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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neuro-oncology 23 (1995), S. 99-108 
    ISSN: 1573-7373
    Keywords: endothelium ; metastasis ; integrin ; selectin ; angiogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Metastasis is one of the most devastating aspects of cancer. It is a complex multistep processes that results in spread of tumorigenic cells to secondary sites in various organs. The actual events that are involved in metastasis are the subject of several recent reviews [1–3]. Upon growth of neoplastic cells beyond a certain mass (2 mm in diameter) an extensive vascularization through angiogenesis occurs. The new capillary network provides a supply of nutrients and gas exchange that allows further growth and development of the tumor mass. The network of the blood vessels also provides an entry site into the circulation for the neoplastic cells that detach from the tumor mass. Only a small percentage of circulating tumor cells (〈 0.01%) survive travel in the circulation and arrest in the capillary beds of distant organs, extravasate and proliferate within the organ parenchyma producing a successful metastasis [1]. Vasculature plays an important role in several steps of the metastatic process; 1) at the site of metastasis, vessels capture the cancer cell and provide the entry route into the secondary organ, and 2) through angiogenesis, vascular endothelial cells provide the supply of nutrients for the growth of the primary tumor mass and the route of intravasation. The lining of all blood vessels are covered with endothelial cells which play an active role in both processes. The metastatic properties of cancer cells have been extensively studied. Here, we will discuss the role of endothelial cells in the metastatic process with focus on their interaction with cancer cells at the site of extravasation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 55 (1994), S. 190-199 
    ISSN: 0730-2312
    Keywords: osteoclast ; osteocalcin ; bone marrow ; differentiation ; resorption ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Murine long-term bone marrow cultures (LTBMCs) were used to generate hematopoietic cells free from marrow stromal cells. These progenitor cells were treated with GM-CSF (5 U/ml) with or without rat bone osteocalcin or rat serum albumin in either α-MEM with 2% heat-inactivated horse serum alone (α) or supplemented with 10% L-cell-conditioned medium (as a source of M-CSF) (L10). Few substrate-attached cells survived in basal α medium, but when treated with L10 medium or GM-CSF, they survived and proliferated. Osteocalcin did not significantly affect survival or proliferation. Subcultures of cells treated with GM-CSF had large numbers of multinucleated cells, more than half of which were tartrate-resistant acid phosphatase-positive (TRAP). Osteocalcin further promoted the development of TRAP-positive multinucleated cells; a dose of 0.7 μg/ml osteocalcin promoted osteoclastic differentiation by 60%. Using a novel microphotometric assay, we detected significantly more tartrate-resistant acid phosphatase activity in the osteocalcin plus GM-CSF group (75.6 ± 14.2) than in GM-CSF alone (53.3 ± 7.3). In the absence of M-CSF, GM-CSF stimulated tartrate-resistant acid phosphatase activity, but osteocalcin did not have an additional effect. These studies indicate that osteocalcin promotes osteoclastic differentiation of a stromal-free subpopulation of hematopoietic progenitors in the presence of GM-CSF and L-cell-conditioned medium. These results are consistent with the hypothesis that this bone-matrix constituent plays a role in bone resorption. © 1994 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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