ABSTRACT
Current radiobiology research appears to have distanced itself from the mechanisms associated with α-and βo-inactivation. In many studies, little regard is given to the fact that two independent mechanisms are in play and that their properties are qualitatively distinct. The dominant mechanisms of cell killing in populations irradiated with doses of 2 and 20 Gy are very different. Much of the current search for molecular factors that might inform about cell radiosensitivity reads like a “molecular taxonomy.” That is, there is a desire to identify individual or groups of molecular expressions that will correlate with intrinsic radiosensitivity. Of that research, the studies that improve our understanding of repair mechanisms of radiation-induced lesions in cellular DNA are the most relevant to radiotherapy. They should inform about the βo-mechanism, particularly in normal tissues, where radiation damage repair between dose fractions is essential. Low-dose hypersensitivity has been researched extensively; how it might relate to linear-quadratic (LQ) radiobiology and radiotherapy prescription of fractioned dose is discussed. The radiation bystander effect consumes a large portion of current radiobiology research funding but its importance for tumor cell eradication in vivo is not particularly clear. The reader is directed to other radiobiology textbooks that describe several other phenomena (cell cycle regulation, immunology, etc.) that might play a role in tumor cell killing by radiation. To have a significant benefit for clinical practice and tumor response modeling, radiobiology studies should be related to the two independent mechanisms of cell killing described by the LQ model.
