Table 1. Potential underlying mechanisms in HRS and IRR doses and in chemopotentiation settings.

Treatments	Mechanisms
	Normal cells	Tumor cells
HRS LDFRT (<0.6 Gy)	ATM activation and DNA repair programs initiated.	Bax upregulation with bcl-2 down regulation; pro-apoptotic proteins upregulated
IRR dose (>1 Gy)	ATM activation and DNA repair programs initiated.	ATM activation, pro-survival transcription factors (NFκB and NF-Y) upregulated, MDR-1 upregulated
LDFRT + chemotherapy	No data	Bax upregulation with bcl-2 down regulation, cytochrome C release; several pro-apoptotic proteins are upregulated
		XIAP was downregulated, but upregulated in LDFRT-resistant cells
IRR dose + chemotherapy	No data	Bcl-2 and MDR1 protein increased; increase in NFκB and NF-Y activity
		XIAP is significantly upregulated

IRR, induced radiation resistance; HRS, hyper-radiation sensitivity; LDFRT, Low Doses Fractionated Radiation Therapy.