Adult Renal Cell Carcinoma: A Review of Established Entities from Morphology to Molecular Genetics

According to the current World Health Organization (WHO), renal cell carcinomas (RCCs) that primarily affect adults are classified into 8 major subtypes. Additional emerging entities in renal neoplasia have also been recently recognized and these are discussed in further detail by Mehra et al (Emerging Entities in Renal Neoplasia, Surgical Pathology Clinics, 2015, Volume 8, Issue 4). In most cases, the diagnosis of a RCC subtype can be based on morphologic criteria, but in some circumstances the use of ancillary studies can aid in the diagnosis. This review discusses the morphologic, genetic, and molecular findings in RCCs previously recognized by the WHO, and provides clues to distinction from each other and some of the newer subtypes of RCC. As prognosis and therapeutic options vary for the different subtypes of RCC, accurate pathologic distinction is critical for patient care.     

胃癌和胃癌前病变Cx43、PCNA的表达及意义

目的　通过观察间隙连接蛋白 Cx4 3和增殖细胞核抗原 (PCNA )在正常胃粘膜、胃癌前病变和胃癌中的表达和分布情况 ,探讨 Cx基因表达与胃癌发生的关系。　方法　运用 SP免疫组织化学方法检测 Cx4 3、PCNA在 70例原发性胃癌 ,6 2例中、重度不典型增生和 16例正常胃粘膜中表达规律。　结果　 Cx4 3在正常胃粘膜 ,中、重度不典型增生和胃癌中表达的阳性率分别为 10 0 % ,83.9%和 17.1% ,三者比较差异有显著性 (P<0 .0 5 )。 Cx4 3表达与胃癌的分化程度相关 (P<0 .0 1)。胃癌前病变、胃癌组中的 PCNA较正常胃粘膜组增高 (P<0 .0 1)。 Cx4 3表达与 PCNA呈负相关 (P<0 .0 1)。　结论　 Cx4 3表达降低在胃癌发生发展中起重要作用 ,Cx4 3可做为胃癌早期诊断的指标     

胃癌组织端粒酶活性与催化亚基hTERT表达的关系

研究胃癌、胃黏膜肠化生及正常黏膜组织端粒酶活性与人端粒酶催化亚基(hTERT)表达的相关性及端粒酶激活在胃癌发生中的作用.方法:通过端粒重复序列扩增(TRAP)和逆转录聚合酶链反应(RT -PCR)方法测定3种胃癌细胞株、26例胃癌、10例胃黏膜肠化生和36例正常胃黏膜组织标本端粒酶活性和hTERT表达.结果:3种胃癌细胞株、24例胃癌组织有端粒酶活性;4例肠化生端粒酶活性较弱;36例正常胃黏膜标本未测到端粒酶活性.hTERT在26例胃癌组织、5例肠化胃黏膜中表达;正常胃黏膜无表达.端粒酶活性、hTERT表达与肿瘤的分期和病理分级无关.结论:hTERT在肿瘤形成的早期阶段表达,端粒酶的激活是胃癌形成的关键步骤.     

胃癌组织p16基因蛋白表达的意义

目的　检测 p1 6基因蛋白在胃癌组织、癌旁组织中的表达及其分布特点 ,分析其与胃癌临床病理学特征及预后的关系 .方法　采用 S- P免疫组织化学法对 53例胃癌组织及 35例癌旁组织进行 p1 6蛋白的定位观察 .结果　各病理类型胃癌组织、癌旁组织均有 p1 6基因蛋白表达 .阳性率分别为 62 .3% (33/53)和 88.6% (31 /35) ,阳性细胞的棕黄色颗粒主要位于细胞核 .胃癌 p1 6基因蛋白表达与性别、年龄、肿瘤部位在统计学上无差异 (P>0 .0 5) ;而与组织学类型、病理分级、淋巴结转移、临床病理分期在统计学上有差异 (P<0 .0 5) .p1 6蛋白阳性者 5年生存率 51 .0 %高于 p1 6蛋白阴性者 2 0 .0 % (P<0 .0 5) .结论　 p1 6基因缺失和表达水平的改变与胃癌发生、发展密切相关 ,检测 p1 6基因蛋白表达可作为辅助临床判断胃癌的生物学行为及推测预后的指标     

雷公藤内酯对人胃癌细胞株FGC_(85)杀伤作用的光镜和电镜观察

本文应用核苷掺入技术及电镜观察首次证实雷公藤内酯对人胃癌细胞株 FGC_(85)的杀伤作用。用药早期,细胞数,分裂指数及 DNA,RNA 合成无明显变化,但出现核仁脱粒及核仁破碎等变化;晚期,电镜观察发现细胞以凋落方式死亡,药物主要作用于间期细胞,其杀伤机构的始动环节可能与核酸代谢障碍无关。     

BIOCHEMICAL CORRECTION IN THE SYNDROME OF HYPERTENSION AND HYPERKALAEMIA BY SEVERE DIETARY SALT RESTRICTION SUGGESTS RENIN-ALDOSTERONE SUPPRESSION CRITICAL IN PATHOPHYSIOLOGY

1. Plasma potassium and chloride concentrations were raised and plasma renin activity, aldosterone, bicarbonate and arterial pH were reduced in two brothers with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome), on unrestricted or moderately restricted sodium diets. 2. These abnormalities were corrected in both patients within 10 days of severe sodium restriction. 3. Pressor sensitivity to cold and angiotensin II decreased on low sodium diet, associated with a fall in blood pressure. 4. Increasing distal tubular sodium delivery by infusion of normal saline increased fractional excretion of potassium when aldosterone had been stimulated by severely restricted sodium diet, but not when aldosterone levels were low on unrestricted sodium diet. 5. These findings are consistent with excessive sodium reabsorption as the primary renal lesion in Gordon's syndrome, leading to volume expansion and suppression of renin and aldosterone. Severe dietary sodium restriction leading to volume contraction, by stimulating renin and aldosterone and promoting kaliuresis, corrects the abnormalities.     

胃癌D17S261和D17S799位点二核苷酸重复序列不稳定性的意义

目的研究二核苷酸重复序列不稳定性〔ＤＲＳＩ〕在胃癌发生中的作用及其临床意义．方法采用ＰＣＲ方法检测了Ｄ１７Ｓ２６１和Ｄ１７Ｓ７９９位点二核苷酸重复序列不稳定性．结果胃癌总ＤＲＳＩ发生率为３４％（１７／５０），其中高中分化腺癌ＤＲＳＩ阳性率（６６７％，１０／１５）显著高于低分化癌（１９４％，６／３１，Ｐ＜００１）；肠型胃癌ＤＲＳＩ阳性率（５５６％，１０／１８）显著高于胃型胃癌（２０％，６／３０，Ｐ＜００５），ＤＲＳＩ与胃癌部位、大小、浸润、分期、淋巴结转移无显著相关．结论ＤＲＳＩ在胃癌的发生中可能起重要作用．     

新生儿胃穿孔14例治疗体会

目的　探讨新生儿胃穿孔的发病特点和治疗方法。方法　对我院近 10年治疗的 14例新生儿胃穿孔进行回顾性分析。结果　 14例新生儿胃穿孔皆行手术治疗 ,术后死亡 7例。结论　新生儿胃穿孔多因先天性胃壁肌层发育不良及胃内张力增高缺血缺氧所致。早期诊断 ,及时手术 ,减少并发症及术后加强支持疗法是提高本病治愈率的关键