Chang K S, Schroeder W, Siciliano M J, Thompson L H, McCredie K, Beran M, Freireich E J, Liang J C, Trujillo J M, Stass S A
Hematopathology Program, University of Texas System Cancer Center, M. D. Anderson Hospital and Tumor Institute, Houston 77030.
Leukemia. 1987 May;1(5):458-62.
The human myeloperoxidase (MPO) gene has recently been cloned in our laboratory. Southern blot hybridization of our MPO cDNA to DNA from a somatic cell hybrid clone panel revealed that the MPO cosegregated with human chromosome 17. In situ hybridization mapped the MPO gene to chromosome 17q22-24. Although this location is close to the translocation breakpoint which occurs in acute promyelocytic leukemia (APL), t(15;17)(q22;q21-22), Southern blot hybridization with different restriction-digested genomic DNA samples from four APL patients did not reveal MPO gene rearrangement. However, RNA dot-blot hybridization showed that APL patients with the translocation expressed high levels of MPO mRNA. This observation raises the possibility that the high levels of MPO gene expression in APL could be due to the arrest of leukemic cells at a specific stage of differentiation or a consequence of the translocation.
人髓过氧化物酶（MPO）基因最近在我们实验室被克隆。我们的MPO cDNA与来自体细胞杂交克隆面板的DNA进行Southern印迹杂交，结果显示MPO与人第17号染色体共分离。原位杂交将MPO基因定位到染色体17q22 - 24。尽管这个位置靠近急性早幼粒细胞白血病（APL）中出现的易位断点，即t(15;17)(q22;q21 - 22)，但对4例APL患者不同限制性酶切基因组DNA样本进行Southern印迹杂交未发现MPO基因重排。然而，RNA斑点印迹杂交显示，发生易位的APL患者表达高水平的MPO mRNA。这一观察结果提示，APL中MPO基因的高表达可能是由于白血病细胞在特定分化阶段停滞，或者是易位的结果。
