Related immunologic mechanisms of chronic prostatitis: Advances in studies / 中华男科学杂志

Chronic prostatitis is a common male disease with a high incidence rate and a serious impact on the patients' quality of life. The pathogenesis of chronic prostatitis remains unclear though it is considered to be possibly related to infection, inflammation, and abnormal pelvic nerve muscle activity. Recently, a growing number of studies have reported immune imbalance and changes of inflammatory cytokines in patients with chronic prostatitis as well as a close correlation of abnormal immune response with the occurrence of diseases, pelvic pain symptoms, mental symptoms, hyperalgesia, and so on. This review summarizes the latest advances in the studies of immunologic mechanisms of chronic prostatitis.

Expressions of E-cadherin and N-cadherin in prostate cancer and their implications / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the differences in the expressions of E-cadherin and N-cadherin between high-risk prostate cancer and low- and medium-risk prostate cancer, and analyze their correlation with the age, serum PSA level, and Gleason score of the patients.</p><p><b>METHODS</b>We retrospectively analyzed the clinical data of 42 cases of prostate cancer, which were divided into a low- and medium-risk group (group A, n = 15) and a high-risk group (group B, n = 27). We measured the expressions of E-cadherin and N-cadherin by immunohistochemical staining, compared their differences between the two groups, and analyzed their correlation with the age, serum PSA level, and Gleason score of the patients.</p><p><b>RESULTS</b>Immunohistochemical staining showed that the expression of E-cadherin was significantly higher in group A than in B (6.1 +/- 0.51 vs 4.2 +/- 0.37, P < 0.01), and so was its positive rate (73.3% vs 25.9%, P < 0.05). The positive rate of E-cadherin was also markedly higher in the patients with serum PSA < 20 microg/L than in those with serum PSA > or = 20 microg/L (66.7% vs 29.6%, P < 0.05), and so was it in the patients with the Gleason score 5-7 than in those with 8-10 (60.9% vs 21.1%, P < 0.05). On the contrary, the N-cadherin expression was significantly lower in group A than in B (3.7 +/- 0.32 vs 7.5 +/- 0.58, P < 0.01), and so was its positive rate (13.3% vs 59.3%, P < 0.01). The positive rate of N-cadherin was also remarkably lower in the patients with the Gleason score 5-7 than in those with 8-10 (26.1% vs 63.2%, P < 0.05). However, there were no statistically significant differences in the N-cadherin expression between the patients with serum PSA < 20 microg/L and those with serum PSA > or = 20 microg/L (P > 0.05), nor in the expressions of E-cadherin and N-cadherin between the patients aged > or = 70 years and those aged < 70 years (P > 0.05).</p><p><b>CONCLUSION</b>The expressions of E-cadherin and N-cadherin are significantly different between high-risk prostate cancer and low- and medium-risk prostate cancer, which suggests that both may correlate with the invasion and metastasis of prostate cancer as well as with the serum PSA level and Gleason score of the patients.</p>

Mammalian target of rapamycin regulates androgen receptor and Akt phosphorylation in prostate cancer 22RV1 cells / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the roles of the mammalian target of rapamycin-1 and -2 (mTORC1 and TORC2) in the proliferation and apoptosis of prostate cancer 22RV1 cells.</p><p><b>METHODS</b>After silencing mTORC1 and TORC2, we examined the proliferation and apoptosis of prostate cancer 22RV1 cells by methylthiazol tetrazolium (MTT) assay and flow cytometry, respectively, and detected the expressions of the androgen receptor (AR) and Akt phosphorylation in the prostate cancer 22RV1 cells by Western blot after transfecting Raptor-siRNA and Rictor-siRNA to the 22RV1 cells.</p><p><b>RESULTS</b>MTT showed that the prostate cancer 22RV1 cells had no significant change in the growth rate after mTORC1 silence (P > 0.05), but their proliferation was markedly inhibited after mTORC2 silence (P < 0.01). Flow cytometry revealed a dramatic increase in the apoptosis of the 22RV1 cells after mTORC1 silence (P < 0.01), but no obvious change after mTORC2 silence (P > 0.05). Western blot exhibited that mTORC1 silence significantly increased the expression of AR and Akt phosphorylation (P < 0.05), while mTORC2 silence markedly decreased them (P < 0.05).</p><p><b>CONCLUSION</b>mTORC2 is not only required for the survival of prostate cancer 22RV1 cells, but also a promising therapeutic target of prostate cancer.</p>

Clinical features on chromophobe renal cell carcinoma / 中华外科杂志

<p><b>OBJECTIVES</b>To explore the clinical, pathological features and prognosis of patients with chromophobe renal cell carcinoma.</p><p><b>METHODS</b>From January 1998 to January 2008, clinical data of 29 patients with chromophobe renal cell carcinoma including clinical manifestations, imaging examinations, treatment models, pTNM stages and follow-up results, were summarized to investigate its features and prognosis.</p><p><b>RESULTS</b>All cases had no obvious clinical and preoperative imaging presentation. There were 23 patients underwent radical nephrectomy, and 6 cases underwent nephron sparing surgery. Postoperative pathological findings confirmed the diagnosis of chromophobe renal cell carcinoma. Macroscopically, the cut surface of the tumors were generally beige in color. Histologically, it showed polygonal chromophobe cells and small round eosinophilic cells with eccentric hyaline degeneration. These tumor cells had a clear and sharp membrane, lightly stained abundant cytoplasm with a fine reticular translucent pattern and irregular nuclei. And a perinuclear halo was often seen in these cells. Histochemically, the tumor cells generally show a diffuse and strong reaction for CK-8 with a negative expression of Vimentin. The pTNM stages of the tumor were as follows, pT1N0M0 in 11 cases, pT2N0M0 in 8 cases, pT3aN0M0 in 5 cases, pT1N1M0 in 3 cases, pT2N1M0 in 2 cases. Twenty-six cases of patients were followed up (24 to 144 months, with an average of 90 months), 3 cases died of cardio-cerebrovascular disease, and local recurrence involved in 6 cases with reoperation in 4 cases, as well as distant metastasis in 1 case. Twenty-one cases survived with tumor-free. The statistical results indicated that the survival rates of the patients with chromophobe renal cell carcinoma in five years and ten years were 83.9%, 77.9%, respectively, compared with renal cell carcinoma of the same stage 63.8% and 49.9% at the same periods, and there is no difference in the survival rate of five years (P > 0.05) but significant difference in that of ten years (P < 0.01).</p><p><b>CONCLUSIONS</b>Chromophobe renal cell carcinoma is a morphologically uncommon subtype of renal cell carcinoma with the good prognosis. Definite diagnosis depends on its typical pathological feature. Radical nephrectomy is the first choice for the treatment of chromophobe renal cell carcinoma.</p>

The mTOR inhibitor enhances chemosensitivity of androgen-independent prostate cancer cell line / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the effect of the mammalian target of rapamycin (mTOR) inhibitor CCI-779 on the chemosensitivity of androgen-independent prostate cancer cell line PC-3.</p><p><b>METHODS</b>Prostate cancer cells PC-3 were cultured and treated with CCI-779, Paclitaxel and combination of the two. Then the inhibitory effects of the three medications on the growth of the PC-3 cells were determined by MTT, and the their cell cycle and apoptosis were detected by flow cytometry.</p><p><b>RESULTS</b>Compared with the control group, the three medications all significantly inhibited the proliferation of the PC-3 cells, and the combined method even enhanced the effect. Flow cytometry showed that CCI-779 and Paclitaxel blocked the cell cycle mainly in the G1/G2 stage, while the combined medication mainly in the G0/G1 stage. Significantly increased apoptosis of the PC-3 cells was observed in the three medication groups as compared with the control group (P < 0.01).</p><p><b>CONCLUSION</b>CCI-779 can inhibit the proliferation of PC-3 cells and enhance the chemosensitivity of prostate cancer.</p>