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Part of the book series: Cancer Treatment and Research ((CTAR,volume 76))

Abstract

Chronic myeloid leukemia (CML) is a relatively common disease mainly afflicting patients older than 40 years. It was the first malignant disease shown to be associated with a change in chromosomal pattern [1,2], and the molecular biology of CML has been intensively investigated [3–6]. It is one of a group of leukemias known to arise because of a translocation that repositions part of the c-ABL proto-oncogene situated on chromosome 9 to a position adjacent to the breakpoint cluster region (BCR) on chromosome 22 [3,4]. This translocation usually produces a distinctively malformed chromosome 22 (referred to as the Ph chromosome) and always creates a length of corrupted genetic information known as the BCR-ABL rearrangement. The resulting fusion gene directs the synthesis of chimeric proteins (p210BCR-ABL or pl90BCR-ABL) with readily detectable in vitro tyrosine kinase activity [5]. It is thought that these proteins arise as a result of different breakpoint locations in the BCR region.

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Clift, R.A. (1995). Marrow Transplantation for Chronic Myeloid Leukemia. In: Buckner, C.D., Clift, R.A. (eds) Technical and Biological Components of Marrow Transplantation. Cancer Treatment and Research, vol 76. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2013-9_1

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