Localization of the c-abl oncogene adjacent to a translocation break point in chronic myelocytic leukaemia

Abstract

The human c-ab1 oncogene maps within the region (q34-qter) of chromosome 9 which is translocated to chromosome 22, the Philadelphia (Ph') chromosome, in chronic myelocytic leukaemia (CML). The position of the Ph' chromosomal break point is shown to be variable and, in one CML patient, has been localized immediately 5' of, or within, the c-ab1 oncogene. A DNA restriction fragment corresponding to this site has been molecularly cloned and shown to represent a chimaeric fragment of DNA from chromosomes 9 and 22.

Review of clinical, cytogenetic, and molecular aspects of Ph-negative CML

“…We have also performed immunoblotting studies to search for EBV-encoded proteins in extracts of tissues from 15 male patients who died of IM [17]. Use of in situ hybridization techniques specific for EBV [18] permits us to identify EBV genome in archival tissues, and use of the polymerase chain reaction [19,20] enables detection of low levels of EBV in blood [21]. hnmunoglobulin levels are quantitated in plasma by radial immunodiffusion (RID) (Kallsted, Austin, TX) or in serum by nephelometry (Beckman ICS, Brea, CA).…”

Deciphering the Key Features of Malignant Tumor Microenvironment for Anti-cancer Therapy

“…The BCR-Abl and Abl-NUP24 fusion proteins derived from chromosomal translocation have constant tyrosine kinase activity in the absence of growth factors, and these oncogenic proteins constitutively activate Abl down-stream signal cascades, resulting in leukemia and genesis of the TME [24][25][26].…”

Characterization of the Different BCR-ABL Transcripts with a Single Multiplex RT-PCR

“…This chromosome, a shortened chromosome 22, results from a t(9;22)(q34;11) reciprocal translocation, allowing the fusion of the 3Ј region of the protooncogene c-ABL (9q34) with the 5Ј region of the BCR (breakpoint cluster region) gene on chromosome 22q11. 1 The Philadelphia chromosome was the first chromosome abnormality to be associated with a specific human disease of malignant origin. The different fusion proteins encoded by BCR-ABL vary in size depending on the breakpoint in the BCR gene but share a high tyrosine kinase activity, in part responsible for the leukemogenesis.…”