1. Epigenome-wide analysis across the development span of pediatric acute lymphoblastic leukemia: backtracking to birth
- Author
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Akram Ghantous, Semira Gonseth Nusslé, Farah J. Nassar, Natalia Spitz, Alexei Novoloaca, Olga Krali, Eric Nickels, Vincent Cahais, Cyrille Cuenin, Ritu Roy, Shaobo Li, Maxime Caron, Dilys Lam, Peter Daniel Fransquet, John Casement, Gordon Strathdee, Mark S. Pearce, Helen M. Hansen, Hwi-Ho Lee, Yong Sun Lee, Adam J. de Smith, Daniel Sinnett, Siri Eldevik Håberg, Jill A. McKay, Jessica Nordlund, Per Magnus, Terence Dwyer, Richard Saffery, Joseph Leo Wiemels, Monica Cheng Munthe-Kaas, and Zdenko Herceg
- Subjects
Pediatric leukemia ,Epigenetics ,DNA methylation ,VTRNA2-1 ,Birth cohort ,Neonatal blood spots ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Cancer is the leading cause of disease-related mortality in children. Causes of leukemia, the most common form, are largely unknown. Growing evidence points to an origin in-utero, when global redistribution of DNA methylation occurs driving tissue differentiation. Methods Epigenome-wide DNA methylation was profiled in surrogate (blood) and target (bone marrow) tissues at birth, diagnosis, remission and relapse of pediatric pre-B acute lymphoblastic leukemia (pre-B ALL) patients. Double-blinded analyses was performed between prospective cohorts extending from birth to diagnosis and retrospective studies backtracking from clinical disease to birth. Validation was carried out using independent technologies and populations. Results The imprinted and immuno-modulating VTRNA2-1 was hypermethylated (FDR
- Published
- 2024
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