Oka Takashi, Ouchida Mamoru, Koyama Maho, Ogama Yoichiro, Takada Shinichi, Nakatani Yoko, Tanaka Takehiro, Yoshino Tadashi, Hayashi Kazuhiko, Ohara Nobuya, Kondo Eisaku, Takahashi Kiyoshi, Tsuchiyama Junjiro, Tanimoto Mitsune, Shimizu Kenji, Akagi Tadaatsu
Department of Pathology, Okayama University Graduate School of Medicine and Dentistry, Okayama 700-8558, Japan.
Cancer Res. 2002 Nov 15;62(22):6390-4.
High-frequent silencing of hematopoietic cell-specific protein-tyrosine phosphatase SHP1 gene by promoter methylation was detected in various kinds of leukemias and lymphomas, as well as in many hematopoietic cell lines, which is supported by our previous observation of strong decrease of SHP1 mRNA and protein. The promoter methylation of the SHP1 gene was clearly correlated with the clinical stage. Loss of heterozygosity with microsatellite markers near the SHP1 gene was shown in 79% of informative acute lymphoblastic leukemia cases. These results suggest that functional loss of SHP1 is associated with the pathogenesis of leukemias/lymphomas.
在各类白血病和淋巴瘤以及许多造血细胞系中,均检测到造血细胞特异性蛋白酪氨酸磷酸酶SHP1基因因启动子甲基化而出现高频沉默,这与我们之前观察到的SHP1 mRNA和蛋白显著减少的结果相符。SHP1基因的启动子甲基化与临床分期明显相关。在79%的信息充分的急性淋巴细胞白血病病例中,SHP1基因附近的微卫星标记显示杂合性缺失。这些结果表明,SHP1的功能丧失与白血病/淋巴瘤的发病机制有关。