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The BCR/ABL hybrid gene.

J Groffen, N Heisterkamp

Bailliere'S Clinical Haematology

|December 1, 1987

Summary

This summary is machine-generated.

The Philadelphia (Ph) translocation in chronic myeloid leukemia (CML) creates a BCR/ABL fusion gene. This fusion produces a novel protein that may drive CML development.

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Area of Science:

Molecular Biology
Genetics
Oncology

Background:

The Philadelphia (Ph) translocation is a hallmark of chronic myeloid leukemia (CML).
This translocation involves breakpoints on chromosomes 9 and 22, specifically within the BCR gene on chromosome 22.

Purpose of the Study:

To investigate the molecular consequences of the Ph translocation in CML.
To identify the genetic and protein products resulting from the BCR/ABL fusion.

Main Methods:

Analysis of DNA from CML patients and cell lines.
Detection and characterization of chimeric BCR/ABL transcripts.
Identification of abnormal ABL protein products.

Main Results:

A specific DNA region, M-BCR, on chromosome 22 is consistently involved in the Ph translocation breakpoint.

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The Ph translocation fuses the 5' portion of the BCR gene with the 3' portion of the ABL oncogene.

Chimeric BCR/ABL mRNA transcripts and abnormally sized BCR/ABL proteins were detected in CML samples.

Conclusions:

The BCR/ABL fusion protein is the likely product of the chimeric mRNA in CML.
The BCR moiety may alter ABL protein activity, potentially conferring transforming capabilities.
The BCR/ABL protein is strongly implicated in the pathogenesis of CML.