Tumor hypoxia, the physiological link between Trousseau's syndrome (carcinoma-induced coagulopathy) and metastasis.
نویسندگان
چکیده
Trousseau first reported over 100 years ago that cancer patients have an increased incidence of coagulopathies (1). Since Trousseau published his findings, thromboembolic disorders have been documented at elevated frequencies in patients with a wide variety of tumors such as lung, pancreas, stomach, and colon tumors (2). These clinical findings have been supported by laboratory studies that have identified altered levels of blood clotting factors in the serum of cancer patients. Indeed, the presence of an unexplained deep venous thrombosis can be clinical reason enough to screen for occult malignancy. Mechanistically, it has been proposed that normal host cells such as platelets, mononuclear phagocytes, and smooth muscle cells are responsible for activating procoagulant and angiogenic pathways (3). However, recent data derived from large “expression profiles” have generated insight into gene expression changes in solid tumors that indicate that tumor cells under microenvironmental stress can produce the same procoagulant and angiogenic factors that host cells secrete. Because studies reveal that solid tumors arising from a number of cell types express and secrete proteins involved in coagulation, it is unlikely that acquired genetic mutations in tumor-promoting genes alone are able to completely explain the clinical data. We propose that tumor-specific physiological changes, such as decreased oxygenation (tumor hypoxia), act to stimulate expression of blood clotting regulators independent of the cancer cell’s origin. In this study, we discuss the supporting evidence for this new concept with regard to both coagulation and fibrinolysis in the vicinity of the tumor and through systemic circulation to distant sites.
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ورودعنوان ژورنال:
- Cancer research
دوره 61 3 شماره
صفحات -
تاریخ انتشار 2001