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Type ii estrogen binding sites in acute lymphoid and myeloid leukemias growth inhibitory effect of estrogen and flavonoids


, : Type ii estrogen binding sites in acute lymphoid and myeloid leukemias growth inhibitory effect of estrogen and flavonoids. British Journal of Haematology 75(4): 489-495

The presence of oestrogen receptors (ER) and type II oestrogen binding sites (type II EBS) have been investigated by a whole cell assay in seven cases of acute lymphoid leukaemia (ALL) and 16 cases of acute myeloid leukaemia (AML). ER were detected in 6/7 ALL patients with values ranging between 133 and 2268 sites/cell and in 12/16 AML patients with values ranging between 274 and 4197 sites/cell. The apparent dissociation constant (KD) for ER was 0.6 .+-. 0.3 nM (mean + SD of 20 cases). All blasts from ALL and AML patients expressed type II EBS at variable levels ranging between 3109 and 239 450 sites/cell. The mean KD value for these sites was 18.3 .+-. 5.6 nM (mean .+-. SD of 23 cases). Specificity experiments demonstrated that type II EBS are oestrogen specific relative to the class of steroid hormones. In addition, the flavonol quercetin was able to compete for [3H] 17 beta-oestradiol (E2) binding to type II EBS, the relative binding affinity (RBA) of quercetin being greater than that of diethylstilboestrol (DES). DES and quercetin exerted a dose-dependent inhibition of ALL and AML blast proliferation in the range of concentrations between 10-8 and 10-5 M. The RBA of DES and quercetin for type II EBS correlated well with their potency as cell growth inhibitors. Moreover, the flavonols rutin and hesperidin which complete slightly for [3H]E2 binding to type II EBS, were scarcely effective in inhibiting leukaemic cell proliferation. The inhibitory effect of DES and quercetin was not due to a non-specific cytotoxic action since after a 1 d culture period, cell viability did not vary between control and treated cells, being greater than 80%. Our results suggest that high oestrogen concentrations and the flavonol quercetin may inhibit leukaemic blast proliferation through a common mechanism involving a binding interaction with type II EBS.

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