[The reaction of the immune system to insulinlike growth factor-1 in postmenopausal women with breast cancer].

Taking into account the information about the role of insulin-like growth factor -1 (IGF-1) in breast cancer the main aim of the present study was to investigate the cellular immune response to IGF-1. There were examined 58 patients with breast cancer (61 +/- 1 years, BMI 31,2 +/- 0,9 kg/m2, all postmenopausal) and 10 with benign tumors of the breast (56 +/- 2 years, BMI 30,8 +/- 0,7 kg/m2 all menopausal) as well as 17 patients suffering from cancer of different sites. Sensibilization of lymphocytes to IGF-1 was measured in the reaction of blast transformation of peripheral blood lymphocytes. The majority of breast cancer patients (47/58) revealed the sensibilization of peripheral blood lymphocytes to IGF-1. Thus in a part of patients (29 /47) this reaction was suppressed and revealed after suppression of cyclooxygenase and/or blocking of the histamine H2-receptors by corresponding pharmaceutics drugs in vitro.

[Immunologic predictors of diabetes mellitus in menopausal breast cancer patients].

Although the relations between diabetes mellitus (DM) and breast cancer (BC) are lately widely discussed, the actual causes for cancer predisposition in patients with diabetes are currently unclear. This study was designed to define the frequency of DM immunological predictors occurrence and immune system function shifts in patients with breast cancer. Sixty four BC patients, 19 patients with benign breast conditions and 40 healthy individuals were included. The lymphocyte sensibilization with insulin suppressed by prostaglandin-synthesizing cells or cells with histamine receptor expression (DM predictor) is more common in BC patients than in control group (29 of 56 vs 5 of 37, p < 0.001). This is not a tumor marker, but rather is an objective factor reflecting higher occurrence of insulin resistance in this group. For BC patients is also characteristic the lower PHA-stimulated peripheral lymphocyte proliferation rate probably caused by increase in short-lived suppressor cell activity, a usual sign of the impairment of cell-mediated immunity. It is also possible, that the immunologic predictors of DM associated with insulin resistance, combined with the effects of short-lived suppressor cells, promote tumor cell proliferation.