TO THE EDITOR:
We read with interest the report of whole (epi)genome analyses in 8-month-old monozygotic twins with pro-B CD10− “B other” B-cell precursor (BCP)–acute lymphoblastic leukemia (ALL) that described a common TCF3-ZNF384 rearrangement and distinct converging PTPN11 mutations.1
Bueno et al1 also concluded that the initial prenatal oncogenic event(s) arose in an early hematopoietic fetal pre–B-cell receptor (BCR) progenitor or stem cell, rather than in a prehematopoietic precursor, because the shared and the individual leukemia-specific somatic mutations were not found in cultured bone marrow–derived mesenchymal stem cells and clonal immunoglobulin (Ig) variable diversity joining (VDJ) rearrangements were not identified in leukemic blasts from either twin. We contest this conclusion for 2 reasons.
First, the complex rearrangement leading to the TCF3-ZNF384 fusion resulted from a 3-way t(12;14) and t(14;19) translocation, with chromosome 14 breakpoints compatible with involvement of...