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| 1 | PTEN encoding product:a marker for tumorigenesis and progression of gastric carcinoma显示文摘AIM: To detect the expression of PTEN encoding productin normal mucosa, intestinal metaplasia (IM), dysplasia andcarcinoma of the stomach, and to investigate its clinicalimplication in tumorigenesis and progression of gastriccarcinoma.METHODS: Formalin-fixed paraffin embedded specimens from184 cases of gastric carcinoma, their adjacent normal mucosa,IM and dysplasia were evaluated for PTEN protein expressionby SABC immunohistochemistry. PTEN expression wascompared with tumor stage, lymph node metastasis, Lauren'sand WHO's histological classification of gastric carcinoma.Expression of VEGF was also detected in 60 cases of gastriccarcinoma and its correlation with PTEN was concerned.RESULTS: The positive rates of PTEN protein were 100 %(102/102), 98.5 %(65/66), 66.7 % (4/6) and 47.8 %(88/184)in normal mucosa, IM, dysplasia and carcinoma of the stomach,respectively. The positive rates in dysplasia and carcinomawere lower than in normal mucosa and IM (P<0.01).Advanced gastric cancers expressed less frequent PTEN thanearly gastric cancer (42.9 % v567.6 %, P<0.01). The positiverate of PTEN protein was lower in gastric cancer with thanwithout lymph node metastasis (40.3 % v563.3 %, P<0.01).PTEN was less expressed in diffuse-type than in intestinal-type gastric cancer (41.5 % v557.8 %,P<0.05). Signet ringcell carcinoma showed the expression of PTEN at the lowestlevel (25.0 %, 7/28); less than well and moderatelydifferentiated ones (P<0.01). Expression of PTEN was notcorrelated with expression of VEGF (P>0.05).CONCLUSION: Loss or reduced expression of PTEN proteinoccures commonly in tumorigenesis and progression of gastriccarcinoma. It is suggested that PTEN can be an objective markerfor pathologically biological behaviors of gastric carcinoma. | Lin Yang Li-Ge Kuang Hua-Chuan Zheng Jin-Yi Li Dong-Ying Wu Su-Min Zhang Yan Xin No.4 Lab,Cancer Institute,The First Affiliated Hospital,China Medical University,Shenyang 110001,China Ying Chen Shen Yang Gynecology & Obstetrics Hospital,Shenyang 110014,China | 2003 | World Journal of Gastroenterology2003，9，1： | 127 |
| 2 | 胃癌中survivin、PTEN、cyclinD1和p53基因的表达及其相关性显示文摘目的 探讨survivin基因表达与胃癌生物学行为及PTEN、cyclinD1、p5 3和凋亡指数 (AI)的相关性。 方法 用免疫组化EnVision法检测 15 6例胃癌组织、4 6例正常胃黏膜和 4 6例癌旁不典型增生组织中survivin、PTEN、cyclinD1和 p5 3的表达以及AI。结果 survivin、PTEN、cyclinD1和p5 3的阳性检测率分别为 6 5 %、4 1%、6 1%和 5 8%。survivin未见核内表达。survivin、cyclinD1和 p5 3表达与胃癌的组织学类型相关 (P <0 0 1,P <0 0 5和P <0 0 1) ;survivin和cyclinD1表达与胃癌的浸润深度相关 (P <0 0 1和P <0 0 5 ) ;4种基因蛋白表达均与淋巴结转移相关 ,survivin的表达与p5 3和cyclin阳性表达呈正相关 ,与PTEN的阳性表达呈负相关 ;survivin、p5 3和cyclinD1高表达均有患者术后 <3年生存期相关 (P <0 0 5 ,P <0 0 1和P<0 0 1) ;survivin阳性组的平均AI为 0 6 1,明显低于survivin阴性组 (P <0 0 1) ;PTEN阳性组明显高于阴性组 (P <0 0 1)。结论 survivin、PTEN、p5 3和cyclinD1基因在胃癌的发生、发展中起着不同程度的作用 ,它们的检测对胃癌恶性度的判定、预后和进一步治疗提供有效的依据。survivin、p5 | 董吉顺 倪灿荣 | 2003 | 临床与实验病理学杂志2003，19，4： | 45 |
| 3 | 胃癌组织中PTEN,VEGF,MMP-9的表达及相关性研究显示文摘目的 探讨胃癌中PTEN,VEGF,MMP-9的表达及其与胃癌生物学行为的关系。方法 应用免疫组织化学SP法检测 7 1例胃癌组织及 3 7 例远癌胃黏膜中PTEN,VEGF,MMP-9 的表达。结果 胃癌组织中PTEN蛋白表达 ( 7 1. 8% )显著低于远癌胃黏膜的表达 ( 1 0 0% ) (P < 0. 0 1 ) , 且与肿瘤的组织分化程度、浸润深度及淋巴结转移呈负相关 (均P< 0. 0 5 ),而与年龄、性别等无关 (均P> 0. 0 5 ) 。VEGF在胃癌中的表达 ( 6 2. 0% ) 显著高于远癌胃黏膜的表达 ( 2 9. 7% ) (P < 0. 0 1 ) ,且与淋巴结转移呈正相关 (P< 0. 0 1 ) ,而与年龄、性别、组织分化程度及肿块浸润深度无关 (均P> 0. 0 5 )。MMP-9在胃癌中的表达 ( 6 9% ) 显著高于远癌胃黏膜的表达 ( 4 0. 5% ) (P < 0. 0 1 ),且与淋巴结转移呈正相关 (P< 0. 0 5 ) , 而与年龄、性别、组织分化程度及癌组织浸润深度无关 (均P> 0. 0 5 )。PTEN在胃癌中的表达与VEGF和MMP-9呈负相关 (P < 0. 0 5 )。结论 胃癌中PTEN蛋白表达降低,其表达与肿瘤的组织分化程度、浸润深度及淋巴结转移密切相关,且与VEGF,MMP-9表达呈负相关。联合检测PTEN,VEGF,MMP-9有助于提高胃癌侵袭转移能力的评估,对胃癌的预后判断具有重要的临床意义。 | 贺荣芳 胡忠良 沈明 文继舫 | 2005 | 中国普通外科杂志2005，14，3： | 39 |
| 4 | 二参三草汤治疗慢性萎缩性胃炎癌前病变的临床观察及其对PTEN、ERK、AKT表达影响的研究显示文摘目的:观察二参三草汤对慢性萎缩性胃炎癌前病变的治疗效果及对PTEN、ERK和AKT表达的影响。方法:40例符合纳入标准的患者随机分为两组,每组20例,治疗组给予二参三草汤,对照组给予胃复春片,疗程均为6个月。观察两组患者临床疗效、内镜、病理疗效及治疗前后PTEN、AKT、ERK表达积分的变化。结果:临床症状缓解总有效率:治疗组95%,对照组65%;内镜下黏膜表现及病理组织学改善情况:治疗组愈显率70%,对照组30%;两组间比较差异显著(P<0.05)。免疫组化结果:治疗组治疗前后PTEN、AKT、ERK的表达差异具有显著统计学意义(P<0.01),而对照组治疗前后AKT、ERK表达水平变化不明显。结论:二参三草汤能明显改善CAG癌前病变的临床症状、内镜下表现及病理组织学表现,其上调抑癌基因PTEN和下调癌基因AKT、ERK的表达可能是二参三草汤治疗慢性萎缩性胃炎癌前病变的部分作用机理。 | 黄婷婷 周晓虹 | 2016 | 中医药信息2016，33，1： | 38 |
| 5 | Inactivation of PTEN is associated with increased angiogenesis and VEGF overexpression in gastric cancer显示文摘AIM: To investigate the expression of PTEN/MMAC1/TEP1 and vascular endothelial growth factor (VEGF), their roles in biologic behavior and angiogenesis and their association in gastric cancer.METHODS: Immunohistochemical staining was used to evaluate the expression of PTEN, VEGF and microvascular density (MVD) on paraffin-embedded sections in 70 patients with primary gastric cancer and 24 patients with chronic superficial gastritis (CSG). Expression of PTEN, VEGF and MVD were compared with clinicopathological features of gastric cancer. The relationship between expression of PTEN, VEGF and MVD as well as the relationship between PTEN and VEGF expression in caner cells were investigated. RESULTS: PTEN expression significantly decreased (t= 3.98, P<0.01) whereas both VEGF expression and MVD significant increased (t = 4.29 and 4.41, respectively, both P<0.01) in gastric cancer group compared with CSG group. PTEN expression was significantly down-regulated (t=1.95, P<0.05) whereas VEGF expression (t = 2.37, P<0.05) and MVD (t= 3.28, P<0.01) was significantly up-regulated in advanced gastric cancer compared with early-stage gastric cancer. PTEN expression in gastric cancer showed a negative association with lymph node metastasis (t= 3.91, P<0.01), invasion depth (t= 1.95, P<0.05) and age (t= 4.69, P<0.01). MVD in PTEN-negative gastric cancer was significantly higher than that in PTEN-positive gastric cancer (t=3.69, P<0.01), and there was a negative correlation betweenPTEN expression and MVD (γ=-0.363, P<0.05). VEGF expression was positively associated with invasion depth (especially with serosa invasion, t = 4.69, P<0.01), lymph node metastasis (t= 2.31, P<0.05) and TNM stage (t= 3.04, P<0.01). MVD in VEGF-positive gaslyic cancer was significantly higher than that in VEGF-negative gastric cancer (t=4.62, P<0.01), and there was a positive correlation between VEGF expression of and MVD (y = 0.512, P<0.05). VEGF expression in PTEN-negative gaslyic cancer was significantly stronger than that in PTEN-positive gastric cancer (t=2.61, P<0.05), and there was a significantly negative correlation between the expression of VEGF and PTEN (γ=-0.403, P<0.05).CONCLUSION: Our results imply that inactivation of PTEN gene and over-expression of VEGF contribute to the neovascularization and progression of gastric cancer. PTEN-related angiogenesis might be attributed to its up-regulation of VEGF expression. PTEN and VEGF could be used as the markers reflecting the biologic behaviors of tumor and viable targets in therapeutic approaches to inhibit angiogenesis of gastric cancers. | Ye-JiangZhou Yu-XiaXiong Xiao-TingWu DeShi WeiFan TongZhou Yue-ChunLi XiongHuang | 2004 | World Journal of Gastroenterology2004，10，21： | 31 |
| 6 | Loss of heterozygosity on 10q23.3 and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions显示文摘AIM: To investigate the loss of heterozygosity (LOH) and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions.METHODS: Thirty cases of normal gastric mucosa, advanced and early stage gastric cancer, intestinal metaplasia, atrophic gastritis, and atypical hyperplasia were analyzed for PTEN LOH and mutations within the entire coding region of PTEN gene by PCR-SSCP denaturing PAGE gel electrophoresis,and PTEN mutation was detected by PCR-SSCP sequencing followed by silver staining.RESULTS: LOH rate found in respectively atrophic gastritis was 10% (3/30), intestinal metaplasia 10% (3/30), atypical hyperpiasia 13.3% (4/30), early stage gastric cancer 20%(6/30), and advanced stage gastric cancer 33.3% (9/30),None of the precancerous lesions and early stage gastric cancer showed PTEN mutations, but 10% (3/30) of the advanced stage gastric cancers, which were all positive for LOH, showed PTEN mutation.CONCLUSION: LOH of PTEN gene appears in precancerous lesions, and PTEN mutations are restricted to advanced gastric cancer, LOH and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer. | Yi-LingLi ZhongTian Dong-YingWu Bao-YuFu YahXin | 2005 | World Journal of Gastroenterology2005，11，2： | 34 |
| 7 | Upregulation of PTEN involved in rosiglitazone-induced apoptosis in human hepatocellular carcinoma cells显示文摘瞄准:调查 rosiglitazone 的效果, peroxisomeproliferator-ac-tivated 受体 gamma ( PPARy )收缩筋在在 hepatocellular carcinomacells 在染色体 10 基因( PTEN )和房间生长上删除的磷酸酶 andtensin 相当或相同事物的表示上,象这些 effects.Methods 的内在的机制一样: RT-PCR 和西方的 blottinganalyses 被执行在 Hep3B 房间 treatedwith rosiglitazone.3-( 4,5-Dimethylthiazol-2-yl )检测抄写和 PTEN 的表示 -2,5-diphenyl | Liang-qi CAO Xi-lin CHEN Qian WANG Xiao-hui HUANG Mao-chuan ZHEN Long-juan ZHANG Wen LI Jiong BI | 2007 | Acta Pharmacologica Sinica2007，28，6： | 32 |
| 8 | PTEN和p53蛋白在肝癌组织中的表达及意义显示文摘背景和目的:抑癌基因PTEN于1997年首次被报道之后即成为研究热点。国外曾有研究小组检测人类肝癌中PTEN基因突变情况,但对有关PTEN蛋白在肝癌中的表达情况了解甚少;p53基因突变是肝癌发生的机制之一,但对于p53基因突变与肝癌某些生物学行为的相关性,不同研究的结果不一。我们拟通过检测PTEN、p53蛋白在肝癌中的表达来了解PTEN、p53与肝癌发生和进展的关系。方法:本研究共取62例石蜡包埋的肝癌标本,所有组织切片均含肝癌组织及癌旁组织。采用免疫组化SP法检测PTEN及突变的p53蛋白的表达情况。结果:62例标本中癌旁肝组织均呈现明确的PTEN阳性染色(胞浆),只有29例(46.8%)标本中肝癌组织呈阳性染色,PTEN在有包膜或无侵袭性肝癌中的表达明显高于无包膜或有侵袭性的肝癌。所有标本癌旁肝组织均未见p53阳性染色,21例肝癌组织p53染色呈阳性(胞核)。p53蛋白的表达与肝癌侵袭性或分化程度无关。结论:PTEN的失表达及p53基因突变可能在肝癌发生中发挥作用,PTEN失表达还可能与肝癌的恶性进展有关。 | 程黎明 王思元 林菊生 | 2003 | 癌症2003，22，1： | 32 |
| 9 | Growth,invasion,metastasis,differentiation,angiogenesis and apoptosis of gastric cancer regulated by expression of PTEN encoding products显示文摘AIM: To investigate expression of PTEN in gastric cancer and to explore its roles in tumorigenesis and progression of gastric cancer.METHODS: Formalin-fixed and paraffin-embedded tissues of adjacent non-tumor mucosa and primary foci from 113cases of gastric cancers were studied for the expression of PTEN and Caspase-3 andmicrovessel density (MVD)by streptavidin-peroxidase (S-P) immunohistochemistry with antibodies against PTEN, Caspase-3, and CD34. The relationship between PTEN and Caspase 3 expression and clinicopathological parameters of tumors was compared.RESULTS: Primary gastric cancer cells expressed PTEN less frequently than adjacent epithelial cells of primary foci (54.9% vs89.4%; P=0.000, χ2=33.474). PTEN expression was significantly associated with invasive depth (P=0.003,rs=0.274), metastasis (P=0.036, rs=0.197), growth pattern (P=0.008, rs=0.282), Lauren′s classification (P=0.000,rs=0.345), and histological classification (P=0.005, rs=0.262)of tumors, but not with tumor size (P=0.639, rs=0.045),Borrmann′s classification (P=0.544, rs=0.070) or TNM staging (P=0.172, rs=0.129). PTEN expression was negatively correlated with MDV in primary gastric cancer (P=0.020,F=5.558). Primary gastric cancer cells showed less frequent immunoreactivity to Caspase-3 than adjacent epithelial cells of primary foci (32.7 % vs 50.4 %; P=0.007,χ2=7.286).Caspase-3 expression was dependent of PTEN expression in primary gastric cancer cells (P=0.000, χ2=15.266).CONCLUSION: Down-regulated expression of PTEN plays an important role in tumorigenesis, progression, growth,differentiation and angiogenesis of gastric cancer. Low expression of PTEN can decrease expression of Caspase-3to disorder apoptosis of tumor cells, which might explain the molecular mechanisms of PTEN contributions to tumorigenesis and progression of gastric cancer. | Wei-GuoJiang Yin-ChangZhang YanXin Hua-ChuanZheng Yi-LingLi Jin-MinSun Xue-FeiYang Xiao-HanLi | 2003 | World Journal of Gastroenterology2003，9，8： | 33 |
| 10 | Expression and significance of PTEN, hypoxia-inducible factor-1 alpha in colorectal adenoma and adenocarcinoma显示文摘AIM: To investigate the expression and significance of PTEN,hypoxia-inducible factor-1 alpha (HIF-1α), and targeting gene VEGF during colorectal carciogenesis.METHODS: Total 71 cases colorectal neoplasms (9 cases of colorectal adenoma and 62 colorectal adenocarcinoma)were formalin fixed and paraffin-embedded, and all specimens were evaluated for PTEN mRNA, HIF-1α mRNA and VEGF protein expression. PTEN mRNA, HIF-1α mRNA were detected by in situ hybridization. VEGF protein was identified by citrate-microwave SP immunohistochemical method.RESULTS: There were significant differences in PTEN, HIF1α and VEGF expression between colorectal adenomas and colorectal adenocarcinoma (P<0.05). The level of PTEN expression decreased as the pathologic stage increased.Conversely, HIF-1α and VEGF expression increased with the Dukes stage as follows: stage A (0.1029±0.0457:0.1207± 0.0436), stage B (0.1656±0.0329: 0.1572±0.0514),and stage C+D (0.2335±0.0748: 0.2219±0.0803). For PTEN expression, there was a significant difference among Dukes stage A, B, and C+D, and the level of PTEN expression was found to be significant higher in Dukes stage A or B than that of Dukes stage C or D. For HIF-1α expression,there was a significant difference between Dukes stage A and B, and the level of HIF-1α expression was found to be significantly higher in Dukes stage C+D than that of Dukes stage A or B. The VEGF expression had similar results as HIF-1α expression. In colorectal adenocarcinoma,decreased levels of PTEN were significantly associated with increased expression of HIF-1α mRNA (r=-0.36, P<0.05)and VEGF protein (r=-0.48, P<0.05) respectively. The levels of HIF-1 were positively correlated with VEGF expression (r=0.71, P<0.01).CONCLUSION: Loss of PTEN expression and increased levels of HIF-1α and VEGF may play an important role in carcinogenesis and progression of colorectal adenocarcinoma. | Ying-AnJiang Li-FangFan Chong-QingJiang You-YuanZhang He-ShengLuo Zhi-JiaoTang DongXia MingWang | 2003 | World Journal of Gastroenterology2003，9，3： | 33 |
| 11 | Notch1和PTEN在胃癌组织中的表达及其意义显示文摘背景与目的:Notch1属于Notch跨膜受体家族,在细胞分化中发挥关键作用。最近研究发现Notch1具有促癌和抑癌双重作用,在肿瘤发生机制中作用复杂,在胃癌组织中的表达以及与临床病理特征的关系目前尚不清楚。本研究旨在研究Notch1与PTEN在胃癌组织中的表达及其意义。方法:通过免疫组化方法检测168例胃癌组织和27例正常胃组织的组织芯片中Notch1和PTEN的表达,分析两者的表达水平与临床病理特征的关系以及两者的相互关系。结果:Notch1在胃癌组织中的阳性率为61.9%(104/168),明显高于正常胃组织25.9%(7/27)(P<0.05),其表达与肿瘤大小、分化程度、浸润深度及脉管浸润的相关性均有统计学意义(P<0.05)。PTEN在胃癌组织中的阳性率为47.0%(79/168),明显低于正常胃组织92.6%(25/27)(P<0.01),且与肿瘤大小、分化程度、浸润深度、脉管浸润、淋巴结转移和远处转移的相关性均有统计学意(P<0.05)。Notch1和PTEN的表达呈负相关(r=-0.170,P<0.05)。Kaplan-Meier分析显示,Notch1阴性组3年生存率为78.0%,显著高于阳性组的34.0%(P<0.01);PTEN阴性组3年生存率为38.0%,显著低于阳性组的62.0%(P<0.01)。Cox回归多因素分析显示Notch1表达是一个独立预后因素。结论:Notch1与PTEN的表达失调可能与胃癌的发生发展相关。Notch1表达可作为评价胃癌预后的指标。 | 李大卫 吴晴 彭志海 杨兆瑞 王一 | 2007 | 癌症2007，26，11： | 30 |
| 12 | PTEN-FAK信号传导通路在白血病细胞迁移、侵袭中的作用显示文摘目的探讨肿瘤抑制基因10号染色体缺失的磷酸酶基因(PTEN)对人慢性粒细胞白血病细胞系K562增殖和凋亡的影响以及PTEN-FAK信号传导通路在白血病细胞迁移、侵袭中的作用。方法将携带有野生型PTEN及绿色荧光蛋白的腺病毒(Ad-PTEN-GFP)及空载体腺病毒(Ad-GFP)转染K562细胞和慢性粒细胞白血病急变期患者白血病细胞,用MTT法检测细胞增殖,流式细胞术检测细胞凋亡率,荧光定量PCR(FQ-PCR)检测PTEN mRNA、FAK mRNA水平变化,Western blot方法检测蛋白水平变化,Transwell小室检测K562细胞及原代白血病细胞迁移及侵袭能力。结果Ad-PTEN-GFP以感染复数为200转染K562细胞后,与Ad-GFP组相比,最大生长抑制率为35.2%;Transwell小室结果显示,转染Ad-GFP组漏入下室内荧光细胞数量为转染Ad-PTEN-GFP组漏入下室细胞数量的9.1倍;转染PTEN基因后原代细胞侵袭迁移能力亦减弱。转染PTEN基因后K562细胞FAK、p-FAK蛋白表达下调为Ad-GFP组的0.72与0.16倍。结论PTEN可能通过下调FAK及P-FAK表达抑制白血病细胞增殖、迁移及侵袭能力。 | 成志勇 郭晓玲 李世辉 王素云 杨晓阳 薛芳 温树鹏 潘崚 | 2009 | 中华血液学杂志2009，30，2： | 29 |
| 13 | PTEN-PI3K/AKT细胞信号转导通路与肿瘤显示文摘PTEN基因是近年来发现的一种新的肿瘤抑制基因,其产物PTEN蛋白具有脂质磷酸酶活性和蛋白磷酸酶活性。PI3K/AKT信号通路为生物体内重要的生存信号通路。实验证实PTEN主要是通过其脂质磷酸酶活性作用于PI3K的下游靶分子PIP3从而阻断PI3K/AKT信号通路来实现其抑癌作用,故有学者将它们称为PTEN-PI3K/AKT信号转导通路。本文中从细胞凋亡、细胞周期调节、细胞迁移与侵袭、血管形成、肿瘤耐药、肿瘤免疫逃逸等多个角度综述了PTEN-PI3K/AKT信号转导通路与肿瘤的关系。 | 陈培 张钦宪 | 2010 | 癌变.畸变.突变2010，22，6： | 28 |
| 14 | Beclin1、PTEN在子宫内膜癌组织中的表达及其意义显示文摘背景与目的:子宫内膜癌的确切发病机制尚不明确。本研究旨在探讨抑癌基因Beclin1(BECN1)、PTEN在子宫内膜癌组织中的表达情况及其与临床病理参数之间的关系。方法:采用免疫组织化学PowerVision二步法测定79例子宫内膜癌、34例子宫内膜增殖症以及22例正常子宫内膜组织中BECN1、PTEN的表达并加以分析。结果:BECN1在正常子宫内膜组织、子宫内膜增殖症、子宫内膜癌组织中的阳性率分别为93.33%、58.82%、34.18%;PTEN的阳性率分别为93.33%、64.71%、32.91%。BECN1、PTEN在正常子宫内膜组织、子宫内膜增殖症、子宫内膜癌组织中的表达率逐渐下降差异有显著性(χ2=42.318,P<0.001;χ2=31.746,P<0.001)。BECN1表达程度与子宫内膜癌细胞分化、组织学类型相关,与手术病理分期和肌层浸润深度无关。PTEN蛋白表达与细胞分化程度、组织学类型以及肌层浸润深度有关,而与手术病理分期无关。BECN1与PTEN表达之间呈正相关。结论:BECN1、PTEN低表达与子宫内膜样腺癌的发生、发展相关。 | 赵剑虹 万小云 谢幸 周彩云 吴琼燕 | 2006 | 癌症2006，25，6： | 26 |
| 15 | 抑癌基因PTEN在乳腺癌组织中的表达显示文摘目的 探讨 10号染色体有缺失且与tensin同源的磷酸酯酶基因 (PTEN )在乳腺癌组织中的表达及其意义。方法 采用免疫组织化学S P法 ,检测 71例乳腺癌组织中PTEN蛋白的表达水平。结果 正常乳腺组织中PTEN呈高表达 ;有腋淋巴结转移的乳腺癌组织中PTEN高表达率为 3 7.8% ,明显低于无腋淋巴结转移者 (P <0 .0 5 ) ;ER阳性者PTEN高表达率明显低于ER阴性者 (P <0 .0 5 ) ;出现远处转移的乳腺癌组织其PTEN高表达率也显著降低 (P <0 .0 1)。PTEN表达水平与患者年龄、肿瘤大小、组织学分级及临床分期无关 ,但随组织学分级和临床分期的增高 ,PTEN高表达率呈下降趋势。结论 PTEN表达异常与乳腺癌发生发展密切相关 ,PTEN低表达的乳腺癌恶性程度高。 | 袁火忠 | 2002 | 实用癌症杂志2002，17，1： | 25 |
| 16 | PTEN-L is a novel protein phosphatase for ubiquitin dephosphorylation to inhibit PINK1-Parkin-mediated mitophagy显示文摘Mitophagy 是为损坏线粒体的特定的消除的选择 autophagy 的一种重要类型。(PINK1 )导致 PTEN 的通常认为的 kinase 蛋白质 1 催化 ubiquitin (Ub ) 的 phosphorylation 在 PINK1-Parkin-mediated mitophagy 的发作起一个关键作用。(PTEN-L ) 磷酸酶和 tensin 相当或相同的事物(PTEN ) 长是 PTEN 的最新识别的 isoform,与到它的 N 终点的 173 氨基酸的增加。这里,我们报导 PTEN-L 是经由它对 phosphorylated ubiquitin 的蛋白质磷酸酶活动的 mitophagy 的一个新奇否定管理者。我们发现 PTEN-L 在外部 mitochondrial 膜(OMM ) 本地化,而 PTEN-L 的删除支持, PTEN-L 的 overexpression 禁止, mitophagy 由各种各样的损坏线粒体的代理人导致了。机械学地, PTEN-L 能够有效地阻止 Parkin mitochondrial translocation,减少 Parkin phosphorylation,维持它的关上的不活跃的符合构造,并且禁止它的 E3 ligase 活动。更重要地, PTEN-L 在 vivo 减少 phosphorylated ubiquitin (pSer65-Ub ) 的水平,并且在 vitro,磷酸酶试金经由它的蛋白质磷酸酶活动证实那 PTEN-L dephosphorylates pSer65-Ub,独立于它的类脂化合物磷酸酶功能。一起拿,我们的调查结果为 ubiquitin 作为蛋白质磷酸酶表明 PTEN-L 的新奇功能,它抵抗在 mitophagy 正式就职和 mitophagy 的最终的抑制导致前馈控制机制的阻塞的调停 PINK1 的 ubiquitin phosphorylation。因此,理解 PTEN-L 的这新奇功能在控制 mitophagy 的分子的难题提供一关键错过片,在包括象 Parkinsons 那样的 neurodegenerative 混乱的许多重要人的疾病的一个批评过程疾病。 | Liming Wang Yik-Lam Cho Yancheng Tang Jigang Wang Jung-Eun Park Yajun Wu Chunxin Wang Yan Tong Ritu Chawla Jianbin Zhang Yin Shi Shuo Deng Guang Lu Yihua Wu Hayden Weng-Siong Tan Pornteera Pawijit Grace Gui-Yin Lim Hui-Ying Chan Jingzi Zhang Lei Fang Hanry Yu Yih-Cherng Liou Mallilankaraman Karthik Boon-Huat Bay Kah-Leong Lim Siu-Kwan Sze Celestial T. Yap Han-Ming Shen | 2018 | Cell Research2018，28，8： | 25 |
| 17 | PTEN与肿瘤的相关性研究进展显示文摘抑癌基因PTEN是在1997年被发现的,具有双重特异性磷酸酶活性。该基因突变,可导致多种肿瘤的发生。本文就PTEN的研究进展及其与肿瘤的关系进行综述。 | 赵红霞 | 2014 | 武汉大学学报(医学版)2014，35，1： | 24 |
| 18 | 胃癌抑癌基因PTEN突变对PI3K/AKT通路的影响显示文摘目的 观察张力蛋白类似物(PTEN)基因突变在胃癌肿瘤形成中的作用及其对PI3K/AKT通路的影响.方法 取144例经病理证实的胃癌组织及癌旁正常黏膜,提取样品DNA,PTEN基因全部9个外显子经扩增、纯化后直接测序筛查突变,Western blot检测PTEN/PI3K/AKT通路蛋白表达.结果 在144例胃癌中27例检测到突变,其中15例错义突变(55.6%),9例无义突变(33.3%),2例单碱基缺失突变(7.4%),1例内含子6剪切位点突变(3.7%).突变热点位于密码子36、75、232和393.与癌旁正常黏膜比较,胃癌组织中PTEN、E-钙黏蛋白(E-cadherin)蛋白表达明显下调,而PI3K、AKT、MMP-2、基质金属蛋白酶(MMP)-9、核转录因子-κB(NF-κB)p65蛋白表达则明显升高.结论 胃癌中PTEN基因突变并不显著,但突变所致PTEN失活可能在胃癌发生发展中起重要作用.PTEN表达缺失与PI3K、AKT、MMP-2、MMP-9、NF-κBp65蛋白表达升高相关. | 温玉刚 王权 周崇治 裘国强 彭志海 唐华美 | 2010 | 中华实验外科杂志2010，27，10： | 22 |
| 19 | PTEN、p16和CyclinD1在胃癌及癌前病变中表达的研究显示文摘目的探讨PTEN、p16和CyclinD1表达与胃癌发生发展的关系。方法应用免疫组化S-P法检测正常胃黏膜、慢性萎缩性胃炎、胃黏膜不典型增生及胃癌组织中PTEN、p16和CyclinD1蛋白的表达情况。结果 PTEN表达从正常胃黏膜、慢性萎缩性胃炎、胃黏膜不典型增生至胃癌,阳性表达率逐渐降低,不典型增生组阳性表达率显著高于胃癌组(P<0.05);p16在慢性萎缩性胃炎组中阳性表达率显著高于不典型增生组(P<0.05);CyclinD1在不典型增生组中阳性表达率显著低于胃癌组(P<0.05)。在胃癌组织中PTEN表达和p16呈正相关(rs=0.585,P<0.01),和CyclinD1呈负相关(rs=-0.587,P<0.01),p16表达与CyclinD1呈负相关(rs=-0.522,P<0.01)。结论胃癌发生机制涉及PTEN、p16和Cy-clinD1等基因的异常,随着病变进展,PTEN、p16表达降低,CyclinD1表达升高,提示PTEN、p16和CyclinD1可能是胃癌早期分子事件。 | 孙桂彬 杨景国 李永华 陈哲 汪威 韩樱松 | 2012 | 现代中西医结合杂志2012，21，15： | 23 |
| 20 | PTEN/MMAC1/TEP1基因研究新进展显示文摘PTEN/MMAC1/TEP1基因是Steck等 3个研究小组在 1997年克隆到的一个新基因 ,具有酪氨酸磷酸酶的核心基序 ,并与张力蛋白、辅助蛋白高度同源 ,是目前发现的第一个具有磷酸酶活性的抑癌基因。本文介绍了其抑癌作用的几条不同途径及在人体多种肿瘤组织中的突变和丢失情况。 | 常青 郭丽娜 | 2000 | 国外医学(肿瘤学分册)2000，27，4： | 23 |
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