serum-free medium conditioned by the prior cultivation of cells of the IPT line (derived from a poorly differentiated carcinoma of the lung) contained material of a high MW which stimulated proliferation in cultures of endothelial cells from human umbilical vein. A response was shown by cells seeded on plastic, gelatin or collagen of type I or type IV, at densities of 25 to 200/mm2, and in media with serum concentrations ranging from 0.5 to 20% v/v. Cells plated on biological substrata showed a greater response than those on plastic.
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PMID:Proliferative response of human venous endothelial cells to medium conditioned by human tumour cells. 620 19

Four cases of small cell carcinoma of the lung were studied ultrastructurally. The tumor cells contained scattered neurosecretory granules. Areas of the tumor that showed the characteristic crush phenomenon were found to be surrounded by myofibroblasts. It is proposed that the crush phenomenon is caused by contraction of the encircling myofibroblasts. The myofibroblasts and collagen may also cause degeneration and necrosis of the tumor cells. Myofibroblasts have not been observed in other histologic types of carcinoma of the lung.
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PMID:Electron microscopy of small cell carcinoma of the lung with special reference to the crush phenomenon. 630 63

Interactions between cancer cells and host macrophages might have important regulatory roles in controlling the expression of the metastatic phenotype, particularly by regulating the production of proteases necessary for tissue invasion. To investigate that possibility, mouse macrophages and Lewis lung carcinoma (LLC) cells from four clonal subpopulations with either low or high metastatic ability were cultured on [14C]collagen (type l)-coated plates. They did not degrade collagen when they were cultured independently on that substrate, but they were induced to do so when macrophages and cancer cells were cultured together. An increased production of neutral collagenase and other neutral protease activities was observed simultaneously. The degree of stimulation of collagen degradation varied according to the cancer cell subpopulation present in the cocultures. For a given LLC cell subpopulation, similar degrees of stimulation of collagen degradation were achieved with either bone marrow-derived or resident peritoneal macrophages, either syngeneic (from C57BL/6 mice) or allogeneic; lower stimulations were obtained with thioglycolate-elicited peritoneal macrophages. Macrophage-conditioned culture media could be substituted for living macrophages to stimulate collagen degradation or collagenase secretion by LLC cells, but LLC cell-conditioned media did not stimulate collagen degradation by macrophages. This suggests that, in the cocultures, collagen degradation is achieved mainly by the cancer cells, not by the macrophages, and that it is induced by a soluble factor, a monokine, produced by the macrophages. That factor might be identical to a recently identified rabbit monokine that stimulates fibroblasts or synovial cells to degrade collagen and proteoglycan and to activate plasminogen, because rabbit macrophage-conditioned media containing that monokine also stimulated collagen degradation by LLC cells.
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PMID:Collagen degradation by metastatic variants of Lewis lung carcinoma: cooperation between tumor cells and macrophages. 635 18

The co-culture of mouse peritoneal macrophages and Lewis lung carcinoma cells induces the release of a metal-dependent type IV collagen-degrading proteinase which is not produced in detectable amounts by either cell type cultivated alone. Conditioned media of the co-cultures degrade both pepsin-extracted type IV collagen from human placenta and mouse type IV procollagen. Thus macrophages can interact with tumor cells to degrade basement membrane type IV collagen: this might be of importance to allow cancer invasion and metastasis.
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PMID:Co-operation between metastatic tumor cells and macrophages in the degradation of basement membrane (type IV) collagen. 661 77

ELectron microscopic observations were made on the Lewis lung carcinoma, which has frequently been used in various experiments. Although the tumor cells had desmosomes, interdigitation, microvilli and basement membranes which were of epithelial nature, they did not show either squamous or adenomatous differentiation. On the basis of microscopic and ultrastructural findings, this tumor falls into the category of large cell carcinomas. At the periphery of the tumor, sinusoidal clefts between the strands of tumor cells contained many red blood cells without fibrin. While perfect blood vessels were observed towards the center of the tumor, large necrotic areas were observed. Dilated large vessels possessed some endothelial fenestrations. Light endothelial cells were also observed, which were penetrated by red blood cells. Interstitial components were very scant and collagen fibres were frequently observed to be dissolved.
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PMID:Ultrastructure of the Lewis lung carcinoma. 688 14


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