REVERSAL OF ACQUIRED-RESISTANCE TO DOXORUBICIN IN P388 MURINE LEUKEMIA-CELLS BY TAMOXIFEN AND OTHER TRIPARANOL ANALOGS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 44  (10) , 4392-4395
Abstract
The effects of the triparanol analogs chlorotrianisene, clomiphene, tamoxifen, 5-[p-(fluoren-9-ylidenemethyl)phenyl]-2-piperidineethanol (MDL 10393), MDL 8917v, nafoxidine, 2-[p-(6-methoxy-2-phenylinden-3-yl)phenoxy]triethylamine (U-11555A), 2-[p-(3,4-dihydro-6-methoxy-2-phenyl-1-naphthyl)phenoxy]triethylamine (U-10520A) and nitromifene, as well as triparanol itself, were studied in the P388 murine leukemia cell line and in a doxorubicin-resistant subline (P388/ADR). At noninhibitory concentrations, all the analogs increased the sensitivity of P388/ADR cells to doxorubicin but did not have such an effect on the doxorubicin-sensitive cells. Diethylstilbestrol, deacetylated cyclofenil (F6060), hexestrol and 17.beta.-estradiol did not have such an activity. The effects of tamoxifen on doxorubicin sensitivity of P388/ADR cells could not be reversed by 17.beta.-estradiol. Estrogen receptors could not be demonstrated in either cell line. The reversal of the doxorubicin-acquired resistance by the triparanol analogs evidently is unrelated to their estrogenic or antiestrogenic activities. The possible clinical implications of these findings are discussed.

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