Figure 5.
Figure 5. Model for the role of deletions of the derivative chromosome 9 in the progression of CML. In patients without deletions, the BCR-ABL gene rearrangement and resultant expression of BCR-ABL protein initiates the chronic phase of the disease. Blast crisis develops with the accumulation of further mutations. However, in the subset of patients with deletions, the recombination event produces not only the translocation but also a deletion (black bar) with the resultant loss of one or more tumor suppressor genes (TSG) from the derivative chromosome 9. The time to blast crisis is therefore reduced since fewer additional mutations are required.

Model for the role of deletions of the derivative chromosome 9 in the progression of CML. In patients without deletions, the BCR-ABL gene rearrangement and resultant expression of BCR-ABL protein initiates the chronic phase of the disease. Blast crisis develops with the accumulation of further mutations. However, in the subset of patients with deletions, the recombination event produces not only the translocation but also a deletion (black bar) with the resultant loss of one or more tumor suppressor genes (TSG) from the derivative chromosome 9. The time to blast crisis is therefore reduced since fewer additional mutations are required.

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