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Abstract
Activation of cellular oncogenes by chromosomal translocation has been implicated in the pathogenesis of several malignant disease. One of the most striking example of this phenomenon occur in leukemias involving Philadelphia (ph’) chromosome. The ph’ chromosome is a
shortened chromosome 22 that arise from the reciprocal translocation with chromosome 9;ie~,(9;22) (q34;qll). This cytogenic finding occur in the majority of patients with chronic myelogenous leukemia (CML), and in much smaller proportion of patient with acute lymphoblastic leukemia
(ALL) or acute myeloblastic leukemia (AML). The Ph’ translocation results in a transcription of the cellular protooncogene ABL gene from its usual residence on chromosome 9 to chromosome 22 on the BCR gene. The breakpoint on ABL gene appears to be distributed over an area >200kb between exon Ib and exon 2. The breakpoint in Ph’ chromosome (22q-) is confined to a very small regions (5.8kb) which has been designed the major breakpoint cluster region (M-bcr). This forms a part of a larger gene the BCR gene. the Ph’ translocation results in a fusion of the BeRfABL gene in a head to tail fashion which transcripts a m-RNA that encodes P2l OBCRlABL protein that has a tyrosine kinas activity. This protein appears to be the underlying mechanism of the disease. The use of polymerase chain reaction (PCR) and fluorescent in situ hybridization for the detection of genetic rearrangements in BCR-ABL fusion gene resulting from the t(9:22) and encoding oncoproteins may offer
advantages over cytogentic techniques and furthermore provide a useful tool for monitoring of residual disease.