Objective To investigate the pathological characters of clinical T1b (4 ＜ diameter ≤7 cm) renal cell carcinoma and provide reference basis for the nephron sparing surgery (NSS).Methods From January 2002 to December 2014, the pathological features of clinical T1b renal cell carcinoma were studied in 710 cases, including 505 male cases and 205 female cases.The mean age was 58 years old, ranged from 26 to 88 years old.The location of tumor included 377 in left side and 383 in right side.In the recorded 372 cases, the accurate site of tumor included 137 in upper portion, 96 in middle portion and 139 in lower portion.The initial symptom included hematuria in 103 cases, back pain in 62 cases, hematuria accompanied with back pain in 34 cases and asymptom in 511 cases.The diameter of tumor ranged from 4.0 to 7.0 cma, mean 5.4 cm.We analyzed pathological features, Fuhrman grades, histologic subtype, tumor metastasis, perirenal fat invasion and vein tumor thrombosis in all patients.Results The proportions of the clear cell, papillary, chromophobe, unclassified and mixed cell histologic subtype were 75.8％ (538/710), 5.1％ (36/710), 4.6％ (33/710), 1.1％ (8/710) and 13.4％ (95/710), respectively.The proportions of hemorrhage, necrosis, cystic degeneration and fibrosis were 51.0％ (362/710), 30.1％ (214/710), 35.4％ (251/710) and 7.8％ (55/710), respectively.The rates of perirenal fat invasion and vein tumor thrombosis were 4.1％ (29/710) and 3.1％ (22/710).Among the 710 clinical T1b renal cell carcinoma, 144 (20.3％) were Fuhrman grade Ⅰ , 513 (72.3％) were grade Ⅱ, 43 (6.1％) were grade Ⅲ, 10 (1.4％) were grade Ⅳ.In 657 cases with low Fuhrman grade (Ⅰ/Ⅱ), 17 cases were noticed perirenal fat invasion.In 53 cases with high Fuhrman grade (Ⅲ/Ⅳ), 10 cases were noticed perirenal fat invasion.The analysis showed that high Fuhrman grading was concerned with the perirenal fat invasion.Conclusions Clinical T1b renal cell carcinoma has obvious heterogeneity in its biological behavior.Most of them has characters of high differentiation, low malignant tendency and good biological behavior.Rare carcinoma exhibits the aggressive character or early distant metastasis.During the nephron sparing surgery, perirenal fat should be removed and perform pathological examination.Vein tumor thrombosis should be bolt out and radical nephrectomy is recommended at the same time.

目的:探讨膀胱尿路上皮癌透明细胞变异亚型的临床病理特点及预后.方法:回顾性分析2005年1月～2014年12月收治的5例膀胱尿路上皮癌透明细胞变异亚型患者的临床病理资料,均为男.年龄46～78岁,中位年龄60岁.临床表现为单纯无痛性肉眼血尿3例,血尿伴腰痛1例,体检发现膀胱占位1例.肿瘤直径2.0～6.1 cm,平均3.4 cm.其中行TURBT术1例,根治性膀胱切除术4例,均未行盆腔淋巴结清扫术.结果:5例术后病理均诊断为膀胱尿路上皮癌透明细胞变异亚型.病理分级Ⅱ～Ⅲ级2例,Ⅲ级3例;病理分期pT2a1例,pT2b3例,pT3a1例;4例脉管内可见瘤栓;1例合并腺癌样分化;1例合并鳞状分化.免疫组化染色:CK7+,CK20+,EMA+,CEA+,Vimentin-,PSA-.5例均获得随访,1例TURBT术后随访10个月未见肿瘤复发及转移,4例行根治性膀胱切除术中,1例于术后26个月死于转移,3例分别随访5、12、14个月未见肿瘤复发及转移.结论:膀胱尿路上皮癌透明细胞变异亚型发病率极低,恶性度较高,肿瘤分期晚,预后差,根治性膀胱切除术是主要的治疗方法.

目的:探讨肾透明细胞癌内血管抑制蛋白-1(Vasohibin-1,VASH1)以及微血管密度(microvesseldensity,MVD)检测与肾透明细胞癌患者预后之间的关系.方法:采用免疫组织化学方法半定量测定肾透明细胞癌标本VASH1染色的平均细胞累积光密度(average optical density,AOD),并测定CD34标记的MVD.用Cox回归模型分析患者的临床和病理因素与生存预后之间的关系.结果:肾癌组织中VASH1的AOD为0.0435±0.0178,MVD均值为55±34,两者的表达均与病理分期和肿瘤内的凝固性坏死有显著相关性(P＜0.05).相关性分析显示VASH1与MVD的表达呈负相关(r=-0.641,P＜0.01).单因素回归分析证明高VASH1组肾透明细胞癌预后显著差于低VASH1组,差异均有统计学意义(HR=2.96,P＜0.05).多因素回归分析显示患者年龄、病理分期以及肿瘤内凝固性坏死与患者的总体生存(HR=4.90,P＜0.05;HR=3.08,P＜0.05;HR=3.05,P＜0.05)和无复发生存(HR=3.91,P＜0.05;HR=2.85,P＜0.05;HR=3.24,P＜0.05)呈显著相关性.结论:在肾透明细胞癌中,低VASH1表达提示较好的预后,而患者年龄、病理分期以及肿瘤内凝固坏死是肾透明细胞癌的独立预后因素.此研究仍待前瞻性大规模临床试验的验证.

目的:分析阴茎癌近年的发病特点,并对临床和病理特点作初步探讨.方法:回顾性分析我院2004年6月～2014年6月收治的79例阴茎癌患者的临床资料:腹股沟淋巴结双侧肿大50例,单侧肿大24例,无明显肿大5例.71例行阴茎部分切除术,5例行阴茎全切术加会阴部尿道造口术,3例行局部肿物切除术.结果:腹股沟淋巴结双侧肿大50例,单侧肿大24例,淋巴结大小介于1～3 cm之间,平均1.77 cm.术后病理检查报告示高分化鳞状细胞癌43例,中分化鳞癌18例,低分化鳞癌3例,疣状癌12例,乳头状瘤局部恶变3例.结论:超过60％阴茎癌患者伴有腹股沟淋巴结肿大,而活检证实淋巴结肿大者仅一半存在转移癌;肿大的淋巴结约半数与炎症反应有关;如患者存在活动性差的多发肿大淋巴结且伴随脉管瘤栓,则淋巴结转移的风险较高,预后较差.

Prostate cancer remains a leading cause of cancer-related mortality worldwide owing to our inability to treat effectively castration-resistant tumors. To understand the signaling mechanisms sustaining castration-resistant growth, we implemented a mass spectrometry-based quantitative proteomic approach and use it to compare protein phosphorylation in orthotopic xenograft tumors grown in either intact or castrated mice. This investigation identified changes in phosphorylation of signaling proteins such as MEK, LYN, PRAS40, YAP1 and PAK2, indicating the concomitant activation of several oncogenic pathways in castration-resistant tumors, a notion that was confirmed by tumor transcriptome analysis. Further analysis demonstrated that the activation of mTORC1, PAK2 and the increased levels of YAP1 in castration-resistant tumors can be explained by the loss of androgen inhibitory actions. The analysis of clinical samples demonstrated elevated levels of PAK2 and YAP1 in castration-resistant tumors, whereas knockdown experiments in androgen-independent cells demonstrated that both YAP1 and PAK2 regulate cell colony formation and cell invasion activity. PAK2 also influenced cell proliferation and mitotic timing. Interestingly, these phenotypic changes occur in the absence of obvious alterations in the activity of AKT, MAPK or mTORC1 pathways, suggesting that PAK2 and YAP1 may represent novel targets for the treatment of castration-resistant prostate cancer. Pharmacologic inhibitors of PAK2 (PF-3758309) and YAP1 (Verteporfin) were able to inhibit the growth of androgen-independent PC3 xenografts. This work demonstrates the power of applying high-resolution mass spectrometry in the proteomic profiling of tumors grown in vivo for the identification of novel and clinically relevant regulatory proteins.