Cancer risk in children born after assisted reproductive technology
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Endokrinologie Leitthema Gynäkologische Endokrinologie https://doi.org/10.1007/s10304-020-00334-x
A. Arshad1 · A. G. Sutcliffe2 1 2
© Springer Medizin Verlag GmbH, ein Teil von Springer Nature 2020 Redaktion B. Sonntag, Hamburg G. Griesinger, Lübeck R. Felberbaum, Kempten
Introduction Since 1978 more than 8 million children worldwide have been born via assisted reproductive technology (ART), with the use of ART increasing by 2.5% per year in the UK [1]. It has been well established that children conceived via ART are at risk of adverse perinatal outcomes, including an increased risk of preterm birth, low birth weight and congenital defects [2, 3]. However, the association between ART and cancer risk in children is less clear. The results from the contemporaneous literature range from there being an increased cancer risk, to there being no risk or to even a protective effect from receiving ART [4, 5]. This article overviews the current literature as to the risk of childhood cancer after ART.
Pathophysiology The aetiology of childhood cancers is complex. It has been suggested that fertility treatments may increase the risk of their occurrence in children. This could be mediated by epigenetic changes caused by the fertility drugs, the ART process or both. Alternatively, these genetic changes that increase the risk of childhood cancer may be pre-existent within the gametes of the infertile partner/partners.
Epigenetic changes secondary to fertility drugs It is considered that childhood cancer pathways may start in early foetal development, where exposure to fertility treatments leads to epigenetic changes in the
North Middlesex University Hospital, London, UK Policy, Practice and Populations Unit, Great Ormond Street Institute of Child Health, University College London, London, UK
Cancer risk in children born after assisted reproductive technology
gametes or embryo. Exposure to fertility medications occurs at each phase of the ART procedure, including during stimulation of the follicles, the process of oocyte retrieval, culture of the embryos, cryopreservation and during embryo transfer. Evidence to support this hypothesis comes from studies that have assessed genetic imprinting. Imprinting is an epigenetic form of gene regulation that regulates the expression of certain genes depending on their parental origin [6]. Aberrant functioning of these imprinting genes is associated with an increased risk of both childhood (retinoblastoma, neuroblastoma and acute myeloid leukaemia) and adult cancers (breast, bladder and cervical cancer) [7]. The development and maintenance of imprinting genes occurs during gametogenesis and embryogenesis. However, environmental and physical stressors can cause abnormalities in these genes [8]. Fertility treatments may act as a chemical stressor, with the medications influencing either their formation or function. There is a paucity of evidence exploring the influence of fertility treatments on the imprinting genes in humans. However, there is better evidence in animal studies. Observationa
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