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| http://dx.doi.org/10.3343/alm.2020.40.5.417 | DOI Listing |
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A case of familial donor-derived acute myeloid leukemia with underlying pre-leukemic mutations.
Haematologica
October 2024
Department of Translational and Precision Medicine, Sapienza University of Rome (Rome, Italy).
Maternal Lifestyle and Prenatal Risk Factors for Childhood Leukemia: A Review of the Existing Evidence.
Fetal Diagn Ther
August 2024
BCNatal Fetal Medicine Research Center (Hospital Clínic and Hospital Sant Joan de Déu), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Background: Acute leukemia is the most common pediatric cancer, with an incidence peak at 2-5 years of age. Despite the medical advances improving survival rates, children suffer from significant side effects of treatments as well as its high social and economic impact. The frequent prenatal origin of this developmental disease follows the two-hit carcinogenesis model established in the 70s: a first hit in prenatal life with the creation of genetic fusion lesions or aneuploidy in hematopoietic progenitor/stem cells, and usually a second hit in the pediatric age that converts the preleukemic clone into clinical leukemia.
View Article and Find Full Text PDFA Pre-Leukemic DNA Methylation Signature in Healthy Individuals at Higher Risk for Developing Myeloid Malignancy.
Clin Cancer Res
May 2024
Department of Haematology, Singapore General Hospital, Singapore, Singapore.
Purpose: DNA methylation alterations are widespread in acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS), some of which appear to have evolved independently of somatic mutations in epigenetic regulators. Although the presence of somatic mutations in peripheral blood can predict the risk of development of AML and MDS, its accuracy remains unsatisfactory.
Experimental Design: We performed global DNA methylation profiling in a case control study nested within the Singapore Chinese Health Study to evaluate whether DNA methylation alterations were associated with AML/MDS development.
Interaction between birth characteristics and variants in the childhood lymphoblastic leukemia risk.
Front Oncol
January 2024
Research Center, Molecular Carcinogenesis Program, Instituto Nacional de Câncer (INCA), Rio de Janeiro, Brazil.
Background: The incidence rate of childhood acute lymphoblastic leukemia (ALL) differs worldwide, and the interplay between hemostasis actors and the maladaptive responses to environmental exposures has been explored. It has been proposed that endogenous cortisol, induced by different triggers, would eliminate pre-leukemic clones originated . Herein, we tested if the interaction between , and (players in glucocorticoid secretion) and birth characteristics would be associated with ALL risk.
View Article and Find Full Text PDFPresence of leukemic clone-specific immunoglobulin heavy chain rearrangements in neonatal blood spots of children with B-cell precursor acute lymphoblastic leukemia.
Int J Lab Hematol
April 2024
Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Belgrade, Serbia.
Introduction: Childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL) can be traced back to birth using leukemic clone-specific immunoglobulin heavy chain (IGH) rearrangements, implying prenatal origin of this disease.
Methods: We retrospectively analyzed neonatal blood spots (Guthrie cards) of 24 patients with childhood BCP-ALL aged 1-9.6 years (median 3.
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