The molecular biology of CML: a review

The t(9;22) generating the Ph1 chromosome in CML creates a new fusion gene (bcr/abl), which combines bcr sequence from chromosome 22 with abl sequence from chromosome 9. This gene generates a new fusion protein which has a much greater protein tyrosine kinase activity than the normal abl protein, an...

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Bibliographic Details
Published inCancer investigation Vol. 7; no. 2; p. 195
Main Authors Leibowitz, D, Young, K S
Format Journal Article
LanguageEnglish
Published England 1989
Subjects
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Oncogenes
Philadelphia Chromosome
Restriction Mapping
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Summary:The t(9;22) generating the Ph1 chromosome in CML creates a new fusion gene (bcr/abl), which combines bcr sequence from chromosome 22 with abl sequence from chromosome 9. This gene generates a new fusion protein which has a much greater protein tyrosine kinase activity than the normal abl protein, and it is this ptk activity which has been shown to be essential for the transforming activity of the v-abl gene and for other related oncogenes which contain the homologous ptk region. The fusion gene is present in almost all patients with CML, including a sizable fraction of the patients with Ph1(-) CML. The Ph1 chromosome and CML have provided one of the most exciting stories of oncogene activation in human malignancy, and much more information, at both the level of basic and of clinical science, will result from the investigations currently underway in a number of laboratories.
ISSN:0735-7907
1532-4192
DOI:10.3109/07357908909038285