Princess Máxima Center for Pediatric Oncology, Heidelberglaan 25, 3584 CSUtrecht, the Netherlands.
Oncode, Utrecht, the Netherlands.
Expert Rev Mol Med. 2021 Apr 27;23:e5. doi: 10.1017/erm.2021.6.
Children show a higher incidence of leukaemia compared with young adolescents, yet their cells are less damaged because of their young age. Children with Down syndrome (DS) have an even higher risk of developing leukaemia during the first years of life. The presence of a constitutive trisomy of chromosome 21 (T21) in DS acts as a genetic driver for leukaemia development, however, additional oncogenic mutations are required. Therefore, T21 provides the opportunity to better understand leukaemogenesis in children. Here, we describe the increased risk of leukaemia in DS during childhood from a somatic evolutionary view. According to this idea, cancer is caused by a variation in inheritable phenotypes within cell populations that are subjected to selective forces within the tissue context. We propose a model in which the increased risk of leukaemia in DS children derives from higher rates of mutation accumulation, already present during fetal development, which is further enhanced by changes in selection dynamics within the fetal liver niche. This model could possibly be used to understand the rate-limiting steps of leukaemogenesis early in life.
与青少年相比,儿童白血病的发病率更高,但由于年龄较小,其细胞受损程度较轻。唐氏综合征(DS)患儿在生命的头几年患白血病的风险更高。DS 中 21 号染色体的组成性三体(T21)的存在是白血病发生的遗传驱动因素,但需要额外的致癌突变。因此,T21 为更好地了解儿童白血病的发生提供了机会。在这里,我们从体细胞进化的角度描述了儿童 DS 中白血病的风险增加。根据这一观点,癌症是由组织背景中受选择压力影响的细胞群体中可遗传表型的变异引起的。我们提出了一个模型,即 DS 儿童白血病风险的增加源于突变积累率的增加,这种积累率在胎儿发育过程中就已经存在,并且在胎儿肝脏龛位内选择动态的变化进一步增强了这种积累率。该模型可用于了解生命早期白血病发生的限速步骤。