Are submicroscopic chromosomal inversions predisposing factors for the t(9;22)(q34;q11.2) translocation in chronic myeloid leukemia?
A complex chromosomal rearrangement observed in a patient with chronic myeloid leukemia was explained as the consequence of a multistep process. The explanation involved an initial t(9;22) translocation with breakpoints distant from the BCR and ABL1 genes followed by genomic deletions that produced the BCR-ABL1 hybrid gene. We present an alternative model that fits the origin of the patient's rearrangement better. The present model links submicroscopic inversions with the occurrence of the t(9;22) translocation and opens a new approach on the research on the disease.
División de Genética, CIBO-Instituto Mexicano del Seguro Social, Sierra Mojada # 800, Colonia Independencia, CP 44340 Guadalajara, Jalisco México.
Juan Ramón
JR
González García
División de Genética, CIBO-Instituto Mexicano del Seguro Social, Sierra Mojada # 800, Colonia Independencia, CP 44340 Guadalajara, Jalisco México ; Doctorado en Genetica Humana, CUCS-Universidad de Guadalajara, Guadalajara, Jalisco México.
Martín Daniel Domínguez
MD
Cruz
División de Genética, CIBO-Instituto Mexicano del Seguro Social, Sierra Mojada # 800, Colonia Independencia, CP 44340 Guadalajara, Jalisco México ; Doctorado en Genetica Humana, CUCS-Universidad de Guadalajara, Guadalajara, Jalisco México.
César Borjas
CB
Gutiérrez
Chronic myeloid leukemia; Duplicons; Non-allelic homologous recombination; Submicroscopic inversion; t(9;22) translocation