Receptor-Ck-dependent regulation of genes in HL-60 cell line.

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.