Revista Brasileira de Hematologia e Hemoterapia
Print version ISSN 1516-8484
ANDRADE, Gabriela V.. P190 BCR-ABL role in myeloid chronic leukemia relapse. Rev. Bras. Hematol. Hemoter. [online]. 2008, vol.30, n.4, pp. 297-302. ISSN 1516-8484. http://dx.doi.org/10.1590/S1516-84842008000400013.
Chronic myeloid leukemia (CML) is a myeloproliferative clonal disorder caused by a mutation in a stem cell, resulting in the proliferation and accumulation of myeloid cells and their progenitors. The Philadelphia chromosome (Ph1) is a result of a mutual translocation of genetic material between the abl gene (Abelson murine leukemia) in chromosome 9 and bcr gene (breakpoint cluster region) in chromosome 22, resulting in the formation of the chimerical gene, BCR-ABL. In this work 45 patients were sequentially followed up in individual periodic evaluations, and 360 samples were selected and analyzed by PCR using the qualitative technique for isoforms characteristic of P210CR-ABL (b3a2 and b2a2) and P190BCR-ABL (e1a2). In our pre-bone marrow transplant study, a prevalence of isoforms characteristic of CML was observed (b3a2 and/or b2a2), a fact essential for the patients to be followed up within the CML protocol. The e1a2 isoform, characteristic of LLA, was detected in 11 patients together with the isoforms characteristic of CML. The detection of the e1a2 transcript was evaluated in respect to its probable role in LMC and was one of the parameters evaluated in this study.
Keywords : Leukemia; leukemia research; chronic myeloid leukemia; polymerase chain reaction; kinase tyrosine.