Several reports have suggested that peri-operative blood transfusion promotes tumour recurrence and death after surgery for cancer. We have studied the effect of transfusion in 156 patients operated on for prostatic cancer. A retrospective review was made of the clinical, histopathological and transfusion data in their hospital records. Sixty patients received blood transfusions and 96 did not. The 5-year prostatic cancer specific survival rate was 0.56 in the transfused patients and 0.69 in the non-transfused group. The transfused patients had a higher prevalence of risk factors than did the non-transfused. When the differences in risk factors were accounted for by Cox regression analysis, peri-operative blood transfusion reduced the prostatic cancer death intensity by 36%. The study does not support the hypothesis that blood transfusion promotes recurrence following surgery for prostatic cancer.

The transcription factors and proto-oncogenes STAT3 and STAT5 are highly activated in hematological malignancies and represent promising therapeutic targets. Whereas the importance of STAT5 as tumor promoter is beyond doubt, the role of STAT3 in hematological cancers is less well understood. Both, enforced as well as attenuated expression of STAT3 were reported in hematopoietic malignancies. Recent evidence implicates STAT3 as key player for tumor immune surveillance as it both mediates the production of and response to inflammatory cytokines. Here we investigated the effects of STAT3 deletion in a BCR/ABL-induced lymphoma model, which is tightly controlled by natural killer (NK) cells in vivo. Upon STAT3 deletion tumor growth is significantly enhanced when compared to STAT3-expressing controls. The increased tumor size upon loss of STAT3 was accompanied by reduced NK cell infiltration and decreased levels of the cytokine IFN-γ and the chemokine RANTES. Upon transplantation into NK cell-deficient mice differences in lymphoma size were abolished indicating that STAT3 expression in the tumor cells controls NK cell-dependent tumor surveillance. Our findings indicate that STAT3 inhibition in lymphoma patients will impair NK cell-mediated tumor surveillance, which needs to be taken into account when testing STAT3 inhibitors in preclinical or clinical trials.