Tumor growth leads to tissue hypoxia and tissue hypoxia, in turn, is a strong stimulus for expression of genes encoding factors that promote tumor growth. Likewise, hypoxia is a key condition within the vicious cycle of autogenous neoplastic dissemination. A marker of the presence of tissue hypoxia may be the presence of high blood viscosity, which is found in a number of neoplastic diseases including gynecological cancer. At the time of diagnosis of breast cancer, patients dying of this disease had had significantly higher initial pv (1.40+/-0.18 mPa s; p<0.0001) when compared to patients not dying of cancer (1.30+/-0.10 mPa s). In multivariate proportional hazard regression analysis, next to tumor size (p=0.03) and nodal status (p=0.004), pv was found an independent prognostic marker for overall survival of breast cancer patients (RR=130.2; 95% CI: 11.6-1,460.6; p<0.0001). An optimized preoperative cut-off value above 1.40 mPa s was significantly associated with poor outcome (log-rank-test) in the Kaplan-Meier survival-estimates, even in node-negative breast cancer (n=153; 54.6%). The most likely explanation for these findings is that increased fibrinogen/fibrin turnover and breakdown products characteristically associated with tumor-cell dissemination contribute to the increased plasma viscosity while the hematocrit, leukocyte count, and platelet count contributed little to the increased blood viscosity in patients with breast cancer. These findings may constitute an approach for new strategies in cancer therapy since it might be possible that reduction of plasma viscosity by treatment improves responsiveness to radio/chemotherapy and thus survival of patients.