CD44v6、P27蛋白在乳腺癌组织中的表达及意义

目的 探讨乳腺癌中CD44v6、p27蛋白表达的意义。方法 应用免疫组化S-P法检测65例乳腺癌中CD44v6、p27蛋白表达。结果 65例乳腺癌中CD44v6、p27蛋白表达总阳性率分别为58.4％、38.4％。CD44v6蛋白阳性表达率与乳腺癌组织学类型、腋淋巴结转移呈正相关(P<0.05,P<0.01),与预后呈负相关(P<0.01),与组织学分级无明显相关性(P>0.05);p27蛋白阳性表达与乳腺癌组织学类型、组织学分级及腋淋巴结转移呈负相关(P<0.05),与预后呈正相关(P<0.05)。结论 CD44v6、p27蛋白表达与乳腺癌浸润、转移及预后显著相关,检测乳腺癌中CD44v6、p27蛋白表达水平,对判断乳腺癌恶性程度、复发转移潜能,评估患者预后及术后选择合理治疗方案有一定参考价值。     

PCNA AND P53 EXPRESSION IN ORAL LEUKOPLAKIA WITH DIFFERENT DEGREES OF KERATINIZATION

Leukoplakias are oral lesions that may have many clinical and histological aspects and they are usually associated with malignancy when dysplastic alterations are shown. However, these transformations may occur in non-dysplastic lesions that show harmless clinical aspect. For this reason, the proposal was to study the p53 and PCNA immunohistochemical expression in non-dysplastic leukoplakias, trying to correlate the results only with the epithelial keratinization degree. For this, 24 leukoplakias degrees I, II and III of Grinspan were used, all of them located in oral mucosa. Most of the leukoplakias showed p53 and PCNA expression in their different keratinization degrees. The p53 marking was confined to the basal and parabasal layers, while the PCNA marking occurred in practically all epithelial layers. The expression pattern of these markers was histologically and statistically similar between the lesions with these keratinization variations. It was evident that non-dysplastic epithelium of leukoplakias showed submicroscopical signs of alterations that lead to malignant transformation, and that the keratinization degree did not correlate to a greater risk of this event.     

转移相关基因nm23和P53及S100A4在晚期胃癌中的表达及与侵袭转移的相关性研究

目的探讨转移相关蛋白（nm23和P53及S100A4）在晚期胃癌转移发展过程中的意义。方法应用组织芯片和免疫组织化学方法研究nm23、P53和S100A4在74例胃癌患者的癌、癌旁、淋巴结转移、远处转移（肝脏、胰腺、卵巢等）组织中的表达。结果同癌旁组织相比，癌组织中P53和S100A4表达明显升高（P〈0．01），而nm23的表达明显降低（P〈0．05）；同癌组织相比，淋巴结中nm23的表达明显降低（P〈0．05）。远处转移组织S100A4表达明显升高（P〈0．01）。3者的阳性表达与胃癌的部分恶性生物学行为有关。癌组织中nm23^＋／P53^＋、P53^＋／S100A4^＋和nm23^＋／S100A4^＋的基因表型比例分别为48例（64．9％）、50例（67．6％）和39例（52．7％），其中P53^＋／S100A4^＋、nm23^＋／S100A4^＋和nm23^＋／P53^＋／S100A4^＋均与胃癌的高转移潜能相关。结论nm23和S100A4在肿瘤转移中发挥了重要作用；联合检测nm23、P53和S100A4的表达可用于评定胃癌的转移潜能。     

脂多糖诱导大鼠肺泡巨噬细胞p38蛋白激酶基因的表达

目的探讨脂多糖 (LPS)诱导的肺泡巨噬细胞 (AM) p3 8蛋白激酶mRNA及其蛋白质表达的变化。方法分离培养AM ,分别采用原位分子杂交和免疫细胞化学方法检测AM p3 8蛋白激酶mRNA及其蛋白质的表达。结果p3 8mRNA在正常对照组AM中有少量表达 ,LPS刺激后 p3 8mRNA表达显著增强 (P <0 .0 1 )。p3 8蛋白质在正常对照组AM中的表达呈弥散性分布 ,以胞浆为主 ,胞核较少 ;LPS刺激后 ,胞浆染色明显减弱 ,胞核染色明显增强 ,胞核染色阳性细胞的百分比由正常对照组的 6.1 2± 2 .0 5 %上升到 3 5 .2± 8.3 5 % ,为正常对照组的 5 .75倍 ,二者比较差异具有显著性 (P <0 .0 1 )。结论LPS刺激AM p3 8mRNA的表达增强 ,诱发 p3 8蛋白激酶由胞浆转位到胞核     

p53、nm23蛋白在宫颈鳞癌中的表达及其临床意义

目的研究p53、nm23基因在宫颈鳞癌中的表达及其临床意义.方法采用免疫组织化学S-P法检测45例宫颈鳞癌组织、10例宫颈上皮内瘤变和10例正常宫颈鳞状上皮中p53、nm23蛋白的表达.结果p53、nm23蛋白在宫颈鳞癌中的阳性表达率分别为64.44%、46.67%;在CIN中阳性表达率分别为0、30.00%;在NE组均无表达.p53蛋白在宫颈鳞癌中阳性表达与在CIN、NE中的不表达差异均有显著性(P＜0.01).nm23蛋白在宫颈鳞癌组织中的阳性表达与在NE中的不表达差异有显著性(P＜0.05),但与在CIN中的表达差异无显著性(P＞0.05);与病理学分级、淋巴结转移均呈负相关(P＜0.05,P＜0.01).结论p53、nm23基因参与了宫颈鳞癌的发生发展过程.p53蛋白的过表达是宫颈癌组织恶性变的生物学标志;检测nm23蛋白对判断宫颈癌淋巴结转移和预后有重要意义.     

SB203580对肾缺血/再灌注损伤时细胞凋亡及p38MAPK影响的实验研究

目的　探讨不同时间及不同浓度p38MAPK特异性抑制剂SB2 0 35 80对肾缺血 /再灌注损伤过程中肾功能、细胞凋亡及 p38MAPK活性、表达量、p38MAPK底物的影响。 方法　 4 9只大鼠按缺血 /再灌注及给药时间的不同 ,随机分为 7组 ,每组7只大鼠按正交拉丁方表的顺序 ,经尾静脉注射相同体积、不同剂量的SB ,使其在大鼠体内达到不同的浓度。测定BUN和Scr;用TUNEL试剂盒检测细胞凋亡情况 ;Westernblot技术用于蛋白定性及半定量分析。结果　SB可显著减轻大鼠肾缺血 /再灌注损伤造成的Scr和BUN的升高、肾小管上皮细胞的凋亡及 p38MAPK的激活 ,但存在模型、剂量及给药时机的差异 (P<0 .0 5 ) ,缺血前 3h之前给药 ,使其体内血药浓度达到 5 μmol/L左右可取得较好的效果。 结论　SB可显著减轻大鼠肾缺血 /再灌注损伤 ,在缺血前 3h之前给药 ,同时使其血药浓度达到 5 μmol/L左右可取得最佳效果。     

P27 Cyclin D_1在胆囊癌中的表达及意义

目的研究p2 7、CyelinDl 在胆囊癌中的表达情况 ,并探讨它们与肿瘤分化程度及生物学行为的关系。方法应用免疫组织化学S -P法检测 10例胆囊炎及 32例胆囊癌标本p2 7及CyelinDl的表达状况。结果p2 7在胆囊炎上皮中为低表达 ,在胆囊癌中少部分表现出高表达。而CyelinDl 在胆囊炎上皮中低表达 ,而在胆囊癌中大部分呈现高表达 ,两者间差异显著 (P <0 .0 5 )。结论CyclinDl在胆囊癌的发生发展中有重要作用 ,且与患者预后有关。     

Effect of N-tosyl-L-phenylalanylchloromethyl Ketone on Tumor Necrosis Factor-alpha -induced NF-κB Activation and Apoptosis in U937 Cell Line

Summary: To investigate the effect of N-tosyl-L-phenylalanylchloromethyl ketone (TPCK) on tumor necrosis factor-alpha-induced NF-κB activation and apoptosis in U937 cell line, changes and subcellular localization of NF-κB/p65 and IκB-α were observed by fluorescencemicroscopy and expression and degradation of IκB-α by flow cytometry. The apoptosis of U937 cells was measured by flow cytometry and electrophoresis of DNA. Immunolfluorescence assay showed that NF-κB/p65,IκB-α only localized in cytoplasm. After TNF-α stimulation, p65 was localized only in nuclei, and IκB-α was only localized in cytoplasm and decreased. The changes of TNF-α stimulation were specifically inhibited by TPCK. Flow cytometry also revealed the downregulation of IκB-α protein during TNF-α-induced apoptosis and the down-regulation was specifically inhibited by TPCK. Flow cytometry also showed the apoptosis of U937 cells after TNF-α induction. DNA ladder can be detected in cells treated by TNF-α. It is concluded that degradation of IκB-α protein and NF-κB/p65 translocation occur during TNF-α-induced apoptosis of U937 cells, suggesting the activation of NF-κB.TPCK-sensitive protease plays an important role in the degradation of IκB-α protein induced by TNF-α in U937 cells. TPCK sensitive protease also plays an important role in the apoptosis of U937 cells induced by TNF-α.     

皮肤鳞状细胞癌中p53、bcl-2和c-myc的表达及意义

目的 研究p53、bcl—2和c—myc在皮肤鳞状细胞癌中的异常表达及其与癌分化程度的关系。方法 应用免疫组织化学S-P法检测58例皮肤鳞状细胞癌中p53、bcl—2和c—myc的表达水平。结果 58例皮肤鳞状细胞癌中p53、bcl-2和c—myc的阳性表达率分别为48．3％、67．2％和32．8％。结论 p53、bcl—2和c—myc异常表达在皮肤鳞状细胞癌的发生、发展中起重要作用，并与皮肤癌的恶性程度有关。