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Objective:To investigate the curative efficacy of radical prostatectomy (RP) for T 4 stage prostate cancer invading bladder neck. Methods:The clinical data of 22 patients with T 4 stage prostate cancer invading bladder neck treated with RP from April 2013 to March 2021 were analyzed retrospectively. The mean age of the patients was (64.09±6.33) years, and the preoperative blood PSA was 57.70(39.40, 68.56) ng/ml. Preoperative MRI or PSMA-PET examination revealed bladder neck invasion, including 16 cases (72.73%) of urinary retention. Clinical stage of T 4N 0M 0 accounted for 40.91% (9/22), T 4N 1M 0 accounted for 45.45% (10/22), and T 4N 1M 1 accounted for 13.64% (3/22). Preoperative patients were not treated with neoadjuvant endocrine or chemotherapy. Laparoscopic or robotic assisted laparoscopic radical prostatectomy and pelvic lymph node dissection were performed. Results:The 22 operations were successfully completed without conversion. The operation time was(184.27±34.82) min, the amount of intraoperative bleeding was (210.91±83.03) ml, the retention time of drainage tube was (4.73 ± 1.03) days, the recovery of gastrointestinal function took 3 (2, 3) days, and the postoperative hospital stay was (6.68 ± 1.39) days. Postoperative pathology showed that the Gleason score of 7 points accounted for 4.54% (1/22), 8 points accounted for 13.64% (3/22), and 9 points accounted for 81.82% (18/22). The positive rate of margin was 81.82% (18/22). Pathological stage of T 4N 0M 0 accounted for 22.73% (5/22), T 4N 1M 0 accounted for 63.64% (14/22), and T 4N 1M 1 accounted for 13.64% (3/22), of which extracapsular or seminal vesicle invasion accounted for 90.91% (20/22). The incidence of postoperative complications above grade 3 was 9.09% (2/22), and the rate of urinary control recovery after 3 months of surgery was 90.91% (20/22). 16 patients with preoperative urinary retention were able to urinate normally after operation. All patients were treated with adjuvant androgen deprivation therapy (ADT) with or without antiandrogens, and 13 cases (59.09%) were treated with adjuvant radiotherapy. The postoperative PSA value before adjuvant treatment was 2.53 (0.51, 5.44) ng/ml. The median survival time was not reached. Two patients died of prostate cancer at 71 and 84 months and one patient died of heart disease at 28 months. Conclusions:RP surgery could effectively relieve the condition of urinary retention with low incidence of operative complications. Although the positive rate of surgical margin is high, RP could be used as one of the treatment options for T 4 stage prostate cancer invading bladder neck, while the long-term effect is still needed to be further analyzed.
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Objective To analyze the effect of endophytic renal tumor growth characteristic on the short-term outcomes of robot-assisted laparoscopic partial nephrectomy (RALPN).Methods From March 2015 to October 2016,23 RALPN cases of endophytic renal masses and 68 RALPN cases of intermediate and exophytic renal tumors were retrospectively analyzed.There were no significant differences in age,gender,tumor side,history of abdominal surgery,benign and malignant cases of the two groups of patients (P > 0.05).Patients with a completely endophytic mass had smaller tumors [(2.4 ± 0.5) cm vs.(3.9 ± 1.1) cm],and higher overall R.E.N.A.L.score (P < 0.05).The differences of perioperative period and postoperative follow-up results were analyzed.Results All 91 RALPN cases were successfully done without conversion to open or radical nephrectomy.There were no significant differences in intraoperative blood loss,postoperative Hb decrease,intraoperative and postoperative blood transfusion rate,hospital days,positive tumor margins,and the incidence of Clavien-Dindo grade Ⅲ or above in the two groups (P > 0.05).The endophytic group showed longer operative time [(95.6 ± 19.4) min vs.(75.3 ± 16.9) min],and longer renal warm ischemia [(25.2 ±5.4)min vs.(17.6 ±7.0)min].In the postoperative follow-up of 3 months to 22 months,all patients got disease-free survival.Conclusions RALPN for completely intraparenchymal renal tumors can be safely and effectively performed in experienced institutes.However,the long-term period of follow-up is still missing.
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Connexin-43 (Cx43) expression in prostate cancer (PCa) cells and the potency of gap junctional intercellular communication (GJIC) in the cells were investigated, with an attempt to elucidate the reason why the so-called "bystander effect" mediated by thymidine kinase (TK) suicide gene therapy on PCa cells is not of significance and to explore the role of GJIC in PCa carcinogenesis. mRNA and protein expression of Cx43 in a PCa cell line PC-3m was detected by reverse-transcription polymerase chain reaction (RT-PCR) and strapt-avidin-biotin-enzyme complex (SABC) immunohistochemical staining, and inherent GJIC of PC-3m cells was assayed by scrape-loading and dye transfer (SLDT) assay. The expression of Cx43 in human normal and malignant prostate tissues was determined by SABC immunohistochemistry as well. It was found that Cx43 mRNA and protein expression in PC-3m cells was slightly reduced as compared with positive controls and the location of Cx43 protein was aberrant in cytoplasm rather than on membrane. Assessment of paraffin sections demonstrated that the expression of Cx43 protein in PCa cells was abnormally located and markedly diminished as compared with normal prostatic epithelial ones, displaying a negative correlation to the pathological grade (chi2=4.025, P<0.05). Additionally, capacity of inherent GJIC in PC-3m cells was disrupted, which was semi-quantified as (+) or (-). It was indicated that both down-regulated expression of Cx43 mRNA and aberrant location of Cx43 protein participated in the mechanisms leading to deficient GJIC in PC-3m cells. Lack of efficient GJIC is a molecular event, which may contribute not only to limited extent of "bystander effect", but also to initiation and progression of prostatic neoplasm.
Résumé
Connexin-43 (Cx43) expression in prostate cancer (PCa) cells and the potency of gap junctional intercellular communication (GJIC) in the cells were investigated, with an attempt to elucidate the reason why the so-called "bystander effect" mediated by thymidine kinase (TK) suicide gene therapy on PCa cells is not of significance and to explore the role of GJIC in PCa carcinogenesis.mRNA and protein expression of Cx43 in a PCa cell line PC-3m was detected by reverse-transcription polymerase chain reaction (RT-PCR) and strapt-avidin-biotin-enzyme complex (SABC) immunohistochemical staining, and inherent GJIC of PC-3m cells was assayed by scrape-loading and dye transfer (SLDT) assay. The expression of Cx43 in human normal and malignant prostate tissues was determined by SABC immunohistochemistry as well. It was found that Cx43 mRNA and protein expression in PC-3m cells was slightly reduced as compared with positive controls and the location of Cx43 protein was aberrant in cytoplasm rather than on membrane. Assessment of paraffin sections demonstrated that the expression of Cx43 protein in PCa cells was abnormally located and markedly diminished as compared with normal prostatic epithelial ones, displaying a negative correlation to the pathological grade (χ2=4.025, P<0.05). Additionally, capacity of inherent GJIC in PC-3m cells was disrupted, which was semi-quantified as (+) or (-). It was indicated that both down-regulated expression of Cx43 mRNA and aberrant location of Cx43 protein participated in the mechanisms leading to deficient GJIC in PC-3m cells. Lack of efficient GJIC is a molecular event, which may contribute not only to limited extent of "bystander effect", but also to initiation and progression of prostatic neoplasm.
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The killing effects of herpes simplex virus thymidine kinase gene/ganciclovir (HSV-tk/GCV) approach by the addition of several commonly clinical chemotherapeutic agents on hormone refractory prostate cancer (HRPC) cells PC-3m were investigated. After transferring of the HSV-tk gene into PC-3m cells, mRNA and protein expression of HSV-tk was detected by reverse-transcript polymerase chain reaction (RT-PCR) and strept avidin-biotin complex (SABC) immunohistochemical method. The killing effect of GCV, cisplatin (CDDP), etoposide (VP-16), vincristine (VCR), methotrexate (MTX), 5-fluorouracil (5-Fu), and suramin on PC-3m cells was evaluated by morphological assessment analysis, trypan blue exclusion assay and MTT assay respectively. Additionally, the cooperative effect of HSV-tk/GCV system combined with the above agents on the target cancer cells was determined by MTT. Furthermore, apoptosis and necrosis induced by GCV plus 5-Fu or suramin was analyzed by flow cytometry (FCM). The results showed that that there was HSV-tk mRNA and protein expression in pDR2-tk plasmid transduced PC-3m cell. Combination of GCV with VP-16, VCR, 5-Fu or suramin led to an enhanced cellular killing effect, but with CDDP resulted in a reduced one and with MTX in an approximate one. FCM revealed that synergistic use of GCV and 5-fu or suramin resulted in a rather large proportion of apoptosis and necrosis with the apoptosis index being 36.38% and 35.51%, and the proportion of necrosis being 33.05% and 28.87%, respectively. In conclusion, HSV-tk/CGV approach by addition of certain clinical available chemotherapeutic drugs brings on statistically significant enhanced cell killing over single-agent treatment. Our results highlight the potential for such new combination therapies for future treatments of HRPC.
Résumé
The killing effects of herpes simplex virus thymidine kinase gene/ganciclovir (HSV-tk/GCV) approach by the addition of several commonly clinical chemotherapeutic agents on hormone refractory prostate cancer (HRPC) cells PC-3m were investigated. After transferring of the HSV-tk gene into PC-3m cells, mRNA and protein expression of HSV-tk was detected by reverse-transcript polymerase chain reaction (RT-PCR) and strept avidin-biotin complex (SABC) immunohistochemical method. The killing effect of GCV, cisplatin (CDDP), etoposide (VP-16), vincristine (VCR), methotrexate (MTX), 5-fluorouracil (5-Fu), and suramin on PC-3m cells was evaluated by morphological assessment analysis, trypan blue exclusion assay and MTT assay respectively. Additionally, the cooperative effect of HSV-tk/GCV system combined with the above agents on the target cancer cells was determined by MTT. Furthermore, apoptosis and necrosis induced by GCV plus 5-Fu or suramin was analyzed by flow cytometry (FCM). The results showed that that there was HSV-tk mRNA and protein expression in pDR2-tk plasmid transduced PC-3m cell. Combination of GCV with VP-16, VCR, 5-Fu or suramin led to an enhanced cellular killing effect, but with CDDP resulted in a reduced one and with MTX in an approximate one. FCM revealed that synergistic use of GCV and 5-fu or suramin resulted in a rather large proportion of apoptosis and necrosis with the apoptosis index being 36.38 % and 35.51%, and the proportion of necrosis being 33.05 % and 28.87 %, respectively. In conclusion, HSV-tk/CGV approach by addition of certain clinical available chemotherapeutic drugs brings on statistically significant enhanced cell killing over single-agent treatment.Our results highlight the potential for such new combination therapies for future treatments of HRPC.