Secondary chromosomal changes in 34 Philadelphia-chromosome– positive chronic myelocytic leukemia patients from the Mexican West.

Meza Espinoza, Juan Pablo; Picos Cárdenas, Verónica Judith; Gutiérrez Angulo, Melva; González García, Juan Ramón

Por favor, use este identificador para citar o enlazar este ítem: https://hdl.handle.net/20.500.12104/72571

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Campo DC	Valor	Lengua/Idioma
dc.creator	Meza Espinoza, Juan Pablo	-
dc.creator	Picos Cárdenas, Verónica Judith	-
dc.creator	Gutiérrez Angulo, Melva	-
dc.creator	González García, Juan Ramón	-
dc.date	2015-08-17T14:31:38Z	-
dc.date	2015-08-17T14:31:38Z	-
dc.date	2004	-
dc.date.accessioned	2019-04-07T23:48:12Z	-
dc.date.available	2019-04-07T23:48:12Z	-
dc.identifier	0165-4608	-
dc.identifier	DOI:10.1016/S0165-4608(03)00283-8	-
dc.identifier	http://repositorio.cualtos.udg.mx:8080/jspui/handle/123456789/374	-
dc.identifier.uri	https://hdl.handle.net/20.500.12104/72571	-
dc.description	The clonal evolution in t(9;22)-positive chronic myelocytic leukemia (CML) is well established. Four major changes occur in more than 70% of patients: +8, i(17q), +19, and an extra Philadelphia chromosome. The frequencies of secondary chromosomal changes in 34 patients from the states of Jalisco, Nayarit, Michoacán, and Colima (the Mexican West) with Philadelphia-chromosome–positive CML were assessed. The most frequent abnormalities were tetraploidy (12 cases); +8, inv(3)(q21q26), and octoploidy (3 cases each); and +der(22)(2 cases). Some translocations not previously associated with CML were observed, such as t(2;7)(p12;q36), t(3;6)(q26;p25), t(3;17)(q26;p13), and t(6;17)(q21;q23∼q25). Significant differences were found for +8 with respect to population results from Japan and from southern, eastern, and western Europe; for i(17)(q10) from eastern Europe; for +19 from Japan and western Europe; and for +der(22) from Japan, southern Europe, and western Europe. Although polyploidy could result from endomitosis, there is no direct evidence that the BCR/ABL protein influences such a process; however, protein kinases such as MAPK, which are involved in endomitosis, are activated by the BCR/ABL protein, and so the BCR/ABL protein could promote endomitosis through the MAPK pathway.	-
dc.description	Doctorado en Genética Humana, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico Laboratorio de Citogenética, División de Genética, Centro de Investigación Biomédica de Occidente, Centro Médico Nacional de Occidente,Instituto Mexicano del Seguro Social (CIBO-IMSS), Guadalajara, Jalisco, Mexico	-
dc.language	en	-
dc.publisher	Elsevier Inc.	-
dc.relation	Cancer Genetics and Cytogenetics;148 (2004) 166–169	-
dc.title	Secondary chromosomal changes in 34 Philadelphia-chromosome– positive chronic myelocytic leukemia patients from the Mexican West.	-
dc.title	Short communication	-
dc.type	Article	-
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