José Alexandre Rodrigues de Lemos, Ciane Martins de Oliveiraz, Ana Carolina Costa Scerni, Alessandra Q. Bentes, Ana Cristina Beltrão, Iê Regina G. Bentes, Tereza Cristina Azevedo, Luciana Maria Cunha Maradei-Pereira
Published December 27, 2005
Genet. Mol. Res. 4 (4): 803-811 (2005)

About the Authors
José Alexandre Rodrigues de Lemos, Ciane Martins de Oliveiraz, Ana Carolina Costa Scerni, Alessandra Q. Bentes, Ana Cristina Beltrão, Iê Regina G. Bentes, Tereza Cristina Azevedo, Luciana Maria Cunha Maradei-Pereira

Corresponding author
J.A.R. Lemos
Email: lemos@ufpa.br

ABSTRACT

Chronic myeloid leukemia (CML) originates from the hematopoietic stem cell and is characterized by the reciprocal translocation t(9;22)(q34;q11), which results in the BCR-ABL fusion gene on chromosome 22q-, also known as the Philadelphia chromosome. This chimeric gene codes for a cytoplasmic protein with constitutive tyrosinekinase activity, responsible for cellular transformation and leukemogenesis in CML. The aim of this observational cohort study was to discriminate and quantify BCR-ABL transcripts in the peripheral blood of patients with CML who were treated with imatinib mesylate (Glivec®, Novartis). Twenty-two patients were followed for six months during treatment. Quantitative real time polymerase chain reaction was performed before treatment and after 3 and 6 months from treatment initiation. As compared with the third month, there was a significant decrease in BCR-ABL expression in the sixth month of treatment (P = 0.0002). At the sixth month, there was a significant difference in the levels of the two major transcripts of BCR-ABL, B2A2 and B3A2 (P = 0.0347), indicating that B2A2 may be more sensitive to imatinib. The results of our study indicate that imatinib is able to modify the natural history of CML, and raise the hypothesis that patients who express the B2A2 transcript may have a better prognosis.

Key words: Chronic myeloid leukemia, Imatinib mesylate, RQ-PCR.