In discriminating prostate carcinoma,when the value of PSA was 4ng/ml,6ng/m l and 10ng/ml,the sensitivity was 92.5%, 67.5%and 30% respectively,and the speci ficity was 45.7%,78.3%and 91.3% respectively.
The normal serum level of γ-Sm in 140 healthy males was 0.83 ±0.71 μg/L, in 50 healthy women was 0.1 μg, L In 26 patients with prostatic cancer at various stages, the mean value of serum yerm being 205.4 μg, L The positive rate was 23/26 (88.5%).
To explore the role of Fas/APO1 in the occurrence and progression of human urinary malignant tumors, expression of Fas/APO1 was tested with immunocytochemical technique in 6 kinds of urinary tumor cell lines consisting of bladder cancer (T24, EJ, BIU87), renal cell carcinoma (GRC1,RCC949),prostatic cancer (PC3M) and a primary in vitro cultured normal renal fibroblast.
The p27kip1 protein expression in prostatic carcinoma was inversely correlated with preoperative serum prostate specific antigen level (r=-0 399,P=0.010), extraprostatic extension (r=-0 329,P=0.036), tumor stage (r=-0 453,P=0.003), and histological grade (r=-0 290,P=0.046).
The Skp2 protein expression in prostatic carcinoma was positively correlated with preoperative serum prostate specific antigen level (r=0 360,P=0.021), extraprostatic extension (r=0 570,P< 0.001), tumor stage (r=0 531,P< 0.001), and histological grade (r=0 514,P=0.001).
The possibility of using AGR2 as a diagnostic marker of prostate cancer is discussed.
Calcitriol induces transcription of the placental transforming growth factor β gene in prostate cancer cells via an androgen-ind
Calcitriol (1α,25-dihydroxycholecalciferol) suppresses the growth of prostate cancer cells.
Growth suppression of hormone-sensitive LNCaP prostate cancer cells by calcitriol is believed to depend on androgens, but the mechanisms of the interactions between the calcitriol-and androgen-dependent signaling pathways is unclear.
It was assumed that calcitriol stimulates production of PTGF-β independently of 5α-dihydrotestosterone and that its effect on prostate cancer cell growth is partly mediated by an androgen-independent mechanism.