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Oncogenes and their involvement in chronic myelogenous leukemia

This review highlights recent developments in the oncogene field relating to the molecular biology of chronic myelogenous leukemia (CML). At least 90% of patients diagnosed with CML carry an abnormal chromosome within their tumor cells. This chromosome is known as the Philadelphia chromosome. It results in most cases from an exchange of genetic material between chromosomes 9 and 22. As a result of this exchange the cellular abl gene from chromosomes 9, which is related to a viral oncogene, becomes fused to a region of chromsome 22 called the breakpoint cluster region (bcr). The hybrid bcr‐abl gene is believed to play an important role in the disease process. The product of the fused bcr and abl genes is a 210,000 mol. wt. protein termed P210bcr‐abl. It has an associated protein kinase activity that phosphorylates tyrosine residues. Tyrosine protein kinases are thought to play an important role in the formation of tumors by rapidly acting RNA tumor viruses such as Abelson mouse leukemia virus. This virus has acquired part of the cellular abl gene from the mouse genome; viral infected tumor cells express a hybrid protein called P120gag‐abl, a tyrosine kinase believed to be responsible for the tumor phenotype. Similarly, P210bcr‐abl may play a key role in maintaining the tumor properties of leukemic cells of the CML patient.