Acute Lymphoblastic Leukemia with Chromosomal Translocation t (5; 14) (q31; q32) and Hypereosinophilia in a Child.
- Author:
Kyong A LEE
1
;
Jin Seok LEE
;
Kyoung Seob SIN
;
Il Hun BAE
;
Sun Hwa LEE
;
Hyeon Jin PARK
Author Information
1. Department of Pediatrics, College of Medicine and Medical Research Institute, Chungbuk National University, Cheong-ju, Korea. hjpark@chungbuk.ac.kr
- Publication Type:Case Report
- Keywords:
Hypereosinophilia;
Acute lymphoblastic leukemia;
t (5;
14) (q31;
q32)
- MeSH:
Child*;
Clone Cells;
Collagen;
Eosinophilia;
Humans;
Hypereosinophilic Syndrome;
Immunoglobulin Heavy Chains;
Interleukin-3;
Leukemia;
Male;
Precursor Cell Lymphoblastic Leukemia-Lymphoma*;
Promoter Regions, Genetic;
Translocation, Genetic*;
Vascular Diseases
- From:Korean Journal of Pediatric Hematology-Oncology
2005;12(1):108-113
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Hypereosinophilia has been associated with a variety of underlying disorders such as parasitic, fungal and mycobacterial infections, allergic disorders, collagen vascular diseases, or hypereosinophilic syndrome (HES). The association of acute lymphoblastic leukemia (ALL) and symptomatic eosinophilia is rare and only a few cases have been reported. HES probably occurs in less than 1% of all patients with ALL. The chromosomal translocation t (5; 14) (q31; q32) was cloned at the molecular level in ALL with eosinophilia. This translocation joined the immunoglobulin heavy chain region to the promoter region of the interleukin-3 (IL-3) gene in opposite transcriptional orientation. The IL-3 gene translocated with the immunoglobulin heavy chain gene may play a central role in the pathogenesis of this leukemia and the associated eosinophilia. We describe a 8-year-old boy who presented with hypereosinophilia and concurrent ALL with t (5; 14).
