Abstract: bcr-abl Fusion gene is the pathogenic gene in chronic myelogenous leukemia, localized at t (9; 22) (q34; q11). Part of the cellular abl proto-oncogene is transposed from its normal residence on q34 of chromosome 9 to q11 of chromosome 22, which is the breakpoint cluster region, and results in the creation of this abnormal fusion gene on chromosome 22. In most cases, the breakpoints on chromosome 22 are restricted to the 5.8 kb M-BCR. This kind of fusion produces two dominant forms of transcripts, b2a2 and b3a2, with 75 bp or 25 aa difference in length. The presence of bcr-abl fusion gene has important diagnostic and prognostic implications in CML. The results of Southern blot and FISH confirm the existence of bcr-abl fusion gene in Ph negative or variant Ph patients. Many new types of junction are observed with these methods. They also reveal that the relapses of leukemic blasts are of host-MRL (minimal residual leukemia) origin. Optimized RT-PCR, quantificated RT-PCR and RNA in situ hybridization are available to detect rare or mixed variants junctions. They also reveal the presence of bcr-abl transcripts in normal blood cells and indicate a significant tendency to increase in frequency with age. The results of BCR-ABL protein Western blot or ELISA demonstrate that the level of BCR-ABL expression in samples from peripheral blood is similar to that in marrow, and the ratio of BCR-ABL/ABL proteins is nearly linear to the percentage of Ph+ cells. The dual expression of P190 and P210 types of BCR-ABL is a factor indicating a poor prognosis.
Publication Year: 1998
Publication Date: 1998-01-01
Language: en
Type: article
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