Surgical trauma and anesthesia may lead to the postoperative immunosuppression, the exact mechanism of which is still unresolved. Among various factors, the role of prostaglandine PGE2-mediated suppression was also proposed. We investigated the influence of surgery and two anesthetic regimes on lymphoproliferative response (LPR) to PHA and on NK cell activity (MTT) in breast cancer patients, as well as the effect of indomethacin, a PGE2 synthesis inhibitor, on these lymphocyte functions in vitro. In 36 previously untreated patients the lymphocyte functions were assayed before, 24 hours and seven days after the surgery. In regard to LPR, three distinct response patterns were observed: a) significant (p < 0.05) increase of initially lowered LPR; b) significant (p < 0.001) decrease of initially normal LPR 24 hours after operation, followed by normalization after seven days; c) no change of initially normal LPR. Indomethacin in vitro significantly (p < 0.05) enhanced the diminished LPR only before surgery, no effect being seen after the operation. The NK cell function was unaffected by surgery regardless the initial level of activity. Indomethacin had no effect on this lymphocyte function. There was no difference between the patient groups submitted to the different anesthetic regimes. In conclusion, our results show that surgical trauma variably affect the lymphocyte functions of cancer patients, the effect not being related to the particular anesthetic regime used. The PGE2-mediated suppression is not likely to be involved in postoperative immune function impairment.