Oncogene activation by chromosomal rearrangement in chronic myelocytic leukemia.
A considerable number of human tumors, especially leukemias and lymphomas is associated with a consistent specific chromosome translocation. At a number of the breakpoint regions of these specific aberrations are c-oncogenes (c-onc) located. The structure and/or expression of some of these c-onc is altered as a result of the specific translocation. In the CML-specific (9;22) translocation the transposition of the c-abl oncogene to the chromosome 22 bcr sequences results in the production of a chimeric bcr/c-abl fusion protein. This result strongly suggests that tumor-specific chromosomal aberrations can lead to the activation of cellular oncogenes.
De Klein
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D001483:Base Sequence; D002892:Chromosomes, Human, Pair 22 / Q000648:ultrastructure; D002899:Chromosomes, Human, Pair 9 / Q000648:ultrastructure*; D004273:DNA, Neoplasm / Q000235:genetics; D005786:Gene Expression Regulation; D006801:Humans; D007951:Leukemia, Myeloid / Q000235:genetics*; D008954:Models, Biological; D009857:Oncogenes; D010677:Philadelphia Chromosome; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics*; D016315:Proto-Oncogene Proteins c-abl; D011519:Proto-Oncogenes; D014178:Translocation, Genetic
D004273:DNA, Neoplasm; D011518:Proto-Oncogene Proteins; D016315:Proto-Oncogene Proteins c-abl