Estudio de pacientes diagnosticados con Leucemia Mielógena Crónica tratados con STI 571 (Gleevec) en Ecuador

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César Paz y Miño
Melissa Arévalo
María Eugenia Sánchez
Claudio Cañizares
María José Muñoz
Paola E Leone

Abstract

The main marker of Chronic Myeloid Leukemia (CML) is considered to be the translocation t(9;22) or Ph chromosome, which occurs in 90-95% of patients with CML. One of the most effective treatments is Gleevec whose target is Ph positive cells. An advantage of this new drug is the differentiation between normal and abnormal cells, and the induction of apoptosis. Thirty-one patients were studied: 13 in chronic phase, 12 in accelerated phase, and 6 in blast crisis over 1 year. Hematological remission was obtained in all cases of chronic phase, but approximately 50% of patients in accelerated phase and blast crisis responded. Cytogenetic remission occurred in 79% of the chronic phase and varied from 17 to 32% in the accelerated phase and blast crisis. There was no molecular remission in any patient. Genetic analysis is a good tool to determine the efficacy of treatment and monitoring of leukemia cases.

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How to Cite
1.
Paz y Miño C, Arévalo M, Sánchez ME, Cañizares C, Muñoz MJ, Leone PE. Estudio de pacientes diagnosticados con Leucemia Mielógena Crónica tratados con STI 571 (Gleevec) en Ecuador. REMCB [Internet]. 2017Aug.9 [cited 2024Jul.3];28(1-2):7-10. Available from: https://remcb-puce.edu.ec/remcb/article/view/196
Section
Artículos Científicos

References

NAKAMURA, K.; MYASHITA, T.; OZAKI, M.; IWAYA, M.; NAKAZA­WA, S.; OKAMURA, J.; KAMADA, N.; TANAKA, K.; KOBAYASHI, N. & MIZUTANI, S. 1991. Molecular stud­ies of Chronic Myelogenous Leukemia usíng the polimerase chain reaction. Caneer; 68:2426-2430.

BUCHDUNGER, E.; MATTER, A. & DRUKER, B. J. 2001. Bcr-Abl inhibí­tion as a modality of CML therapeu­tieso Bioehim Biophys Acta; 1551:M1I M18.

MAURO, M. J. & DRUKER, B. J. 2001. STI571: Targeting BCR-ABL as thera­py for CML. Oneologist; 6:233-238.

DRUKER, B. J.; TALPAZ, M.; RESTA, D. J.; BIN-PENG, R. N.; BUCH­ DUNGER, E.; FORD, J. M.; LYDON, N. B.; KANTARJIAN, H.; CAPDEV­ILLE, R.; OHNO-JONES, S. & SAWYERS. 2001. Efficaey and safety inhibitor of the BCR-ABL tyrosine kinase in chronic myeIoid leukemia. D New Engl J Med, 344:1031-1037.

DOBROVIC, A.; MORLEY, A. A.; SESHADRl, R. & JANUSZEWICZ, E. H. 1991. Molecular diagnosis of philadelphia negative CML using the polymerase chain reaction and DNA analysis: clínical features and course of Mbcr negative and M-ber positíve CML. Leukemia, 5:187-190.

CORTES, J. E.; TALPAZ, M.; BERAN, M.; O'BRIEN, S. M.; RIOS, M. B. & KANTARJIAN, H. M. 1995. Philadelphia chromosome. Negative Chronic Myelogenous Leukemia with rearrangement of the breakpoint cluster region. Cancer, 75:434-469.

YAISH, P.; GAZIT, A. & GILON, C. 1988. Blocking ofEGF~dependent cell proliferation by EGF receptor kinase inhibitors. Science, 242:933-935.

PAZ Y MIÑO, c.; BURGOS, R.; MORIL­LO, S. A.; SANTOS, 1. c.; FIALLO, B. F. & LEONE, P. E. 2002. BCR-ABL rearrangement frequencies in chronic myeloid leukemia and acute lymphoblas­tic leukemia in Ecuador. Cancer Genel Cylogen;123, 65-67.