Figure 6-3. (continued) (B) Subsequent hybridization with probes specific for chromosome 17 centromere (green) and p53 (red) shows the rearrangement to be more complex. The der(5) is a dicentric chromosome with an inactive centromere (centromeres indicated with arrows); p53 has been lost as a result of the rearrangement. (C) Although not found as frequently in CLL as in some other hematologic malignancies, a dicentric isochromosome for the long arm of chromosome 17 also results in the loss of p53 in this CLL patient. In the partial metaphase shown, two separate centromere signals, but no p53 signal, are visible on the isochromosome to the left, whereas both can be seen on the normal chromosome 17 to the right.

proteoasomic degradation. Overexpression of MDM2 mRNA and/or protein in CLL has been shown in several studies.39-41 However, neither the mechanism of overexpression nor the clinical significance is understood. MDM2 function is also inhibited by the ARF tumor suppressor gene encoded at the p16/ARF locus on chromosome 9p21. Loss of ARF function enables MDM2 to inhibit p53, but the role of this pathway in CLL has yet to be established.

Table 6-3. p53 Mutation or Deletion in Chronic

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