t(14;19)(q32;q13): A recurrent translocation in B‐cell precursor acute lymphoblastic leukemia

Abstract

The recurrent t(14;19)(q32;q13) translocation associated with chronic B-cell lymphoproliferative disorders, such as atypical chronic lymphocytic leukemia, results in the juxtaposition of the IGH@ and BCL3 genes and subsequent overexpression of BCL3. We report six patients with B-cell precursor acute lymphoblastic leukemia who have a cytogenetically identical translocation with different breakpoints at the molecular level. Fluorescence in situ hybridization with locus-specific probes confirmed the involvement of the IGH@ gene but showed that the breakpoint on 19q13 lay outside the region documented in t(14;19)(q32;q13)-positive chronic lymphocytic leukemia. This newly described translocation constitutes a distinct cytogenetic subgroup that is confined to older children and younger adults with B-cell precursor acute lymphoblastic leukemia.

Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL)

“…[36][37][38][39] While the involvement of IGH was confirmed by fluorescence in situ hybridization (FISH), the partner genes were unknown. In the t(14;19)(q32;q13) patients the involvement of BCL3, rearranged with IGH in chronic lymphocytic leukemia (CLL) and other mature B-cell malignancies was excluded.…”

t(6;14)(p22;q32): a new recurrent IGH@ translocation involving ID4 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL)

“…Rearrangements involving the immunoglobulin heavy chain locus (IGH@) at chromosome band 14q32 are frequently observed in mature B-cell neoplasms, 1,2 although a number are now emerging in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). [3][4][5][6][7][8][9][10] The translocation, t(6;14)(p22;q32), has been reported in 2 independent cases of BCP-ALL. 7,8 It was shown that as a consequence of juxtaposing to the IGH@ enhancer, the partner gene, ID4, was overexpressed.…”

Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia

“…One such translocation, t(14;19)(q32;q13), has been previously described in 6 patients with BCP-ALL, in which the breakpoint on chromosome 19 differs from the t(14;19)(q32;q13) identified in mature B-cell malignancies. 12 The Groupe Francophone de Cytogénétique Hématologique (GFCH) has collected 8 additional patients for hematologic, cytogenetic, and molecular studies. Here we report that this translocation involves the CEBPA gene on chromosome 19, resulting in a marked up-regulation of its expression and the production of an apparently normal CEBPA protein.…”