Info

}BCR Jc-ABL

Philadelphia chromosome

9.31 A reciprocal translocation between chromosomes 9 and 22 causes chronic myeloid leukemia.

shortened chromosome 22, called the Philadelphia chromosome because it was first discovered in Philadelphia. At the end of a normal chromosome 9 is a potential cancer-causing gene called c-ABL. As a result of the translocation, part of the c-ABL gene is fused with the BCRgene from chromosome 22. The protein produced by this BCR-c-ABL fusion gene is much more active than the protein produced by the normal c-ABL gene; the fusion protein stimulates increased, unregulated cell division and eventually leads to leukemia.

A third mechanism by which chromosome rearrangements may produce cancer is by the transfer of a potential cancer-causing gene to a new location, where it is activated by different regulatory sequences. Burkitt lymphoma is a cancer of the B cells, the lymphocytes that produce antibodies. Many people having Burkitt lymphoma possess a reciprocal translocation between chromosome 8 and chromosome 2, 14, or 22, each of which carries genes for immunological proteins ( FIGURE 9.32). This translocation relocates a gene called c-MYC from the tip of chromosome 8 to a position in one of the aforementioned chromosomes that is next to a gene for one of the immunoglobulin proteins. At this new location, c-MYC comes under the control of regulatory sequences that normally activate the production of immunoglobulins, and c-MYC is expressed in B cells. The c-MYC protein stimulates the division of the B cells and leads to Burkitt lymphoma.

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