Activation of the interleukin-3 gene by chromosome translocation in acute lymphocytic leukemia with eosinophilia [see comments]

Abstract

The t(5;14)(q31;q32) translocation from B-lineage acute lymphocytic leukemia with eosinophilia has been cloned from two leukemia samples. In both cases, this translocation joined the IgH gene and the interleukin-3 (IL-3) gene. In one patient, excess IL-3 mRNA was produced by the leukemic cells. In the second patient, serum IL-3 levels were measured and shown to correlate with disease activity. There was no evidence of excess granulocyte/macrophage colony stimulating factor (GM-CSF) or IL-5 expression. Our data support the formulation that this subtype of leukemia may arise in part because of a chromosome translocation that activates the IL-3 gene, resulting in autocrine and paracrine growth effects.

Cutaneous B‐lymphoblastic lymphoma with IL3/IgH translocation presenting with hypereosinophilia and acute endocarditis

“…The cytogenetic abnormalities identified in ALL associated with hypereosinophilia are varied [7]. In a small number of reported cases, the translocation t(5;14)(q31;q32) has been identified in the underlying leukaemia [6,[8][9][10][11]15]. Alternative more complex rearrangements and deletions involving the long arm of chromosome 5 have also been seen [16,17].…”

“…In childhood, the best recognized, albeit rare, malignant association is that between hypereosinophilic syndrome and acute lymphoblastic leukaemia (ALL) [1,[3][4][5][6][7][8][9][10][11]. In this setting, the reactive hypereosinophilia may precede, accompany or occasionally follow the diagnosis of ALL.…”

Identifying Global Health Competencies to Prepare 21st Century Global Health Professionals: Report from the Global Health Competency Subcommittee of the Consortium of Universities for Global Health

“…22 Nutrition Many public health nutrition programs identify competencies relevant to global health, but the most comprehensive reference was a report developed by the World Public Health Nutrition Association which identified specific competencies for global public health nutrition. 23…”

Further evidence for the clonal nature of the idiopathic hypereosinophilic syndrome: complete haematological and cytogenetic remission induced by interferon‐alpha in a case with a unique chromosomal abnormality

“…Interleukin-3 (IL-3), GM-CSF and interleukin-5 (IL-5) are three cytokines with a marked capacity to increase eosinophil production, activation and degranulation, hence participating in the local inflammatory responses and eosinophil-mediatedtissue damage (Fauci et al, 1982;Liesveld & Abboud, 1991). As the genes encoding for GM-CSF, IL-3 and IL-5 reside on the long arm of chromosome 5 (GM-CSF and IL-3 on 5q23-31 and IL-5 on 5q31) (Meeker et al, 1990;Prin et al, 1991), it may be that through an unidentified mechanism the chromosomal translocations resulted in excess production of these cytokines, causing hypereosinophilia. Activation of the IL-3 gene by a chromosomal translocation has been described before in acute lymphocytic leukaemia with eosinophilia (Meeker et al, 1990).…”

“…As the genes encoding for GM-CSF, IL-3 and IL-5 reside on the long arm of chromosome 5 (GM-CSF and IL-3 on 5q23-31 and IL-5 on 5q31) (Meeker et al, 1990;Prin et al, 1991), it may be that through an unidentified mechanism the chromosomal translocations resulted in excess production of these cytokines, causing hypereosinophilia. Activation of the IL-3 gene by a chromosomal translocation has been described before in acute lymphocytic leukaemia with eosinophilia (Meeker et al, 1990).…”