The oncogene BCR–ABL1 induces the synthesis of a splice variant of Bruton's tyrosine kinase (BTKp52) that hijacks full-length BTK and transforms B cells.

The oncogene BCR–ABL1 hijacks a B cell signaling protein by inducing the synthesis of a linker protein, according to Feldhahn and colleagues on page 1837. This study helps explain how BCR–ABL1 causes B cell leukemias in humans and identifies a potential new target for drug development.

Translocation events that combine unrelated chromosomal sequences are found in up to 65% of human acute leukemias. One such translocation event creates a chimeric protein between the signaling protein BCR and the tyrosine kinase ABL1. The BCR–ABL1 fusion allows precursor B cells to bypass survival signals from the pre-B cell receptor that are normally required for B cell survival. But exactly how BCR–ABL1 ensures B cell survival in the absence of pre-B cell...

The Rockefeller University Press
2005
The Rockefeller University Press
2005
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