Abstract
Recent studies have demonstrated that the cellular tumour antigen p53 (ref. 1) can complement activated ras genes in the transformation of rat fibroblasts, suggesting that the gene encoding p53 may act as an oncogene2,3. Here, by using in situ chromosomal hybridization4,5, we have mapped the p53 gene to human chromosome 17, at bands 17q21–q22, the region containing one of the breakpoints in the translocation t(15;17) (q22;q21) associated with acute promyelocytic leukaemia (APL)6,7. Hybridization of p53 and erb-A (17qll-ql2) probes to malignant cells from three APL patients indicated that the p53 gene is translocated to chromosome 15 (15q+), whereas erb-A remains on chromosome 17. Analysis of variant translocations demonstrates that the 15q+ chromosome contains the conserved junction8, suggesting a role for p53 in the pathogenesis of APL. However, rearrangements of the p53 gene were not detected on Southern blotting of DNA from leukaemic cells of four APL patients with t(15;17).
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Le Beau, M., Westbrook, C., Diaz, M. et al. Translocation of the p53 gene in t(15;17) in acute promyelocytic leukaemia. Nature 316, 826–828 (1985). https://doi.org/10.1038/316826a0
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DOI: https://doi.org/10.1038/316826a0
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