| 1. |
- Fioretos, Thoas, et al.
(författare)
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Standpoint on imprinting of BCR and ABL
- 1995
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Ingår i: Leukemia. - 1476-5551. ; 9:4, s. 743-744
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Tidskriftsartikel (refereegranskat)abstract
- Cytogenetic studies of Ph-positive leukemic patients and their parents have indicated that chromosome 22 involved in the formation of the t(9;22) is of maternal origin, whereas chromosome 9 is preferentially of paternal origin. These data have suggested that the two genes BCR and ABL, which become fused through the translocation, might be imprinted, ie expressed in a parental-specific manner. Recent molecular genetic studies however, have shown that BCR and ABL are expressed on both alleles and that the maternal and paternal ABL genes contribute equally often to the BCR-ABL fusion messenger. The findings make imprinting of these genes unlikely as an explanatory model and necessitate a combined cytogenetic and molecular genetic study.
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| 2. |
- Johansson, B, et al.
(författare)
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Abberant cytogenetic evolution pattern of Philadelphia-positive chronic myeloid leukemia treated with interferon-alpha
- 1996
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Ingår i: Leukemia. - 1476-5551. ; 10:7, s. 1134-1138
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Tidskriftsartikel (refereegranskat)abstract
- The cytogenetic evolution of 32 Philadelphia (Ph)-positive chronic myeloid leukemias (CML) receiving interferon-alpha (IFN-alpha) therapy was compared to the patterns in untreated CML and cases treated with busulfan (Bu), hydroxyurea (Hy), and allogeneic bone marrow transplantation (BMT). Half of the CML receiving IFN-alpha had at least one of the well-known major or minor route aberrations whereas 16 cases displayed unusual secondary abnormalities, of which only del(7p) and del(13q) were recurrent; a frequency significantly higher than in CML without therapy or after Bu and Hy treatment (P < 0.001) but similar to the one found post-BMT. The incidence of cases with cytogenetically divergent subclones, ie cell populations with unrelated aberrations in addition to the t(9;22), was also higher in the IFN-alpha group compared to the untreated, Bu and Hy groups (P < 0.01) but similar to the post-BMT group. Finally, 14 of the 32 IFN-alpha-treated CML displayed cytogenetic evolution already during the chronic phase; again a higher incidence than in the untreated, Bu and Hy groups (P < 0.001) but not different from the post-BMT group. These findings strongly indicate that IFN-alpha, directly or indirectly, can induce clones with aberrant chromosomal evolution patterns to evolve and proliferate, but the mechanisms underlying these cytogenetic peculiarities remain to be elucidated.
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