October 13, 1988New England Journal of Medicine
The Molecular Genetics of Philadelphia Chromosome–Positive Leukemias
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Discussion
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Implication
Review demonstrates oncogene activation by chromosomal translocation in leukemias, highlighting the genetic mechanism of the Philadelphia chromosome.
Key Points
- To review the molecular genetics and oncogenic mechanisms underlying the formation of the Philadelphia chromosome in human leukemias.
- Analysis of cytogenetic aberrations involving reciprocal translocation t(9;22)(q34;q11)
- Evaluation of cellular oncogene transposition, specifically the c-abl gene, across chronic and acute leukemias
- The Philadelphia chromosome is a shortened chromosome 22 resulting from a reciprocal t(9;22)(q34;q11) translocation.
- The cytogenetic abnormality is present in the majority of patients with chronic myelogenous leukemia and a smaller subset with acute lymphoblastic or acute myelogenous leukemia.
- Translocation transposes the cellular abl (c-abl) proto-oncogene from chromosome 9 to chromosome 22, driving oncogenic activation.
Cite This Study
Epstein et al. (1988) studied this question.