Backtracking NOM1::ETV6 fusion to neonatal pathogenesis of t(7;12) (q36;p13) infant AML
Pablo Bousquets‐Muñoz, Òscar Molina, Ignacio Varela, Ángel Álvarez‐Eguiluz, Javier Fernández-Mateos, Ana M. Gómez-Lahoz, Elena G. Sánchez, Milagros Balbı́n, David Ruano‐Gallego, Manuel Ramı́rez, Xosé S. Puente, Pablo Menéndez, Talía Velasco-Hernández
Abstract
Acute leukemia is the most frequently diagnosed malignancy in childhood, with acute lymphoblastic leukemia (ALL) comprising approximately 80% of cases in children aged 0–18 years, and acute myeloid leukemia (AML) accounting for approximately 15–20% [ 1 ]. The early onset (0–10 years) of most childhood acute leukemias and the high concordance rate among monozygotic twins suggest a prenatal origin of the disease [ 1 ]. Indeed, the presence of preleukemic precursors in cord blood (CB) samples or Guthrie blood spots from children who later developed acute leukemia has been demonstrated in several studies [ 2 , 3 ]. However, this has mainly been demonstrated experimentally for the most common cytogenetic subtypes, particularly in ALL.