Radiosensitivity, of tumors

Garg AK, Buchholz TA, Aggarwal BB. 2005. Chemosensitization and radiosensitization of tumors by plant polyphenols. Antioxid Redox Signal 7 1630-1647. 

Munro TR, Gilbert CW (1961) The relation between tumor lethal doses and the radiosensitivity of tumor cells. Br J Radiol 34 246-251... 

Whereas epidermal growth factor (EGF) enhances the radiosensitivity of human squamous ceU carcinoma cells in vitro (197), addition of EGF to hormone-deprived MCE-7 breast cancer cells prior to irradiation results ia iacreased radioresistance (198). An anti-EGE-receptor monoclonal antibody blocks the abiUty of EGE to enhance growth and radioresistance. Tumor cells, the growth of which is stimulated by EGE, appear to be protected those where growth is iohibited are sensitized (198). 

Lloyd RD, Taylor GN, Jee WSS, et al. 1999. Relative radiosensitivity of bone tumor induction among beagles as a function of age at injection of 239Pu or 226RA. Health Phys 76(l) 75-81. 

Several genetic alterations can influence radiosensitivity of cancer cells and radioresponsive tumors are known to allow more easily radiation-induced apoptosis. Therefore, the proper functioning of the apoptotic machinery regulates radiosensitivity. As described above, a cracial role is played by p53, and its downstream genes p21 and bax, in activating the apoptotic process. Those cancers with mutations at these levels are expected to be radioresistant. 

These same authors also report a dose-dependent increase in the apoptotic rate after the administration of gemcitabine (33), which they believe correlates with the elimination of the more radioresistant S phase population of cells and redistribution of the remaining cells into more radiosensitive compartments of the cell cycle. They also report in another study that reoxygenation of the resistant hypoxic fraction of tumor cells is also a mechanism for the action of gemcitabine (34). Therefore, elimination of these S phase tumor cells may aid the radiation response by not only causing cell cycle synchronization but also by leading to reoxygenation of hypoxic cells. 

Bernhard EJ, McKenna WG, Hamilton AD, et al. Inhibiting Ras prenylation increases the radiosensitivity of human tumor cell lines with activating mutations of ras oncogenes. Cancer Res 1998 58 1754-1761. 

S. J. Li, G.Y. Jin, J.E. Moulder, Prediction of tumor radiosensitivity by hexafluoromi-sonidazole retention monitored by [FI-1]/[F-19] magnetic-resonance spectroscopy. Cancer Commun. 3 (1991) 133-139. 

VI. Van den Brenk, H. A. S., Effect of high pressure oxygen on radiosensitivity of Ehrlich s tumor in mice after immunological approximation. Bril. J. Cancer 16, 61-84 (1961). 

In contrast to the success in treating hematological malignancies such as lymphoma and leukemia, RIT of the more common solid tumors such as breast, colon, ovary or prostate has been severely Hmited by toxicity to the bone marrow, poor tumor penetration of the radioimmunoconjugates, a 3-fold lower radiosensitivity of these malignancies, and the development of an immune response to the mAbs, which restricted re-treatment [6]. Although a few patients have achieved CR, most experienced PR or minor responses (MR) (Table 5.2). 

Moeller BJ, Cao Y, Li CY, Dewhirst MW. Radiation activates HIF-1 to regulate vascular radiosensitivity in tumors role of reoxygenation, free radicals, and stress granules. Cancer Cell 2004 5 429-441. 

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