Kaul D, Kaur M
Department of Experimental Medicine & Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Leuk Res. 1997 Nov-Dec;21(11-12):1047-9. doi: 10.1016/s0145-2126(97)00098-2.
The selective and conspicuous absence of a novel receptor-Ck (having affinity for cholesterol moiety in lipoproteins and intrinsic tyrosine kinase activity) in various leukemic cell lines/patients, prompted us to explore the nature of interrelationship between receptor-Ck deficiency and over-expression of genes coding for bcl-2, cyclin 'D', chimeric bcr-abl, c-myc and LDL-receptor in the human promyelocytic leukemic cell line (HL-60). This study revealed unambiguously that deregulated expression of these genes is primarily due to the inability of these cells to express the receptor-Ck gene. Based upon the observations we propose that 'receptor-Ck' deficiency may be responsible for the initiation of chronic myeloid leukemia.
在各种白血病细胞系/患者中，新型受体Ck（对脂蛋白中的胆固醇部分具有亲和力且具有内在酪氨酸激酶活性）选择性且明显缺失，这促使我们探究在人早幼粒细胞白血病细胞系（HL-60）中，受体Ck缺陷与编码bcl-2、细胞周期蛋白D、嵌合bcr-abl、c-myc和低密度脂蛋白受体的基因过表达之间的相互关系本质。这项研究明确揭示，这些基因的表达失调主要是由于这些细胞无法表达受体Ck基因。基于这些观察结果，我们提出“受体Ck”缺陷可能是慢性髓性白血病起始的原因。
