Recent interest has focused on natural killer T (NKT) cells as effector cells in a possible new form of immunotherapy. NKT cells express T cell and natural killer cell receptors. They are CD1d-dependent and can be stimulated by α-galactosylceramide. We have studied peripheral blood levels of NKT cells simultaneously with CD8+ cells and natural killer cells in 54 patients with prostatic carcinoma. Levels of NKT cells in patients with androgen withdrawal and stable PSA levels were 211.8 ± 138.4 cells/µl and in patients with rising PSA levels were 27.0 ± 22.1 cells/µl. A similar but less pronounced difference in CD8+ cells between these groups was found (656.4 vs. 212.0 cells/µl). Comparing all 54 patients studied, a positive correlation was found between the levels of NKT cells and CD8+ cells (r = 0.83). Our results suggest an important and regulatory role of NKT cells in patients with prostatic carcinoma.

In patients with prostatic carcinoma, natural killer (NK) cell activity was monitored in a chromium release assay. Cells from the human myeloid cell line K 562 and from a human prostatic cancer cell line (PC 3) were used as target cells. Additionally, in vitro stimulation with Β-interferon was done in each sample. NK activity in patients with localized prostatic cancer was increased as compared to age-matched controls. Patients with advanced disease showed reduced levels of NK activity. Furthermore, hormonally treated patients in relapse had significantly lower activity than patients in remission or with stable disease. Hormone therapy was without major influence on NK activity. BCG vaccination as an adjuvant immunotherapy was done in a small group of patients. Baseline NK activity and interferon-stimulated activity were enhanced by BCG in most cases.

Serum levels of fucosyltransferase (FT), phosphohexoseisomerase (PHI), tissue polypeptide antigen (TPA), Tennessee antigen (TAG), carcinoembryonic antigen (CEA) and prostatic acid phosphate (PAP) were determined in 75 healthy individuals and in 86 patients with prostatic carcinoma and 38 patients with bladder tumors. The discrimination capacities of the different markers were compared by using inverse distribution plots. At a rate of 5% false positive values the sensitivities for bladder tumors were: FT 30%, TPA 24%, CEA 16%, TAG 15%. The sensitivities for prostatic carcinoma were: PAP 63%, PHI 36%, TPA 18%, CEA 14%, TAG 14%.

Nuclear and cytosolic androgen receptor concentrations in tissues of human benign prostatic hypertrophy (BPH) were determined by use of methyltrienolone (R-1881) and 7Α,17Α-dimethyl-19-nortestosterone (DMNT) as radiolabeled ligands. Cytosolic R-1881-binding sites were 46.1 ± 43 fmol/mg protein and nuclear R-1881-binding sites were 51.8 ± 42 fmol/mg protein. DMNT-binding sites in cytosol were 44.3 ± 38 fmol/mg protein and in nuclear extract 73.4 ± 64 fmol/mg protein. No significant correlation was found between the number of R-1881 – and DMNT-binding sites in either cytosol or nuclear extracts. Cytosolic or nuclear androgen receptor content was not significantly correlated with the percentage of epithelial or stromal cells as determined from the corresponding histological sections. In BPH tissue with marked cystic degeneration, very low androgen receptor levels were found.

No abstract