Cancer regulation

Elcock, M., and Morgan, R. W. (1993). Update on artificial sweeteners and bladder cancer. Regul Toxicol Pharmacol 17, 35-43. 

Azenshtein, E., T. Meshel, S. Shina, N. Barak, I. Keydar, and A. Ben-Baruch. 2005. The angiogenic factors CXCL8 and VEGF in breast cancer regulation by an array of promalignancy factors. Cancer Lett 217 73. 

Ogretmen, B. (2006). Sphingolipids in cancer regulation of pathogenesis and therapy. FEBS Lett 580, 5467-5476. 

Modem cancer therapy has been primarily dependent upon surgery, radiotherapy, chemotherapy, and hormonal therapy (72) (see Chemotherapeutics,anticancer Hormones Radiopharmaceuticals). Chemotherapeutic agents maybe able to retard the rate of growth, but are unable to eradicate the entire population of neoplastic cells without significant destmction of normal host tissue. This serious side effect limits general use. More recentiy, the immunotherapeutic approach to cancer has involved modification and exploitation of the cellular and molecular mechanisms in host defense, regulation of tissue proliferation, tissue differentiation, and tissue survival. The results have been more than encouraging. 

For radiation doses <0.5 Sv, there is no clinically observable iacrease ia the number of cancers above those that occur naturally (57). There are two risk hypotheses the linear and the nonlinear. The former implies that as the radiation dose decreases, the risk of cancer goes down at roughly the same rate. The latter suggests that risk of cancer actually falls much faster as radiation exposure declines. Because risk of cancer and other health effects is quite low at low radiation doses, the iacidence of cancer cannot clearly be ascribed to occupational radiation exposure. Thus, the regulations have adopted the more conservative or restrictive approach, ie, the linear hypothesis. Whereas nuclear iadustry workers are allowed to receive up to 0.05 Sv/yr, the ALARA practices result ia much lower actual radiatioa exposure. 

Environmental tobacco smoke mid gasoline vapors both contain mixtures of trace luiiounts of many of the individual compounds regulated as Air Toxics under Title 111, section 112 of the 1990 Clean Air Act Amendnmts. Much of the general public is more likely to be exposed to these mixtures during the course of their lives tlian to specific compounds on the air toxics list. Hence, estimation of the cancer risk resulting from exposure to these mixtures is a useful and relevant exercise. 

Yart A, Mayeux P, Raynal P (2003) Gabl, SHP-2 and Other Novel Regulators of Ras Targets for Anticancer Drug Discovery. Curr Cancer Drug Targets 3 177-192... 

Kim Y, Yoon JW, Xiao X et al (2007) Selective down-regulation of glioma-associated oncogene 2 inhibits the proliferation of hepatocellular carcinoma cells. Cancer Res 67(8) 35 83-3593... 

The CaR regulates numerous biological processes, including the expression of various genes (e.g., PTH) the secretion of hormones (PTH and calcitonin), cytokines (MCP-1), and calcium (e.g., into breast milk) the activities of channels (potassium channels) and transporters (aquaporin-2) cellular shape, motility (of macrophages), and migration cellular adhesion (of hematopoietic stem cells) and cellular proliferation (of colonocytes), differentiation (of keratinocytes), and apoptosis (of H-500 ley dig cancer cells) [3]. 

---