ESPEYB15 9 Oncology and chronic disease Late effects of tumour therapy: molecular evidences of premature cellular aging (1 abstracts)
9.4 Young adult survivors of childhood acute lymphoblastic leukemia show evidence of chronic inflammation and cellular aging
Ariffin H , Azanan MS , Abd Ghafar SS , Oh L , Lau KH , Thirunavakarasu T , Sedan A , Ibrahim K , Chan A , Chin TF , Liew FF , Jeyamogan S , Rosli ES , Baharudin R , Yap TY , Skinner R , Lum SH & Hainaut P
Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
To read the full abstract: Cancer. 2017;123:4207-4214
Metabolic syndrome and early cardiovascular disease are well-known long-term complications of cancer treatment during childhood, but the underlying causes are still unclear. It had been already demonstrated that the abnormalities of the immune system, that are characteristic of the elderly population, may become evident earlier in childhood cancer survivors (1), and these abnormalities have been interpreted as signs of premature cellular aging. The current study reports that the leukocytes from a cohort of asymptomatic young adult survivors of childhood acute lymphoblastic leukaemia (ALL) show positive markers of chronic inflammation and aging (higher inflammatory cytokines and shorter leukocyte telomere length). The authors speculate that the cellular damage may be more pronounced in younger children because the insults related to cancer treatment occur within a developmental window of high sensitivity, considering that telomere attrition rate is highest during infancy and early childhood (2). In addition, traumatic experiences associated with cancer may become embedded epigenetically and lead to modifications in gene expression (3). Adverse life events at a young age increase the odds of short telomeres, whereas similar experiences in adulthood have not shown comparable biologic effects (4). It is noteworthy that survivors who were diagnosed before 5 years of age had shorter leukocyte telomere length compared with those who were diagnosed later. As the authors state, understanding the cellular processes that drive accelerated aging may facilitate the development of targeted interventions to stop, or at least slow down, these processes.
1. Azanan MS, Abdullah NK, Chua LL, et al. Immunity in young adult survivors of childhood leukemia is more similar to elderly rather than age-matched controls: role of cytomegalovirus. Eur J Immunol. 2016; 46: 1715-1726.
2. Zeichner SL, Palumbo P, Feng Y, et al. Rapid telomere shortening in children. Blood. 1999; 93: 2824-2830.
3. Murgatroyd C, Patchev AV, Wu Y, et al. Dynamic DNA methylation programs persistent adverse effects of early-life stress. Nat Neurosci. 2009; 12: 1559-1566.
4. Puterman E, Gemmill A, Karasek D, et al. Lifespan adversity and later adulthood telomere length in the nationally representative US Health and Retirement Study. Proc Natl Acad Sci U S A. 2016; 113: E6335-E6342.
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ESPE Yearbook of Paediatric Endocrinology
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