[The overlooked in visceral physiopathology: vertebral venous system].
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BACKGROUND: Metastasic deposits from malignancies frequently lodge in the skeleton, including the jaw bones. METHOD: A review of the literature was performed in order to provide a coherent overview on the pathogenesis of bone metastasis. RESULTS: Bone metastasis follows complex molecular interactions that enable tumor cells to detach from the primary site, invade the extracellular matrix, intra-vasate, extra-vasate, and proliferate within bone. They induce local bone changes that could manifest radiologically as either osteolytic or radiodense. In addition to the direct bone changes, malignancies can elaborate mediators that are released in circulation, leading to generalized osteopenia. CONCLUSIONS: The spread of malignant neoplasms to bone is not a random process but rather a cascade of specific molecular events orchestrated through complex interactions between neoplastic cells and their environment.
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The increase of circulating DNA levels, the mutations of tumor characteristic genes and the telomerase expression of circulating tumor cells can be detected not only in advanced stage but also in early stage of tumors. The combinational detection of circulating DNA and telomerase of circulating tumor cells is useful for the early diagnosis of tumors.
Blood vessels facilitate the widespread dissemination of cancer cells in metastasis. Interactions between circulating intravascular cancer cells and the microvasculature involve mechanical contact and transient attachment, mediated by endothelial surface adhesion molecules and their ligands on the neoplastic cells. Initial interactions trigger a sequence of activation pathways that involve cytokines, growth factors, bioactive lipids, and reactive oxygen species produced by the cancer cell or the endothelium. These activation steps elicit the expression of integrin adhesion molecules in cancer cells and the endothelium, matrix metalloproteinases, and chemotactic factors that promote firm attachment of tumor cells to the vessel wall and transvascular penetration. On the other hand, induction of endothelial free radicals can be cytotoxic to cancer cells. Collectively, the sum of these interactions act as a rate-regulating step in the metastatic process.
Dissemination of tumor cells by vascular channels seems to be enhanced by certain surgical procedures, e.g. transurethral resection of the prostate, an operative procedure commonly used in the diagnosis and management of prostatic cancer, the third biggest killer of men in the United States. Circulating tumor cells have been the subject of great controversy as they are considered to be the connecting link between the primary tumor and the hematogenously disseminated metastatic growths. Isolation and identification of tumor cells which get released into the vascular channels is somewhat complicated. We report our experience with a technique for isolating and identifying prostatic tumor cells in the circulation and briefly discuss the role of transurethral resection of the prostate in the management of prostatic cancer.
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