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Blood, 15 September 2000, Vol. 96, No. 6, pp. 2254-2261
NEOPLASIA
The incidence of clonal T-cell receptor rearrangements in B-cell
precursor acute lymphoblastic leukemia varies with age and
genotype
Caren Brumpt,
Eric Delabesse,
Kheira Beldjord,
Frederic Davi,
Jean-Michel Cayuela,
Corinne Millien,
Patrick Villarese,
Pierre Quartier,
Agnes Buzyn,
Françoise Valensi, and
Elizabeth Macintyre
From the Department of Biological and Clinical
Hematology, and CNRS UMR8603, Hôpital Necker-Enfants
Malades and Université Paris V; Biological Hematology,
Hôpital de La Pitié-Salpêtrière; and Biological
Hematology, Hôpital Saint-Louis; Paris, France.
B-cell precursor acute lymphoblastic leukemias (BCP-ALLs) are
increasingly treated on risk-adapted protocols based on presenting clinical and biological features. Residual molecular positivity of
clonal immunoglobulin (IG) and T-cell receptor
(TCR) rearrangements allows detection of patients at an
increased risk of relapse. If these rearrangements are to be used for
universal follow-up, it is important to determine the extent to which
they are informative in different BCP-ALL subsets. We show that
IGH V-D-J rearrangements occur in 89% of 163 BCP-ALL, with
no significant variation according to age or genotype (BCR-ABL,
TEL-AML1, MLL-AF4, and E2A-PBX1). In contrast,
TCRG rearrangements, which occur in 60% of patients overall, are frequent in BCR-ABL and TEL-AML1,
are less so in MLL-AF4, and are virtually absent in infants
aged predominantly from 1 to 2 years and in E2A-PBX1 ALLs.
Incidence of the predominant TCRD V 2-D3 rearrangement
decreases with age but is independent of genotype. These differences
are not due to differential recombination activating gene activity, nor
can they be explained adequately by stage of maturation arrest.
Analysis of MLL-AF4 BCP-ALL is in keeping with
transformation of a precursor at an early stage of ontogenic
development, despite the adult onset of the cases analyzed. We
postulate that the complete absence of TCRG rearrangement in E2A-PBX1 cases may result from deregulated E2A function.
These data also have practical consequences for the use of
TCR clonality for the molecular follow-up of
BCP-ALL.
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