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• W1019309969 abstract "Chronic myeloid leukemia (CML) is a hematopoietic stem cell disorder that accounts for approx 20% of all cases of leukemia (1). The death rate attributed to CML is 1.5/ 100,000/yr (2). CML is characterized by a specific chromosomal abnormality referred to as the Philadelphia chromosome (Ph1) (3,4). The Ph1 results from the reciprocal translocation of the c-abl proto-oncogene on the long arm of chromosome 9 (g34.1) to the 5.8 kb breakpoint cluster region (bcr) on the long arm of chromosome 22 (q11.21). The resulting bcr-abl oncogene produces an 8.5-kb messenger ribonuclease (mRNA), which encodes for a 210-kDa fusion protein (p210) (5). Depending on whether c-abl is between exon 2 or exon 3 of bcr, two different mRNAs may be formed: b2/a2 or b3/a2 (6). The two different mRNAs encode for an identical fusion protein, p210 (7), which has increased tyrosine kinase activity, compared to the normal c-abl protein (8). Cells transfected with bcr-abl cDNA have a demonstrated growth advantage over normal hematopoietic cells (9), which may be very important to the development and maintenance of CML." @default.
• W1019309969 created "2016-06-24" @default.
• W1019309969 creator A5089893290 @default.
• W1019309969 date "2000-01-01" @default.
• W1019309969 modified "2023-09-23" @default.
• W1019309969 title "Stem Cell Transplantation for Chronic Myeloid Leukemia" @default.
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• W1019309969 doi "https://doi.org/10.1007/978-1-59259-657-7_6" @default.
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