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)

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

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

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

Fluorescence in situ hybridization with biotinylated repetitive DNA probe specific for the centromeric region of chromosome 17 (p17H8: Oncor) was applied to suspended nuclei which were isolated by Shutte's method from formalin-fixed paraffin-embedded tissue. The tissues were obtained from surgically resected specimens from nine patients with non-small cell lung carcinoma. The isolated nuclei were prepared with 0.05% pepsin/0.1NHCl for 15 minutes at 37 degrees C. Subsequently, these were immersed in 70% acetic acid for 10 seconds at room temperature. After heat denature with hybridization mixture which contained 3 mu 1 DNA probe for 10 minutesat 70 degrees C, 1 x 10(6) nuclei were incubated overnight at 37 degrees C. After washing with 60% formamide/2 x SSC, the hybridized probes were labeled by FITC conjugated avidin. A number of centromeric signals of chromosome 17 wasevaluated by fluorescence microscopy (BH-2, Olympus). Furthermore, a probe-related FITC intensity was quantified using flow cytometry (FACScan, Becton Dickinson). As the results, there was good correlation between a relative fluorescence intensity determined by flow cytometry and a relative fluorescence signal by fluorescence microscopy (p < 0.05).
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PMID:[Flow cytometric quantification of numerical chromosome aberrations in non-small cell lung carcinomas using formalin-fixed paraffin-embedded tissue]. 943 39