Altered G1 checkpoint control determines adaptive survival responses to ionizing radiation

Typical cell signaling response to ionizing radiation: DNA damage and extranuclear damage

“…Tissue/cells at treatment site (including tumor-associated endothelial cells, normal tissue and remnant cancer cells) that initially survive irradiation may elicit factors. These factor(s) may transduce and alter the physiology of the neighboring bystander cells [18][19][20][21][22] by paracrine feedback signaling that may pre-dispose the cells to carcinogenic processes [23] in normal tissue, and tumor cell growth in surviving cancer cells leading to tumor recurrence at later time. Reports from our laboratory demonstrated that radiation at doses used in fractionated radiotherapy could selectively induce the DNA-binding activity of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) [24][25][26] and the occurrence of a positive feedback loop between tumor necrosis factor-alpha (TNF-α) and NF-κB.…”

An Examination of Radiation Hormesis Mechanisms Using a Multistage Carcinogenesis Model

“…This adaptive response to IR, which occurs after exposures that are so low (0.005-0.01 Gy) that they do not induce discernible aberrations themselves, has been attributed to the induction of a repair mechanism that causes the restitution of X-rayinduced chromosome breaks (Wolff, 1998). Variations and the absence of adaptive responses have also been reported (Jacobson-Kram and Williams, 1988;Bauchinger et al, 1989;Bosi and Olivieri, 1989;Sankaranarayanan et al, 1989;Schmid et al, 1989;Hain et al, 1992;Müller et al, 1992;Wojcik et al, 1992Wojcik et al, , 1993Shadley, 1994;UNSCEAR, 1994;Vijayalaxmi et al, 1995;Boothman et al, 1996;Raaphorst and Boyden, 1999;Sorensen et al, 2002). Azzam et al (1996) exposed quiescent mouse fibroblasts (C3H 10T1/2) cells to doses of 1-100 mGy -rays and observed that the risk of neoplastic transformation was reduced from the spontaneous level to a rate three-to four-fold below that level.…”

Radiation Induced Radioresistance - Role of DNA Repair and Mitochondria

“…Shadley & Wiencke, 1989 The beneficial effects of low dose depended upon total dose, dose rate of pre-irradiated dose but not on dose rate of challenge dose in human lymphocytes. Boothman et al, 1996 Elevated level of PCNA, cyclin D1, cyclin A in human cell line preirradiated with gamma-rays, may play a role in cell cycle regulation and DNA repair. Carette et al, 2002 Implication of PBP74 in low dose irradiated human tumour cell lines HT29 and MCF-7 with gamma-rays within 30 min after irradiation.…”