LYMPHOCYTES FROM CML PATIENTS LACK A 47 KDA FACTOR HAVING AFFINITY FOR A GENOMIC STEROL REGULATORY SEQUENCE

Deranged cellular cholesterol homeostasis has been widely recognized i n the initiation as well as progression of various types of cancers in cluding chronic myeloid leukaemia (CML). Since the human genomic stero l regulatory element (SRE) has been shown to regulate various key gene s involved in this phenomenon, the present study revealed the existenc e of a unique 47 kDa protein factor having affinity for this SRE seque nce in lymphocytes from normal subjects, as well as its absence in lym phocytes from untreated CML patients, However, this factor appeared wh en these CML patients achieved complete haematological remission (CHR) through alpha-interferon therapy. Furthermore, an inverse relationshi p was also observed between the LDL receptor gene expression at the tr anscriptional level and the binding affinity of this 47 kDa protein fa ctor to the SRE sequence. Based upon these results we propose that thi s factor may have a role in pathophysiology of chronic myeloid leukaem ia. Copyright (C) 1996 Elsevier Science Ltd