肿瘤转移相关基因与周围型肺癌CT征象的关系研究

摘要目的：探讨VEGF和nm23-H1基因表达水平与周围型肺癌的病理生理学特征和CT征象之间的关系。方法：回顾性分析确诊的47例周围型肺癌患者CT表现．同时采用免疫组化方法(LSAB法)检测47例肺癌组织中的VEGF和nm23-H1表达水平。结果：1)VEGF、nm23-H1表达水平与原发肿瘤大小、淋巴结转移状态，pTNM分期均有密切关系(P＜0．05)。2)VEGF与nm23-H1表达水平呈负相关(P＜0.05)。3)VEGF基因的高表达和nm23-H1基因的低表达均与分叶征、纵隔淋巴结转移有关(P＜0．05)，且VEGF的高表达也与空洞征有关：二者表达水平与毛刺征、空泡征、胸膜凹陷征和支气管征均无关(P＞0．05)。4)深分叶征、空泡征和支气管征与肿瘤大小有关(P＜0．05)，而与毛刺征、胸膜凹陷征和纵隔淋巴结转移均无关(P＞0.05)。结论：VEGF过度表达和nm23-H1低表达均与周围型肺癌的分叶征、空洞坏死征和纵隔淋巴结转移有密切关系。     

血管内皮生长因子与大肠癌侵袭转移的相关性研究

目的:探讨血管内皮生长因子(VEGF)基因在大肠癌组织中的表达及其与大肠癌发生转移的关系。方法:采用定量逆转录聚合酶链式反应(QRT-PCR)方法,检测45例结直肠癌手术切除标本的癌和切端结肠组织VEGFmRNA的转录水平,同时用免疫组化方法检测VEGF的蛋白表达水平。结果:大肠癌组织中VEGFmRNA及其蛋白的表达阳性率明显高于切端结肠组织。大肠癌组织中VEGFmRNA转录水平及蛋白表达水平与肿瘤的浸润程度、淋巴结转移、Dukes’分期呈明显的正相关(P<0.01),与肿瘤的分化程度等无显著相关性(P>0.05)。结论:VEGF在大肠癌浸润和转移过程中发挥重要作用,肿瘤血管生成与大肠癌浸润和转移关系密切。VEGF可能具有预测大肠癌转移的作用。     

KAI1基因在食管癌组织中的表达及其意义

目的:探讨KA I l基因的表达与食管癌发生及浸润转移的关系。方法:采用RT-PCR及免疫组化方法,检测食管癌组织及其正常粘膜中KA I lmRNA及蛋白的表达。结果:KA I lmRNA的表达在食管癌组织和其正常粘膜中未见显著性差异,且与肿瘤的分化程度、浸润深度及淋巴结转移无关;KA I l蛋白在癌组织中的表达明显低于其正常粘膜,在有淋巴结转移病例中的表达明显低于无淋巴结转移病例,但与肿瘤的分化程度、浸润深度无关。结论:食管癌癌变和转移可能与KM I1蛋白的低表达有关,但与KA I lmRNA的表达无关,推测这可能是由于翻译后修饰所致。     

胃腺癌组织瘦素、瘦素受体表达及其临床意义

目的:研究瘦素和瘦素受体蛋白在胃腺癌组织中的表达及其临床意义。方法:采用免疫组织化学方法检测60例胃腺癌组织中瘦素、瘦素受体蛋白的表达,以其细胞阳性表达率积分和染色强度积分乘积半定量计算其蛋白表达水平,分析其蛋白表达水平与临床病理参数的关系。结果:56例(96.7%)胃腺癌组织具有瘦素蛋白表达,55例(91.7%)具有瘦素受体蛋白表达,其中55例(91.7%)具有瘦素和瘦素受体的双重表达。UICC分期中Ⅳ期瘦素蛋白表达水明显高于Ⅰ、Ⅱ、Ⅲ期(P<0.05)。发生远处转移胃腺癌组的瘦素蛋白表达水平均值显著高于未发生远处转移胃腺癌组[(8.00±1.19)vs(6.44±1.33),P<0.01]。结论:①胃腺癌组织存在瘦素和瘦素受体的双重表达;②胃腺癌组织瘦素蛋白表达水平有助于判断其预后;③瘦素可能在胃腺癌远处转移过程中起重要作用。     

Dukes'A期结直肠癌术后复发转移分析

目的探讨Dukes’A期结直肠癌根治术后复发转移相关的临床病理因素。方法回顾性分析172例行根治术的Dukes’A期结直肠癌病例的临床病理资料。其中，非复发组144例，复发组28例。结果Dukes’A期直肠癌术后复发转移率（20．9％）比结肠癌（8．1％）高（x^2=4．800，P〈0．05）。肿瘤浸润至肌层术后复发转移率（18．4％，28／152）明显高于局限于黏膜下层肿瘤（0．0％，0／20）（P〈0．05）。而性别、年龄、病程、大体类型、肿瘤大小、组织学类型、分化程度与术后复发转移无关。结论Dukes’A期直肠癌比结肠癌术后更易发生复发转移。Dukes’A期结直肠癌浸润至肌层术后复发转移风险高于局限于粘膜下层。     

大肠癌病理分型、浸润深度与淋巴结转移相关关系的研究

目的:探讨大肠癌病理分型及浸润深度与淋巴结转移的关系。方法:回顾性研究了306例大肠癌病理资料,对大肠癌的病理分型分期及浸润深度与淋巴结转移进行分析。结果:低分化腺癌、印戒细胞癌的淋巴结转移率和淋巴结转移度较高分化腺癌高;大肠癌浸润肠壁全层的淋巴结转移率和转移度较仅浸润黏膜层的高。结论:大肠癌分化程度、病变深度与淋巴结转移密切相关。     

Rhodostomin inhibits thrombin-enhanced adhesion of ROS 17/2.8 cells through the blockade of alphavbeta3 integrin.

Osteosarcoma is a very malignant bone tumor which has a high metastatic potential and usually lead to poor prognosis. The adhesion of tumor cells to the endothelium or extracellular matrix (ECM) is an essential step in the metastatic cascade. We investigated the effect of thrombin on the adhesion activity of the osteosarcoma cell line, ROS 17/2.8. Incubation with the low concentrations of thrombin (0.01-5 U/ml, 5 min to 24 h) elevated the adhesion activity of ROS 17/2.8 to both human umbilical vein endothelial cells (HUVEC) and extracellular matrix, with the peak effect at the concentration of 0.5 U/ml for 30 min at 37 degrees C. The ROS 17/2.8 cells responded to thrombin by a peak effect of increased adhesion to HUVEC (5.5 folds vs. control) and fibronectin (4.8 folds) after thrombin pretreatment (0.5 U/ml, 30 min, 37 degrees C). Pretreatment with monoclonal antibodies against beta3 integrins, including anti-alphavbeta3, 10E5 and 7E3, effectively antagonized the thrombin-enhanced cell adhesion activity, whereas anti-alpha3beta1 and anti-alpha5beta1 did not antagonize the enhanced cell adhesion. Rhodostomin, an Arg-Gly-Asp (RGD)-containing snake venom peptide, and synthetic peptide RGDS also blocked the thrombin-enhanced ROS 17/2.8 cell adhesion. This study demonstrated that thrombin enhanced the cell adhesion of ROS 17/2.8 cells to HUVEC or ECM through an upregulation of beta3 integrins, and rhodostomin was a strong inhibitor on thrombin-enhanced cell adhesion, either to HUVEC or fibronectin substratum.     

乳腺癌survivin和TK1的表达及其与腋窝淋巴结转移的关系

目的 探讨乳腺癌survivin蛋白的表达及其与肿瘤细胞增生和腋窝淋巴结转移的关系。方法收集乳腺癌60例，其中有腋窝淋巴结转移的28例，用免疫组化染色检测survivin和胞质胸腺嘧啶核苷激酶(cytosolic thymidinekinase，TK1)蛋白的表达情况。结果 ①乳腺癌组织中有survivin蛋白的表达，其阳性表达率为64．9‰②survivin蛋白表达阳性的乳腺癌细胞TK1的标记指数明显高于survivin蛋白表达阴性者。③无腋窝淋巴结转移的乳腺癌survivin蛋白阳性表达率明显低于有腋窝淋巴结转移者。结论 乳腺癌组织中有survivin蛋白的表达，且其表达与肿瘤细胞增生和腋窝淋巴结转移有关。     

血浆MMPs水平与甲状腺乳头状癌浸润转移的关系

背景与目的:甲状腺乳头状癌是常见的甲状腺恶性肿瘤,目前尚无理想的血液学指标来反映其生物学特性,本研究观察血浆基质金属蛋白酶(MMP)-2、-9活性与甲状腺乳头状癌侵袭和转移的关系。方法:温州医学院附属第二医院1999～2003年共有经病理确诊、行甲状腺癌改良根治术的甲状腺乳头状癌患者74例,用明胶酶谱法测定患者血浆MMP-2和MMP-9活性。结果:淋巴结转移组的血浆活化MMP-2和MMP-9水平(71.9±11.7、15.5±6.1)明显高于无淋巴结转移组(35.2±6.6、7.3±2.3)(P<0.001);包膜及包膜外浸润组的血浆活化MMP-2和MMP-9水平(70.5±13.0、14.7±6.1)明显高于包膜内浸润组(35.4±7.9、8.0±4.2)(P<0.001);而肿瘤直径≥1cm组和<1cm组血浆活化MMP-2和MMP-9水平(55.4±20.4vs.59.3±20.8,10.8±5.7vs.13.7±6.8)无显著性差异(P>0.05),各组之间血浆总MMP-2和MMP-9水平无显著性差异(P>0.05)。结论:明胶酶的活化形式MMP-2和MMP-9的血浆水平与甲状腺乳头状癌的转移、侵袭有关,与肿瘤的大小无关。     

Breast cancer stem cells: Multiple capacities in tumor metastasis

Breast cancer is the leading cause of cancer death among women worldwide. Accumulating evidence indicates that the local recurrent and/or distant metastatic tumors, the major causes of lethality in the clinic, are related to the aggressive phenotype of a small fraction of cancer cells loosely termed as cancer stem cells (CSCs), tumor initiating cells (TICs), or cancer metastasis-initiating cells (CMICs). Breast cancer stem cells (BCSCs) are shown to exhibit unique growth abilities including self-renewal, differentiation potential, and resistance to most anti-cancer agents including chemo- and/or radiotherapy, all of which are believed to contribute to the development and overall aggressiveness of the recurrent or metastatic lesions. It is in the urgent need not only to further define the nature of heterogeneity in each tumor but also to characterize the precise mechanisms governing tumor–host cross-talk which is assumed to be initiated by BCSCs. In this review, we will focus on recently identified key factors, including the BCSCs among circulating tumor cells, interaction of BCSCs with the host, epithelial mesenchymal transition (EMT), tumor microenvironment, the intrinsic resistance due to HER2 expression, potential biomarkers of BCSCs and cancer cell immune signaling. We believe that new evidence coming from both bench and clinical research will help to develop more effective approaches to control or significantly reduce the aggressiveness of metastatic tumors.