Martinez-Serra, Jordidel Campo Garcia, RaquelGutierrez, AntonioAntich, Jose LuisGinard, MagdalenaDuran Pastor, Maria AntoniaBento, LeyreRos, TeresaAmat, Juan CVidal, CarmenIglesias, Julio FOrlinska, IzabelaBesalduch Vidal, Juan2024-07-032024-07-032014Martinez-Serra J, Del Campo R, Gutierrez A, Antich JL, Ginard M, Duran MA, et al. Chronic myeloid leukemia with an e1a3 BCR-ABL fusion protein: transformation to lymphoid blast crisis.. Biomark Res. 2014;2:14.2050-7771http://hdl.handle.net/20.500.13003/17107http://hdl.handle.net/20.500.12105/19952Chronic myelogenous leukemia (CML) results from the neoplastic transformation of a hematopoietic stem cell. CML is cytogenetically characterized by the presence of the Philadelphia chromosome (Ph'). Most patients with CML express e13a2 or e14a2 mRNAs that result from a rearrangement of the major breakpoint cluster regions (M-BCR) generating the 210-kDa (p210BCR-ABL) fusion proteins b2a2 or b3a2 respectively. The e1a3 CML-related atypical translocation has been reported with an indolent clinical course, low leukocyte count, long chronic phase even without treatment and good response to therapy. We report the case of a patient initially diagnosed as CML in chronic phase whose cells expressed the e1a3 variant. The patient readily responded to imatinib 400mg with the achievement of a rapid complete cytogenetic response and the normalization of the blood count values, but after 5months transformed into lymphoid blast crisis.enghttp://creativecommons.org/licenses/by/4.0/ALLCMLbcr-able1a3research articleAttribution 4.0 International2519755421410.1186/2050-7771-2-14Biomarker Researchopen access2-s2.0-85006228432L603849551