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Revista Cubana de Hematología, Inmunología y Hemoterapia
versión On-line ISSN 1561-2996
Resumen
PAVON MORAN, Valia et al. Chronic myeloid leukemia: Updating in cytogenetics and molecular biology. Rev Cubana Hematol Inmunol Hemoter [online]. 2005, vol.21, n.2, pp. 0-0. ISSN 1561-2996.
Chronic myeloid leukemia (CML) is a a chronic myeloproliferative syndrome of clonal nature, originated in the stem cell, that results in an excessive number of myeloid cells in all the maturation stages. It was the first malignat disease in which an acquired genetic abnormality was proved, and it is at present the best studied molecular model of leukemia. In the chronic myeloid leukemia, it is expressed the chromosal translocation t (9;22) (q34;q11), giving rise to the formation of the Philadelphia (Ph) chromosome. Due to this translocation, 2 new hybrid genes are produced: BCR-ABL in chromosome 22q- or Ph chromosome, and the reciprocal gene ABL-BCR in the derivative chromosome 9q+, which , although transcriptionally active, does not seem to play any functional activity in the disease. Nowadays, the identification of the minimal residual disease by molecular methods is very important for the exact evaluation of the evolutive state of the disease
Palabras clave : Chronic myeloid leukemia; BCR-ABL; Philadelphia chromosome; FISH.