In line with this, ER(+)/PR(−) breast tumours have more aggressive phenotypes and are less sensitive to growth factor deprivation compared to ER(+)/PR(+).29 Moreover, strong correlations between high EPOR, ER and PR expression were reported and a specific functional association between EpoR and ERα was postulated.30 Similar studies were performed with different cell types, namely renal carcinoma cells, melanoma, malignant glioma, cervical cancer cells and mesothelioma cells31–34, reporting contradictory effects of Epo on cell survival after cDDP treatment. This evidence concerns the gene PGR and cervical cancer.