Browsing by Author "Cabrera, ME"

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    Analysis of the complementary determining region III of the immunoglobulin heavy chain locus in acute lymphoblastic leukemia in Chilean children
    (1996) Barriga, FJ; Risueno, C; Patillo, JC; Andrade, W; Cabrera, ME; Beressi, V; DelBorgo, P; Salgado, C; Becker, A; Campbell, M; Bertin, P
    We have analyzed the sequence of 40 VDJ rearrangements of the immunoglobulin heavy chain gene locus on 32 unselected children from Chile with precursor B cell ALL at diagnosis. Rearrangements were derived by PCR with VH gene family-specific primers and sequenced directly. The number of VDJ rearrangements, and the pattern of VH, DH and JH gene usage was identical to the one reported by groups from developed countries. CDR3 regions represented an unbiased repertoire; VH to JH joinings were in frame in 36% of cases. Absent N nucleotides in the DJ border, suggestive of fetal origin of ALL, were seen in 9/40 rearrangements but they did not correlate with younger age. More than one rearrangement was sequenced in six patients, representing independent events with no signs of clonal evolution. One patient was analyzed at first bone marrow relapse showing persistence of one rearrangement and evolution of a second one which conserved the DJ border. The subset of B cell precursors which suffer malignant transformation to ALL appear to be common in different parts of the world.
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    Discordant clinical presentation and outcome in infant twins sharing a common clonal leukaemia
    (1996) Campbell, M; Cabrera, ME; Legues, ME; Ridge, S; Greaves, M
    We report the different presentation features and clinical outcome between two identical infant twins with acute lymphoblastic leukaemia with a shared clonal disease and MLL gene rearrangement. One twin relapsed and died, but the other is in complete remission >4 years after diagnosis. These data, and Similar observations on other twin infants with leukaemia, suggest that despite a common clonal in utero, post-natally these leukaemias can evolve independently, at different rates, in the twinned individuals, and that the usually fatal leukaemia associated with t(4;11) MLL gene rearrangement can be effectively treated when the leukaemic burden is small.
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    Rapid intraclonal switch of lineage dominance in congenital leukaemia with a MLL gene rearrangement
    (1995) Ridge, SA; Cabrera, ME; Ford, AM; Tapia, S; Risueno, C; Labra, S; Barriga, F; Greaves, MF
    We describe a case of neonatal mixed lineage leukaemia which presented with a dominant B progenitor lymphoblast population plus a minor monocytic component. Treatment of the patient with corticosteroid and Ara-C resulted in loss of lymphoblasts and a rapid (within 7 days) increase and dominance of the monocytic component. The common clonal origin of the two cell types was evident from the identical rearrangement in the MLL gene and a shared rearrangement of one IGH allele. In common with other neonatal or infant ALL with MLL gene rearrangements, this leukaemia may have originated in a common B-monocytic lineage stem cell during foetal haemopoiesis. The observations further suggest that the therapeutic impact of the MLL gene rearrangement is to some extent dependent on the cellular context in which it is expressed.