Engels H, Menzel H G, Pihet P, Wambersie A
Université Catholique de Louvain, Cliniques Universitaires St-Luc, Bruxelles, Belgium.
Strahlenther Onkol. 1999 Jun;175 Suppl 2:47-51. doi: 10.1007/BF03038888.
The risk of induction of a second primary cancer after a therapeutic irradiation with conventional photon beams is well recognized and documented. However, in general, it is totally overwhelmed by the benefit of the treatment. The same is true to a large extent for the combinations of radiation and drug therapy. After fast neutron therapy, the risk of induction of a second cancer is greater than after photon therapy. Neutron RBE increases with decreasing dose and there is a wide evidence that neutron RBE is greater for cancer induction (and for other late effects relevant in radiation protection) than for cell killing. Animal data on RBE for tumor induction are reviewed, as well as other biological effects such as life shortening, malignant cell transformation in vitro, chromosome aberrations, genetic effects. These effects can be related, directly or indirectly, to cancer induction to the extent that they express a "genomic" lesion. Almost no reliable human epidemiological data are available so far. For fission neutrons a RBE for cancer induction of about 20 relative to photons seems to be a reasonable assumption. For fast neutrons, due to the difference in energy spectrum, a RBE of 10 can be assumed. After proton beam therapy (low-LET radiation), the risk of secondary cancer induction, relative to photons, can be divided by a factor of 3, due to the reduction of integral dose (as an average). The RBE of heavy-ions for cancer induction can be assumed to be similar to fission neutrons, i.e. about 20 relative to photons. However, after heavy-ion beam therapy, the risk should be divided by 3, as after proton therapy due to the excellent physical selectivity of the irradiation. Therefore a risk 5 to 10 times higher than photons could be assumed. This range is probably a pessimistic estimate for carbon ions since most of the normal tissues, at the level of the initial plateau, are irradiated with low-LET radiation.
常规光子束治疗性照射后诱发第二种原发性癌症的风险已得到充分认识和记录。然而，总体而言，这种风险完全被治疗的益处所掩盖。在很大程度上，放射与药物联合治疗也是如此。快中子治疗后，诱发第二种癌症的风险高于光子治疗。中子的相对生物效应（RBE）随剂量降低而增加，并且有大量证据表明，中子诱发癌症（以及与辐射防护相关的其他晚期效应）的RBE高于细胞杀伤的RBE。本文综述了关于肿瘤诱发的RBE的动物数据，以及其他生物效应，如寿命缩短、体外恶性细胞转化、染色体畸变、遗传效应。这些效应可直接或间接地与癌症诱发相关，只要它们表现出“基因组”损伤。到目前为止，几乎没有可靠的人类流行病学数据。对于裂变中子，相对于光子，诱发癌症的RBE约为20似乎是一个合理的假设。对于快中子，由于能谱不同，可假设RBE为10。质子束治疗（低传能线密度辐射）后，相对于光子，诱发继发性癌症的风险可除以3，这是由于积分剂量（平均而言）的降低。重离子诱发癌症的RBE可假设与裂变中子相似，即相对于光子约为20。然而，重离子束治疗后，由于照射具有出色的物理选择性，风险应如质子治疗一样除以3。因此，可以假设风险比光子高5至10倍。对于碳离子，这个范围可能是一个悲观的估计，因为在初始坪区水平，大多数正常组织受到的是低传能线密度辐射。
