Tumors blood supply

Horsman, M. R., Christensen, K. L., and Overgaard, J. (1992) Relationship between the hydralazine-induced changes in murine tumor blood supply and mouse blood pressure. Inti. J. Radiat. Oncol. Biol. Phys. 22,455 458. 

Alternatively, if the tumor vasculature could be made the target, then the drugs would not have to cross the vessel wall or the interstitium. Anti-angiogenesis therapy, pioneered by Judah Folkman (1993), whose aim is to stop the growth of new vessels of a tumor, is a successful example of such an approach. Hyperthermia, photodynamic therapy, and cytokines such as TNF are other approaches which may also impair the tumor blood supply. One attractive hypothesis is that when several of the current cytotoxic therapies work, it is not only because they destroy cancer cells, but also because they may destroy a solid tumor by impairing its blood supply. Thus judiciously combining anti-vascular therapies with anti-cellular therapies may lead to synergistic results. Our recent study with lym-... 

Vaupel P, Jain RK (eds) (1991) Tumor blood supply and metabolic microenvironment. Characterization and implications for therapy. Gustav Fischer, Stuttgart, New York Vaupel P Kallinowski F (1987) Hemoconcentration of blood flowing through human tumor xenografts. Int J Microcirc Clin Exp 6 72... 

Rossi S, Garbagnati P, Lencioni R et al (2000) Percutaneous radio-frequency thermal ablation of nonresectable hepatocellular carcinoma after occlusion of tumor blood supply. Radiology 217 119-126 Seong J, Keum KC, Han KH, Lee DY, Lee JT, Chon CY, Moon YM, Suh CO, Kim GE (1999) Combined transcatheter arterial chemoembolization and local radiotherapy of unresectable hepatocellular carcinoma. Int J Radiat Oncol Biol Phys 43 393-397... 

Palliation of symptoms in nonoperable patients was also included in some outcome analyses. The details of symptoms and therapeutic effects of renal artery embolization are generally lacking, but studies generally reported thathematuria, pain, and paraneoplastic symptoms were alleviated. In one study, severe hematuria resolved in 11 of 14 patients, and incomplete embolization of the tumor blood supply from parasitized lumbar arteries resulted in persistent hematuria in 3 of 14 patients [11]. In another study, malignant hypercalcemia resolved after embolization [10]. Kalman and Varenhorst concluded that a small group of patients with specific, tumor-related symptoms may benefit from embolization. However, the palliative effect of embolization cannot be evaluated from the available data, and the effectiveness of the procedure awaits validation. 

The role of NO in maintaining tumor blood supply is double-edged and both increasing and decreasing intrammoral levels of nitric oxide could have anti-tumor effects. A phase I smdy aiming at reducing mmor blood supply by the administration of inhibitors of iNOS has been launched with clear evidence of proof of concept as reduction of tumor blood flow (Ng et al. 2007). 

State of deviation of plasma pH (systemic acidosis) or tissue extracellular pH (tissue or local acidosis) from normal (ca. pH 7.4) towards lower values. Deviation of 0.1 pH units is significant. Systemic acidosis can be caused by lung or kidney failure. Local acidosis can be the consequence of injury, inflammation, or tumor growth, due to disruption of blood supply. Local acidosis is normally associated with hypoxia. 

Micro-Thromboses Platelets and leucocytes, like other cells, are known to carry surplus negative charge, and can be electrophoretically deposited at (or around) the anode10 owing to the positive electrode potential. These microthromboses in capillaries in or near the treatment site will result in decreased blood flow and may contribute to a local dystrophy of the tissue. A more pronounced version of this effect can be seen sometimes as electrocoagulation and vascular occlusion (i.e., shut, closed or obstructed vasculature) of the tumor tissue. In other words, ECT cuts off the blood supply to the tumor and causes the tumor cell necrosis. 

In order for a solid tumor to grow beyond a certain size, it must develop a blood supply by elaborating factors such as vascular endothelial growth factor (VEGF). VEGF secreted by the tumor cells diffuses to nearby endothelial cells, which respond by dividing and migrating toward the tumor to eventually develop into blood vessels and vascularize the tumor. 

The idea. In 1961, Judah Folkman, a young surgeon, noted that cancer cells injected into isolated in vitro thyroid preparations grew to small tumors and then stopped growing. However, the same cancer cells grew into massive tumors when implanted into mice. Folkman realized that the in vivo tumors had something the in vitro system did not have—a rich vascular bed and blood supply. 

In addition to the treatment of pain and inflammation, COX-2 inhibitors might be of benefit in other indications. Expression of COX-2 in colon cancer, intestinal adenomas, and other cancer cells as well as clinical studies with COX-2 inhibitors, suggest the use of COX-2 inhibitors in cancer (Masferrer et al., 1999). Expression of COX-2 in angiogenesis follows the same route since angiogenesis is important for blood supply and hence the growth of many tumors. 

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