Send to

Choose Destination
Arch Med Res. 2001 May-Jun;32(3):202-7.

Cytogenetics in acute lymphoblastic leukemia in Mexican children: an institutional experience.

Author information

Departamento de Investigación en Genética Humana, Instituto Nacional de Pediatría, Mexico City, Mexico.



Cytogenetic studies in acute lymphoblastic leukemia (ALL) have identified numerical and structural chromosomal abnormalities related to the disease's pathophysiologic characteristics. These findings correlate with prognosis and response to treatment in ALL patients. The purpose of this study was to define the frequency of chromosomal abnormalities in a group of Mexican children with ALL and to compare these data with those reported in the literature.


Bone marrow chromosome studies with GTG bands were performed in 150 pediatric patients with ALL who were naive to antileukemic treatment and aged from 5 months to 16 years; the majority was diagnosed as L1.


Among 131 patients, 30 (22.9%) karyotypes were normal and the remaining 101 (77.1%) had abnormal karyotypes with numerical and/or structural abnormalities. Among patients with numerical abnormalities, the most frequent karyotypes were hyperdiploidy with 51-65 chromosomes (30 patients) and hyperdiploidy with 47-50 chromosomes (18 patients). Among recurrent, non-random, and primary structural abnormalities, the most frequent was t(9;22), followed by t(1;19). Aberrations involving band 11q23 were not detected, and only one of two patients with L3 had the t(8;14). Of the secondary non-random abnormalities, dup(1q), del(6q), and i(7)(q10) were found.


The frequency and type of chromosomal abnormalities found was comparable to those reported in the literature with similar methodology and pediatric populations; however, the number of cases analyzed should be increased to create a database of Mexican children with ALL, and several patients require molecular analysis to identify chromosomal abnormalities not detected through conventional cytogenetic studies.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center