Le Beau M M, Westbrook C A, Diaz M O, Rowley J D, Oren M
Nature. 1985;316(6031):826-8. doi: 10.1038/316826a0.
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 oncogene. Here, by using in situ chromosomal hybridization, 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). Hybridization of p53 and erb-A (17q11-q12) 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 junction, 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).
最近的研究表明，细胞肿瘤抗原p53（参考文献1）在大鼠成纤维细胞转化过程中可与激活的ras基因互补，这表明编码p53的基因可能作为一种癌基因发挥作用。在此，我们通过原位染色体杂交，将p53基因定位于人类染色体17的17q21 - q22带，该区域包含与急性早幼粒细胞白血病（APL）相关的易位t(15;17)（q22;q21）的一个断点。用p53和erb - A（17q11 - q12）探针与三名APL患者的恶性细胞杂交表明，p53基因易位至染色体15（15q +），而erb - A仍位于染色体17上。对变异易位的分析表明，15q +染色体含有保守的连接点，提示p53在APL发病机制中起作用。然而，在对四名患有t(15;17)的APL患者白血病细胞的DNA进行Southern印迹分析时，未检测到p53基因的重排。
