Yamamoto H, Hatano M, Iitsuka Y, Mahyar N S, Yamamoto M, Tokuhisa T
Division of Developmental Genetics, Chiba University School of Medicine, Japan.
Mol Immunol. 1995 Nov;32(16):1177-82. doi: 10.1016/0161-5890(95)00100-x.
HOX11 is identified from the breakpoint of human T cell acute lymphoblastic leukemias with t(10;14). Since overexpression of HOX11 in T cells caused leukemias in transgenic mice, the endogenous HOX11 may play a role in proliferation and differentiation of T cells. In order to elucidate the role, we examined the expression of Hox11 in normal lymphocytes by a reverse transcriptase-polymerase chain reaction analysis. Two alternatively spliced Hox11 mRNAs were expressed in fetal spleens. However, lymphocytes did not express Hox11 mRNA during differentiation. Furthermore, it was not induced in primary lymphocytes after activation. These results suggest that ectopic expression of HOX11 in T cells is responsible for leukemogenesis.
HOX11是从患有t(10;14)的人类T细胞急性淋巴细胞白血病的断点处鉴定出来的。由于HOX11在T细胞中的过表达在转基因小鼠中引发白血病，内源性HOX11可能在T细胞的增殖和分化中发挥作用。为了阐明其作用，我们通过逆转录聚合酶链反应分析检测了正常淋巴细胞中Hox11的表达。两种选择性剪接的Hox11 mRNA在胎儿脾脏中表达。然而，淋巴细胞在分化过程中不表达Hox11 mRNA。此外，在原代淋巴细胞激活后它也未被诱导。这些结果表明T细胞中HOX11的异位表达是白血病发生的原因。
