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  • Title: CML: a model for targeted therapy.
    Author: Cilloni D, Saglio G.
    Journal: Best Pract Res Clin Haematol; 2009 Sep; 22(3):285-94. PubMed ID: 19959080.
    Abstract:
    The discovery of the Philadelphia (Ph) chromosome represented the first step towards understanding the molecular basis of haematological malignancies. Subsequent developments including the characterisation of t(9;22)(q34;q11) translocation, the identification of the breakpoint cluster region as well as the demonstration that retrovirally mediated insertion of a human BCR-ABL gene into murine haematopoietic stem cells induced a leukaemia-like picture and the creation of BCR-ABL transgenic mice established the central role of BCR-ABL in chronic myeloid leukaemia (CML) beyond all reasonable doubt. Many years later an important goal was achieved, that is, the use of BCR-ABL as a therapeutic target. However, it is uncertain whether the BCR-ABL fusion gene is really the initiating lesion for the chronic phase of CML. There is an incomplete understanding of the so-called genomic instability that underlies the production of the fusion gene and predisposes the Ph-positive clone to acquire further genetic events leading to advanced-phase disease.
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