Simmers R N, Webber L M, Shannon M F, Garson O M, Wong G, Vadas M A, Sutherland G R
Blood. 1987 Jul;70(1):330-2.
The human granulocyte-colony stimulating factor gene (G-CSF) is localized at 17q11.2-q21, the region of one of the breakpoints in the 15;17 chromosome translocation specific for acute promyelocytic leukemia (APL). As G-CSF induces differentiation and loss of tumorigenicity in myeloid leukemic cells or cell lines, it was possible that the translocation in APL involved the DNA of the G-CSF coding region or its regulatory region. In situ hybridization to chromosomes with the t(15;17) from patients with the APL translocation using a G-CSF cDNA clone revealed that the coding region of this gene is proximal to the t(15;17) breakpoint on chromosome 17. Southern analysis of DNA from patients with the APL translocation showed no differences in hybridization between normal and leukemic cells. These results indicate that the G-CSF coding sequence is not disrupted by the chromosomal rearrangement characteristic of APL.
人类粒细胞集落刺激因子基因(G-CSF)定位于17q11.2-q21,该区域是急性早幼粒细胞白血病(APL)特有的15;17染色体易位的断点之一。由于G-CSF可诱导髓系白血病细胞或细胞系分化并丧失致瘤性,因此APL中的易位可能涉及G-CSF编码区或其调控区的DNA。使用G-CSF cDNA克隆对APL易位患者的t(15;17)染色体进行原位杂交分析,结果显示该基因的编码区位于17号染色体上t( (15;17) 断点的近端。对APL易位患者的DNA进行Southern分析,结果显示正常细胞和白血病细胞之间的杂交没有差异。这些结果表明,G-CSF编码序列未被APL特有的染色体重排破坏。