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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present paper we have studied: (a) the concentration of fibronectin (FN) in plasma and in ascitic fluid of mice at different times after inoculation of Ehrlich ascites tumor cells; (b) the ability of Ehrlich ascites cells to synthesize and release FN; and (c) the localization of FN in Ehrlich ascites cells by immunofluorescence microscopy. It was found that (a) 4 to 5 days after inoculation of the tumor, the plasma concentration of FN was significantly higher [1.7 +/- 0.07% (S.E.) of total plasma protein] than that in the normal control mice (0.8 +/- 0.035); (b) FN is present in the ascitic fluid in all phases of tumor growth; (c) Ehrlich ascites cells cultured in vitro synthesize and release large amounts of FN in the culture medium; and (d) only about 1 to 2% of the tumor cells show a very small amount of FN, and this is mostly in the area of cell-cell contact.
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PMID:Concentration of fibronectin in plasma of tumor-bearing mice and synthesis by Ehrlich ascites tumor cells. 38 88

Prostate cancer selectively metastasizes to the axial skeleton to produce osteoblastic lesions, which suggests that bidirectional paracrine interactions exist between prostate cancer and bone cells. To evaluate the role of tumor-stromal cell interaction and stromal-specific growth factors in prostate cancer growth and dissemination, we coinoculated nontumorigenic human prostate cancer cells (LNCaP) and various tissue-specific fibroblasts subcutaneously in athymic mice. LNCaP tumors were induced most consistently by human bone fibroblasts (62%), followed by two prostate fibroblast cell lines (31% and 17%), but not by lung, kidney, or embryonic 3T3 fibroblasts. Carcinomas formed preferentially in male hosts, demonstrating in vivo androgen sensitivity. Immunohistochemical and biochemical techniques confirmed the human prostate component of these tumors and were paralleled by elevations in serum prostate specific antigen. In vitro mitogenic assays revealed a two-to three-fold bidirectional stimulation between LNCaP and bone or prostate fibroblast conditioned media, but not lung, kidney, or 3T3 fibroblast conditioned media. A novel method developed to deliver concentrated bone or prostate fibroblast conditioned media in vivo using a slowly absorbed matrix (gelfoam) also induced tumor formation, emphasizing the importance of fibroblast growth factors in LNCaP tumor formation. Northern analysis identified the stromal compartment as the primary source of extracellular matrix (collagen, fibronectin), while only LNCaP cells expressed transforming growth factor alpha. Although LNCaP and stromal cells express basic fibroblast growth factor (bFGF), the bidirectional paracrine-mediated mitogenic activity between these cells is not inhibited by anti-bFGF antibodies, suggesting that other undefined growth factors may be involved in stimulating LNCaP growth. These observations illustrate the importance of stromal-epithelial interaction in prostate tumor growth and suggest that extracellular matrix and paracrine-mediated growth factors play a role in prostate cancer growth and metastasis.
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PMID:Prostate and bone fibroblasts induce human prostate cancer growth in vivo: implications for bidirectional tumor-stromal cell interaction in prostate carcinoma growth and metastasis. 137 62

Interleukin 6 (IL-6) is a multifunctional cytokine important in the inflammatory response. Its potential role as an antitumor agent has been suggested by its demonstrated activity in a variety of tumor models. The mechanism of antitumor activity has been proposed to be its enhancement of cytotoxic T-cell function. In the current work we demonstrate clear antitumor activity for this cytokine in a nonimmunogenic tumor system. B16 melanoma cells transfected with the human IL-6 complementary DNA demonstrated slower tumor growth in vivo. Tumors that developed from these cells had a prominent stromal matrix, an easily recognized infiltration of inflammatory cells, fewer mitotic figures, and fewer blood vessels. These in vivo findings corresponded with a greater adhesion of the IL-6-transfected B16 cells to stromal matrix proteins (laminin, fibronectin, and vitronectin) and a less prominent vascular response in an intradermal angiogenesis assay. Therefore, we propose that with weakly antigenic tumors, such as B16 melanoma, IL-6 may mediate important antitumor responses by nonspecific proinflammatory mechanisms.
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PMID:In vivo and in vitro characteristics of interleukin 6-transfected B16 melanoma cells. 139 47

Plasmatic fibronectin has been studied in tumor patients on the basis of the role that unspecific opsonin may play in tumor growth and spreading. Alterations in fibronectin levels might be used as a biological marker and our purpose has been to evaluate the significance of this test in the biological diagnosis of cancer. When comparing the levels found in the control group (22.86 +/- 1.40 mg/dl) and in tumor patients (23.80 +/- 1.90 mg/dl), we observed no difference in the overall group. However, in relation to the localization of tumors, a significant increase was found in breast cancer (31.83 +/- 3.83 mg/dl) and a significant decrease in squamous cell carcinoma of the head and neck (9.56 +/- 1.68 mg/dl). These results suggest that plasmatic fibronectin could be useful as a biomarker in some types of tumors. Our conclusion was confirmed by analysis of ROC curves related to every one of the studied tumors.
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PMID:Plasmatic fibronectin in malignancies. 149 Nov 80

Adult male rats bearing the Dunning R3327 prostatic carcinoma were randomized to the following treatments: intact controls, castration, and castration + estrogen. After a study period for 6 weeks the rats were killed and the tumors were analyzed morphometrically to determine the amount of epithelium, stroma, and connective tissue fibers in the tumors, and the nuclear size of large stromal cells. Cryostat sections were analyzed with immunohistochemistry using a panel of antibodies against cytokeratins, desmin, vimentin, fibronectin and collagens. Addition of estrogen to castration resulted in an inhibition of tumor growth. The expression of cytokeratin 14 (a marker for basal myoepithelial cells) was reduced, but the expression of cytokeratin 18 (a marker for the luminal epithelial cells) was unaffected by estrogen. The amounts of collagen I, III and fibronectin (plasma and cellular types) were increased in the stroma, and the nuclear size of large stromal cells was also increased by estrogen. It is concluded that castration + estrogen treatment has effects in the epithelium and stroma of Dunning tumors that are qualitatively and quantitatively different from the effects of castration alone.
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PMID:Estrogen treatment of Dunning tumors in castrated rats: qualitative and quantitative morphology. 157 67

Clonal cell lines were derived from rat liver epithelial cells following their transformation with either v-raf or v-raf/v-myc. Cells transformed with v-raf alone showed reduced tumor incidence and tumor growth rates when implanted into nude mice, compared to cells also expressing the v-myc oncogene. A series of additional clones isolated from a tumor obtained following inoculation of an athymic nude mouse with the v-raf-transformed rat liver epithelial cells displayed an intermediate range of tumor aggressiveness. These findings indicate that unknown genotypic and/or phenotypic changes occur during tumor formation in vivo, which are required in addition to raf activation for complete expression of the malignant phenotype. This in vitro model of tumor progression was used to examine alterations in the expression of genes related to the growth control of liver epithelial cells, which may be involved in the malignant conversion of the preneoplastic cells. A close association was observed between the increased level of expression of the transforming growth factors alpha and beta 1, the decreased expression of extracellular matrix proteins fibronectin and collagen I, and the tumor aggressiveness (latency/growth rate), suggesting a causal role for these factors in the progression of v-raf-transformed rat liver epithelial cells to the fully malignant phenotype.
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PMID:Expression of growth-related genes during tumor progression in v-raf-transformed rat liver epithelial cells. 170 45

We have developed a series of variant clonal Chinese hamster ovary cell sublines which are deficient in the expression of the alpha 5/beta 1 integrin fibronectin receptor. When these clonal sublines were injected s.c. into nude mice, there were marked differences in the rate of tumor growth. Tumors from clones expressing very low levels of fibronectin receptor grew most rapidly, clones expressing levels of fibronectin receptor comparable to wild type cells grew at an intermediate rate, while a clone expressing elevated levels of fibronectin receptor grew slowly. Cells recovered from the tumors maintained their original phenotypes in terms of levels of fibronectin receptor expression. These results suggest that there is an inverse correlation between the level of expression of the alpha 5/beta 1 fibronectin receptor and the rate of tumor growth.
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PMID:Increased tumorigenicity of fibronectin receptor deficient Chinese hamster ovary cell variants. 182 19

Basal cell carcinoma is the most common malignancy in humans. Although rarely metastatic, it is capable of significant local destruction and disfigurement. This two-part article reviews the current understanding of basal cell carcinoma biology. Part I examines significant clinical, histologic, and ultrastructural features that relate to invasive potential. Genetic characteristics, including tumor growth rate, chromosomal abnormalities, and oncogene presence, are discussed, and expression of important cell and matrix proteins, including keratin, fibronectin, and HLA antigens, are reviewed. Further topics to be explored in Part II include host immunologic responses, theories of pathogenesis, and valuable second-line therapeutic regimens for treatment of multiple cancers.
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PMID:Biology of basal cell carcinoma (Part I). 199 6

Laminin promotes the modulation of human pancreatic adenocarcinoma cells from a proliferative to a resting phenotype. This process includes restoration of cell polarity, increase of protein biosynthesis, and increase of glycoprotein secretion. The growth correlates with the amount of laminin coated on the culture dish. Adenocarcinoma cells do not synthesize collagen type I, fibronectin or laminin. Prolonged propagation of the cells on laminin substratum enhances the expression of laminin-binding sites on the cell surface. Laminin binds to cell plasma membrane vesicles with a KB of about 2.2 x 10(10). By affinity chromatography of [35S]methionine-labeled, detergent-extracted, cells on immobilized laminin, a Mr 82,000 polypeptide could be enriched. By simultaneous chromatography on immobilized collagen type I, a Mr 34,000 polypeptide was retained. In laminin overlay experiments on transblotted plasma membrane proteins, Mr 82,000 and 70,000 polypeptides were labeled. Affinity chromatography on laminin-Sepharose of tumor cell membranes from cells grown in nude mice tumors retained Mr 100,000, 82,000, 70,000 and 55,000 polypeptides bound to the column. Endoglycosidase F treatment of these proteins reduced the number of higher Mr proteins, leaving a Mr 70,000 polypeptide, together with smaller peptides. Using the enriched binding protein fraction as antigens, monoclonal antibodies (mAbs) were prepared in mice. Two of the mAbs were further analysed; they recognized simultaneously the complete pattern of high and low Mr polypeptides identified to date by the other methods. Antibody 2A1-H7 was capable of inhibiting attachment and spreading of the cells on laminin and collagen I, but not on tissue-culture plastic. These data may indicate a molecular heterogeneity, partly based on diverse glycosylation, responsible for the variations in the molecular weight of the binding proteins. The adaptation processes of the tumor cells during growth on the extracellular matrix may indicate a regulatory function on tumor growth and metastasis in vivo.
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PMID:Laminin interactions with ductal pancreatic adenocarcinoma cells: identification of laminin- and collagen-binding proteins. 216 59

The main components, both intrinsic (laminin and type IV collagen) and extrinsic (fibronectin), of the basement membrane (BM) were analyzed by immunohistochemical methods in normal, dysplastic and neoplastic laryngeal mucosa specimens. The material was obtained from 35 patients who had undergone surgery for glottic or supraglottic cancer. Fibronectin proved to be absent from normal mucosa whereas an immunopositivity was observed close to the dysplastic epithelium, especially around inflammatory cells. Positivity increased as the degree of dysplasia increased from LIN I to LIN III. A strong staining was also seen around nests of well and moderately differentiated squamous cell carcinoma. These findings are in agreement with the theories about the main sites of origin for fibronectin, both from plasma and connective tissue. Laminin and type IV collagen showed the same staining characteristics. In normal and mild dysplastic samples a regular and continuous positivity was found at the boundaries between the epithelium and the mesenchymal stroma. Focal discontinuities were present in areas of intense subepithelial inflammation only. Interruptions and reduplications were more evident in severely dysplastic epithelium. In invasive squamous cell carcinomas a strong correlation has been found between the degree of cell differentiation and the pattern of distribution of the intrinsic BM components. Immunostaining was usually evident and continuous around nests of well differentiated squamous cell carcinoma, whereas positivity progressively decreased in moderately and poorly differentiated neoplasms. Furthermore, staining for intrinsic BM components was also related to the pattern of tumor growth: continuous around the "pushing" edge of neoplastic growth and discontinuous when the neoplastic front had an "invading" appearance. These observations tend to support the theory which considers neoplastic growth a cyclic process. BM components are most likely synthesized during the phases of quiescence and reabsorbed during the phase of invasiveness, following shifts in neoplastic cell metabolism.
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PMID:[Distribution of laminin, type IV collagen and fibronectin in normal, dysplastic and neoplastic laryngeal tissue]. 226 Apr 38


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