A new recurrent and specific cryptic translocation, t (5; 14)(q35; q32), is associated with expression of the Hox11L2 gene in T acute lymphoblastic leukemia
OA Bernard, M Busson-LeConiat, P Ballerini… - Leukemia, 2001 - nature.com
OA Bernard, M Busson-LeConiat, P Ballerini, M Mauchauffe, V Della Valle, R Monni…
Leukemia, 2001•nature.comFISH identified a cryptic t (5; 14)(q35; q32) in T acute lymphoblastic leukemia (ALL),
whereas it was not observed in B ALL samples. This translocation is present in five out of 23
(22%) children and adolescents with T ALL tested. RanBP17, a gene coding for a member of
the importin β protein family, and Hox11Like2, an orphan homeobox gene were mapped
close to the chromosome 5 breakpoints and CTIP2, which is highly expressed during normal
T cell differentiation, was localized in the vicinity of the chromosome 14 breakpoints. The …
whereas it was not observed in B ALL samples. This translocation is present in five out of 23
(22%) children and adolescents with T ALL tested. RanBP17, a gene coding for a member of
the importin β protein family, and Hox11Like2, an orphan homeobox gene were mapped
close to the chromosome 5 breakpoints and CTIP2, which is highly expressed during normal
T cell differentiation, was localized in the vicinity of the chromosome 14 breakpoints. The …
Abstract
FISH identified a cryptic t (5; 14)(q35; q32) in T acute lymphoblastic leukemia (ALL), whereas it was not observed in B ALL samples. This translocation is present in five out of 23 (22%) children and adolescents with T ALL tested. RanBP17, a gene coding for a member of the importin β protein family, and Hox11Like2, an orphan homeobox gene were mapped close to the chromosome 5 breakpoints and CTIP2, which is highly expressed during normal T cell differentiation, was localized in the vicinity of the chromosome 14 breakpoints. The Hox11L2 gene was found to be transcriptionally activated as a result of the translocation, probably under the influence of CTIP2 transcriptional regulation elements. These data establish the t (5; 14)(q35; q32) as a major abnormality, and Hox11 family member activation as an important pathway in T ALL leukemogenesis.
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