Canellos G P, Arseneau J C, DeVita V T, Whang-Peng J, Johnson R E
Lancet. 1975 Apr 26;1(7913):947-9. doi: 10.1016/s0140-6736(75)92007-3.
The incidence of second tumours occurring in the course of Hodgkin's disease has been investigated in a series of 452 patients treated with standard chemotherapy or radiotherapy, combination chemotherapy alone, intensive radiotherapy alone, or both intensive radiotherapy and combination chemotherapy administered in sequence. 16 tumours were noted. When analysed according to mode of treatment, 6 cases occurred in a group of 62 patients who received both modalities. When analysed for age, sex, and man-years of follow-up, this group appears to have 14-5 times the risk of developing a second tumour. However, that subgroup which had a complete remission after intensive radiotherapy followed by a relapse of disease, prior to receiving combination chemotherapy, had the highest risk with 18-5 times greater incidence of second tumour than expected. It is noteworthy that, of the 16 second tumours, 2 were acute myeloid leukaemia; in both cases a similar chromosomal abnormality (45 chromosomes, C-group deletion) was noted. The mechanism of oncogenesis may represent a combination of the immunosuppressive effects and cellular effects of those forms of treatment.
在一组452例接受标准化疗或放疗、单纯联合化疗、单纯强化放疗或先后接受强化放疗和联合化疗的患者中,对霍奇金病病程中发生的第二肿瘤的发病率进行了调查。共发现16例肿瘤。根据治疗方式分析,6例发生在62例接受两种治疗方式的患者组中。按年龄、性别和随访人年分析,该组发生第二肿瘤的风险似乎是14.5倍。然而,在接受联合化疗之前,先接受强化放疗后疾病复发且完全缓解的亚组风险最高,第二肿瘤的发病率比预期高18.5倍。值得注意的是,在这16例第二肿瘤中,有2例是急性髓细胞白血病;在这两例中都发现了类似的染色体异常(45条染色体,C组缺失)。肿瘤发生机制可能是这些治疗形式的免疫抑制作用和细胞效应的结合。