1. Biological consequences of the BCR/ABL fusion gene in humans and mice
- Author
-
M Y Gordon
- Subjects
Fusion Proteins, bcr-abl ,Mice, Transgenic ,Chromosomal translocation ,Mice, SCID ,Biology ,Philadelphia chromosome ,medicine.disease_cause ,Pathology and Forensic Medicine ,Fusion gene ,Mice ,Leukemia, Myelogenous, Chronic, BCR-ABL Positive ,hemic and lymphatic diseases ,medicine ,Animals ,Humans ,neoplasms ,Gene ,ABL ,breakpoint cluster region ,General Medicine ,Hematopoietic Stem Cells ,medicine.disease ,Disease Models, Animal ,Cancer research ,Carcinogenesis ,Tyrosine kinase ,Cell Division ,Research Article - Abstract
The BCR/ABL fusion gene is pathognomonic for the human disease chronic myeloid leukaemia (CML). CML is a malignant myeloproliferative disorder that is characterised at the cytogenetic level by the Philadelphia (Ph) translocation between chromosomes 9 and 22. At the molecular level this results in the juxtaposition of parts of the BCR and ABL genes to form a fusion gene (that is, BCR/ABL). The p210 protein tyrosine kinase product of BCR/ABL is presumed to be responsible for the biological and clinical features of CML in humans. A vast amount of work has been done on the molecular biology and biochemistry of p210 (reviewed in ) but this article is concerned with the cell biological consequences of p210 expression.
- Published
- 1999
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