15-PGDH和COX-2在大肠腺癌中的表达

目的研究NAD+依赖性15-羟基前列腺素脱氢酶(15-PGDH)和环氧合酶-2(Cycboxygenase-2,COX-2)在大肠腺癌组织、大肠腺瘤组织及正常大肠组织中的表达,探讨两者在大肠腺癌组织中的表达情况及其与大肠腺癌临床病理因素的关系。方法应用免疫组织化学(SABC)法检测40例大肠腺癌组织、20例大肠腺瘤组织和20例正常大肠组织中15-PGDH及COX-2的表达情况。结果15-PGDH在大肠腺癌(15%)和腺瘤组织中(20%)的阳性表达率显著低于正常大肠组织(100%)(P0.01),在大肠腺癌和腺瘤中15-PGDH的表达差异无统计学意义(P0.05)。15-PGDH蛋白表达与大肠腺癌患者的性别、年龄、分化程度及Dukes分期和有无淋巴结转移等临床病理参数均无关(P0.05)。COX-2在大肠癌组织(80%)和大肠腺瘤组织中(70%)的表达明显高于正常大肠组织(25%)(P0.01)。且其在大肠癌中的阳性表达率随大肠癌Dukes分期的升高、病理分化程度的降低及远处淋巴结的转移而逐渐增高(P0.05)。大肠癌组织中15-PGDH和COX-2的表达呈负相关(r=-0.544,P=0.000)。结论大肠腺癌组织中15-PGDH的表达缺失或减少可能发生在大肠腺癌发生、发展的早期,是大肠腺癌发生的抑制剂。大肠腺癌组织中COX-2的表达明显增高,其表达的增加可能促进了大肠癌的发生、发展。     

大肠癌组织中EGFR和VEGF的表达及其与临床病理因素的相关性

目的观察大肠癌和大肠正常组织中表皮生长因子（EGFR）和血管内皮生长因子（VEGF）的表达,探讨其与大肠癌临床病理因素及预后的关系。方法应用免疫组化Zn Vision法检测68例大肠癌组织和癌旁正常组织30例中EGFR和VEGF的表达水平。结果大肠癌组织中EGFR和VEGF阳性表达率分别为44.11%、48.52%,均高于癌旁正常组织的6.66%、10.00%（P〈0.05）;EGFR和VEGF的表达与大肠癌的TNM分期以及有无淋巴结转移有关（P〈0.05）;年龄〈40岁的大肠癌组EGFR和VEGF阳性表达率高于年龄≥40岁组（P〈0.05）;在年龄〈40岁的大肠癌患者中,两者共同阳性表达者淋巴结转移率高（P〈0.05）。结论 EGFR和VEGF在大肠癌组织中高表达,与大肠癌临床分期及淋巴结转移密切相关。年龄〈40岁的大肠癌患者具有更高的EGFR和VEGF阳性表达率及共同表达率。     

LRP16、Ki67及EGFR表达与乳腺癌的临床病理因素及预后的关系探讨

目的分析白血病相关性基因(LRP16)、增殖细胞核抗原(K-67,Ki67)及表皮生长因子受体-1(EGFR)在乳腺癌组织中的表达,并探讨其表达与乳腺癌的临床病理因素及预后的关系。方法运用免疫组化的方法检测86例乳腺癌患者组织中LRP16、Ki67及EGFR的表达,并分析其与临床病理因素的相关性及预后的关系。结果 LRP16、Ki67及EGFR在乳腺癌组织中的阳性表达率分别为52.3%、70.9%、16.3%,不同年龄组的各项指标表达均无统计学差异(P0.05)。LRP16表达与临床分期、组织分级、肿瘤大小、淋巴结转移、呈相关性(P0.05);Ki67表达与临床分期、组织分级、肿瘤大小、淋巴结转移呈相关性(P0.05);EGFR表达与组织分级呈相关性(P0.05)。LRP16阳性组与阴性组术后局部复发和转移时间相比较有统计学意义(P0.05);Ki67阳性组与阴性组术后局部复发和转移时间相比较亦有统计学意义(P0.05);而EGFR阳性组与阴性组术后局部复发和转移时间相比较无统计学意义(P0.05)。结论联合检测乳腺癌组织中LPR16、Ki67、EGFR表达情况,能更清楚地了解乳腺癌的生物学行为,可为患者的诊断、治疗及预后评估提供重要的临床指导意义。     

SFRP2和β-catenin在大肠癌中的表达及其临床意义

目的:探讨分泌型Frizzled相关蛋白2(Secreted Frizzled-related proteins 2,SFRP2)和β-连接素(β-catenin)在大肠癌发生、发展中的作用.方法:采用免疫组化SP法检测20例正常大肠黏膜、加例非腺瘤性息肉、36例大肠腺瘤和42例大肠癌组织中的SFRP2和β-catenin蛋白的表达情况,分析二者表达的差异及其与临床病理参数的关系.结果:大肠癌和大肠腺瘤组SFRP2的阳性表达率显著低于正常大肠黏膜和非腺瘤性息肉组(28.57% VS 100.0%,95.0%;36.11% VS 100.0%,95.0%,均P＜0.05);大肠癌中β-catenin膜表达缺失率显著高于正常大肠黏膜、非腺瘤性息肉及大肠腺瘤组(52.4% VS 0%,0%,11.1%,均P＜0.05);大肠癌和大肠腺瘤组β-catenin异位表达率显著高于正常大肠黏膜和非腺瘤性息肉组(64.3% VS 0%,0%;30.6% VS 0%,0%,均P＜0.05),大肠癌β-catenin异位表达率高于大肠腺瘤(P＜0.05);SFRP2表达、β-catenin膜表达缺失及异位表达与大肠癌患者的肿瘤部位、大体形态、肿瘤直径、淋巴转移和Dukes分期无明显关系,而与大肠癌的分化程度密切相关,其中SFRP2表达还与大肠癌的浸润深度密切相关:SFRP2表达与β-catenin膜表达缺失、异位表达均呈明显负相关(r=-0.452,P=0.003;r=-0.519,P=0.000),而β-catenin膜表达缺失与异位表达呈明显正相关(r=0.782,P=0.000).结论:SFRP2和β-catenin的表达与大肠癌的发生、发展密切相关,可能是大肠癌发生的早期事件,且SFRP2表达与β-catenin膜表达缺失、异位表达均呈负相关,前者起抑癌作用,后者起促癌作用.     

大肠癌组织中端粒酶催化亚单位的表达及临床意义

目的:探讨端粒酶催化亚单位(hTERT)在大肠癌患者中的表达情况及与及临床病理类型、淋巴结转移和复发之间的关系.方法:免疫组化法测定大肠癌组织(n=45)、腺瘤组织(n=16)及正常大肠黏膜(n=10)hTERT表达情况,并将hTERT表达情况与大肠癌临床病理类型、淋巴结转移和肿瘤复发之间的关系进行总结.结果:大肠癌患者癌组织中的hTERT阳性率为77.8%,显著高于腺瘤组(2/16)和正常大肠黏膜组(0/10),有显著性差异(P＜0.05).hTERT表达强度与淋巴结转移呈高度相关性(r=5.2,P＜0.05).大肠癌复发转移平均时间阳性组为34±5 mo,阴性组为20±6 mo,差异有显著性(P＜0.05).结论:hTERT在大肠癌组织中有高表达,hTERT免疫组化检测结果可以作为大肠癌早期诊断和淋巴结转移的一个重要参考指标.     

环氧化酶2在大肠癌中的表达及其与大肠癌生物学特性的关系

[目的]通过观察环氧化酶2（Cyclooxygenase-2,COX-2）在大肠腺瘤、大肠癌中的表达及其与大肠癌生物学特性的关系,初步探讨其在大肠癌发生、发展过程中的作用机制。[方法]应用免疫组织化学染色法对78例大肠癌组织、21例大肠腺瘤组织和13例正常大肠黏膜组织进行免疫组化染色;应用它检验分析COX-2的表达情况及其与大肠癌临床病理特征的关系。[结果]大肠癌组织中COX-2阳性表达率为78．21％,明显高于大肠腺瘤的52．38％和正常大肠黏膜组织的7．69％（P〈0．05）;COX-2表达与大肠癌的Duke＇s分期、分化程度、淋巴结转移有相关性（P〈0．05）,而与大肠癌患者的性别、组织学类型无关（P〉0．05）。[结论]COX-2在大肠癌组织中表达率明显高于大肠腺瘤,而正常大肠黏膜中表达率极低或不表达;COX-2表达与大肠癌生物学特性有明显相关性。     

COX-2基因在大肠癌的表达及其意义

目的 探讨COX-2基因在大肠癌中表达的意义.方法 收集手术切除的大肠癌标本58例,同时选取大肠癌远端正常黏膜组织10例,应用流式细胞术(FCM)检测大肠癌及正常黏膜中COX-2表达情况,根据平均荧光强度计算荧光指数(FI). 结果 COX-2表达平均FI值正常黏膜组为1.00±0.28,高、中、低分化及黏液癌组分别为2.47±1.41、2.70±1.08、3.16±1.34和2.01±1.43,高、中、低分化及黏液癌组COX-2表达均明显高于正常黏膜组(P＜0.01);大肠癌淋巴结转移组平均FI值(2.45±1.41)显著高于无淋巴结转移组(1.61±1.27)(P＜0.05).COX-2的表达与患者的年龄、性别、肿瘤的发生部位等无关.结论 COX-2在大肠癌中表达异常增高,并与淋巴结转移密切相关.     

血管内皮细胞生长因子及生长抑制因子4在大肠癌中的表达

目的探讨血管内皮细胞生长因子(VEGF)及生长抑制因子4(ING-4)在大肠癌中的表达及其与患者临床病理特征的关系。方法选择经手术病理证实的68例大肠癌、20例大肠腺瘤及20例正常的肠黏膜组织,采用免疫组化法检测并比较各组VEGF及ING-4表达情况,分析二者与大肠癌患者临床病理特征及生存期的关系。结果 VEGF蛋白在大肠癌组、大肠腺瘤组及正常组中的阳性表达率依次下降(P<0.05、P<0.01),ING-4蛋白在大肠癌组、大肠腺瘤组及正常组中的阳性表达率依次升高(P<0.05)。VEGF蛋白在浸润浆膜外层的大肠癌组阳性率显著高于浸润肌层及浆膜层者(P<0.05),在Dukes C、D期大肠癌患者中的阳性率高于A、B期者(P<0.05),在发生淋巴结转移的大肠癌组阳性率高于无淋巴结转移者(P<0.05);ING-4蛋白在高、中分化大肠癌组阳性率显著高于低分化组(P<0.05),在Dukes A、B期大肠癌患者中的阳性率高于C、D期(P<0.05),在发生淋巴结转移的大肠癌组阳性率高于无淋巴结转移者(P<0.05)。VEGF阳性大肠癌患者3年生存率及5年生存率均显著低于阴性患者(P<0.05),ING-4阳性大肠癌患者3年生存率及5年生存率较阴性患者无显著差异(P>0.05)。结论 VEGF高表达与大肠癌浸润程度、Dukes分期、淋巴结转移及预后有关,ING-4低表达与大肠癌分化程度、Dukes分期及淋巴结转移有关,可以作为大肠癌的术前诊断、制订手术方案的及预测转移的重要指标。     

DR-nm23在大肠癌组织中的蛋白表达及意义

目的:探讨DR-nm23蛋白在大肠癌组织中的表达及其与大肠癌发生发展和转移的关系. 方法:应用SP免疫组织化学法检测98例大肠癌、57例大肠腺瘤及42例正常大肠黏膜组织中DR-nm23蛋白的表达,统计学分析比较DR-nm23蛋白表达差异与大肠癌的发生、进展、淋巴结转移以及大肠癌组织学分型、病理分级的相关性. 结果:DR-tnm23蛋白在正常组、腺瘤组和大肠癌组的表达逐渐下调,3组间表达差异具有显著性(71.4% vs 38.6%,35.7%,均P<0.01).腺瘤组中,高级别上皮内肿瘤的表达率低于低级别上皮内肿瘤(25.7% vs 59.1%,P<0.05);大肠癌无淋巴结转移组表达率高于淋巴结转移组,表达与淋巴结转移呈负相关(44.1% vs 23.1%,P<0.05);DR-nm23表达与组织学分型(χ2=13.731,P<0.01)及病理分级(χ2=12.198,P<0.01)均有相关性.转移组中,淋巴结转移癌DR-nm23蛋白表达率较原发癌高,但二者差异无显著性(P>.05). 结论:DR-nm23参与大肠癌细胞的分化,其表达下调与大肠癌发生发展转移密切相关,可作为反映大肠癌生物学行为和判断预后的潜在重要指征.     

E-钙粘素、基质金属蛋白酶-2及其抑制剂与大肠癌浸润转移的关系

目的:探讨E-钙粘素(E-Cad)、基质金属蛋白酶-2(MMP-2)及其抑制剂(TIMP-2)表达与大肠癌浸润转移的关系。方法:采用S-P免疫组织化学染色技术,检测30例大肠腺癌,60例大肠癌组织E-Cad、MMP-2和TIMP-2的表达情况。结果:E-Cad的表达率在大肠腺瘤中为87.10%,显著高于大肠癌中的55.10%(P<0.05);其表达与大肠癌的大体类型有关,且随着大肠癌分化程度的降低而减少,与淋巴结转移呈负相关,E-Cad表达率越高患者的预后越好(P均<0.05)。MMP-2的表达率在大肠腺瘤中为26.67%,显著低于大肠癌中的86.67％(P<0.05);其表达与大肠癌的Dukes分期、分化程度、淋巴结转移和生存期均密切相关(P均<0.05)。TIMP-2的表达在大肠腺癌和大肠癌组织中没有显著性差异(P均>0.05),但其表达与大肠癌的Dukes分期、淋巴结转移、远隔脏器转移及生存期均有关(P均<0.05)。结论:E-Cad、MMP-2和TIMP-2的检测可以成为临床判断大肠癌的恶性程度、转移及预后的重要参考指标。     

COX-1和COX-2在结直肠腺瘤中的表达

目的观察COX-1和COX-2在结直肠腺瘤中的表达情况。方法16例经病理证实的散发性结直肠腺瘤活组织检查标本，15例肠镜检查无明显病变的IBS患者肠黏膜活组织检查标本。免疫组化染色观察COX-1和COX-2表达水平的变化。结果COX-2在结直肠腺瘤组织中的表达异常增高（P〈0．05），而COX-1在正常组织和腺瘤中的表达水平没有明显的变化。结论在结直肠腺瘤组织中，COX-2表达明显升高，提示COX-2参与结直肠腺瘤的发生和发展。     

环氧合酶-2、基质金属蛋白酶-9和核增殖抗原在胃癌组织中的表达及临床意义

目的 探讨环氧合酶-2(COX-2)、基质金属蛋白酶-9(MMP-9)及核增殖抗原(Ki67)在胃癌中的表达与胃癌发生、浸润和转移的关系.方法 选择2003年1月至2005年12月手术切除、病理证实的胃癌存档蜡块标本58例,其中男37例,女21例.年龄31～76岁,中位年龄58.2岁.另取上述胃癌根治术患者距肿瘤5～6 cm的癌旁组织作对照.采用免疫组化法检测胃癌组织中COX2、MMP-9、Ki67的表达.结果 COX-2、MMP-9在胃癌组织中的表达率分别为82.76%和68.9%,均高于对照组(37.93%和24.14%,P＜0.01).COX-2、MMP-9的表达与胃癌患者性别、年龄、部位及大小无相关性(P＞0.05),与胃癌浸润深度、淋巴结转移及TNM分期有关(P＜0.05),MMP-9还与胃癌分化程度相关(P＜0.05).COX-2与MMP-9在胃癌组织中的表达有相关性(P＜0.05,C=0.359).MMP-9、COX-2表达阳性者Ki67表达水平高于阴性者,两者间差异有统计学意义(P＜0.01).结论 COX-2、MMP-9、Ki67在胃癌浸润、转移过程中起重要作用,共同促进肿瘤的发生、发展.     

Cyclooxygenase-2 expression according to size and location of gastric and colorectal tubular adenomas]

BACKGROUND/AIMS: Recent studies have shown that cyclooxygenase-2 (COX-2) may be involved in the process of invasion, growth and apoptosis in colorectal carcinoma and in the growth and tumorigenesis in familial adenomatous polyposis. This study was conducted to determine the significance of the expression of COX-2 in gastric and colorectal adenomas. METHODS: Forty-nine samples of gastric adenoma and fifty-seven samples of colorectal adenoma were obtained by endoscopic mucosal resection or polypectomy from 106 patients from January 2000 to July 2003. COX-2 expression was determined by immunohistochemistry. Correlation between COX-2 expression and several clinical factors were compared in each gastric and colorectal adenomas. RESULTS: The expression of COX-2 in epithelial cells was significantly higher in the group with large adenoma (>1 cm) compared with the group with small adenoma (< or =1 cm) in gastric (76.5% vs. 46.7%, p=0.04) and colorectal adenomas (75% vs. 41.5%, p=0.023). Moreover, increased COX-2 expression was shown in distal compared to proximal colorectal adenoma (64.3% vs. 37.9%, p=0.047). CONCLUSIONS: COX-2 was expressed in a size-dependent manner in gastric and colorectal tubular adenomas. The expression of COX-2 was different according to the location of colorectal adenoma. The association of COX-2 expression with the size of adenoma may suggest that the role of COX-2 is not related to the early development of adenoma, but related to the progression of adenoma.     

Relationship between cyclooxygenase-2 expression and K-ras gene mutation in colorectal adenomas

BACKGROUND AND AIMS: Cyclooxygenase (COX)-2 has a trophic effect on gastrointestinal epithelial cells and is associated with the progression of colorectal adenomas. Mutation of the K-ras gene is also associated with the progression of colorectal adenomas and has recently been suggested to play an important role in the induction of COX-2. In the present study, we investigated the relationship between COX-2 expression and K-ras mutation in colorectal adenomas. METHODS: Twenty-nine colorectal adenomas were obtained from specimens resected by the use of surgery or endoscopic mucosal resection and analyzed clinicopathologically. Immunohistochemistry was performed to analyze COX-2 expression in the adenoma specimens. The K-ras codon 12 mutations were detected by using the polymerase chain reaction-restriction fragment length polymorphism method. RESULTS: An increase of COX-2-positive cells in adenoma was observed in 11 (37.9%) lesions, 10 (90.9%) of which had a K-ras gene mutation, suggesting a significant correlation between COX-2 expression and K-ras gene mutation in colorectal adenomas. Morphologically, COX-2-positive adenomas (13.8 +/- 2.6 mm) were significantly larger than COX-2-negative ones (5.8 +/- 0.9 mm). In addition, the increase of COX-2-positive cells in the lesion was observed more frequently in tubulovillous (63.6%) than in tubular (36.4%) adenoma. CONCLUSIONS: Cycloxygenase-2 expression in colorectal adenoma cells is strongly correlated with K-ras gene mutation, suggesting that COX-2 and mutated K-ras are connectively associated with the progression of colorectal adenoma.     

PUMA、COX-2、Caspase-3在结直肠癌中的表达及临床意义

目的进一步探讨结直肠癌的发生机制。方法选择手术切除的结直肠癌标本60份（结直肠癌组）、腺瘤组织20份（腺瘤组）,另取癌组织切缘正常黏膜44份（正常组）,采用免疫组化法检测其p53上调凋亡调控因子（PUMA）、环氧合酶-2（COX-2）、半胱氨酸天冬氨酸蛋白酶-3（Caspase-3）表达情况,采用计数资料列联表的相关分析法分析三指标间及与结直肠癌临床病理特征的关系。结果结直肠癌组PUMA、COX-2、Caspase-3阳性表达率分别为31.7%7、8.3%6、6.7%,腺瘤组分别为30.0%、75.0%、70%,正常组分别为63.6%、84.1%、95.5%,结直肠癌和腺瘤组PUMA、Caspase-3阳性表达率明显低于正常组,P均〈0.01;COX-2阳性表达率亦低于正常组,P均〉0.05;结直肠癌组和腺瘤组三指标间阳性率比较均无统计学差异。PUMA的表达与结直肠癌肿瘤直径相关,与其他临床病理特征无关;Caspase-3和COX-2的表达均与结直肠癌中临床病理参数无关。PUMA与Caspase-3表达呈正相关。结论 PUMA和Caspase-3的表达下调可能在结直肠癌发生的早期阶段起作用。     

Cyclooxygenase (COX)-2 immunoreactivity and relationship to p53 and Ki-67 expression in colorectal cancer

The tumor-suppressive effects of nonsteroidal antiinflammatory drugs (NSAIDs) have been suggested to be due to a reduction in cyclooxygenase (COX)-2 activity, although the effects of COX-2 in the colonic mucosa and in colorectal cancer have not been determined. Ki-67 immunoreactivity in cancers is also attracting attention, as Ki-67 reflects cell proliferation, while p53 immunoreactivity is also of interest, as it reflects the malignancy of colorectal lesions. Accordingly, to determine these correlation, we investigated the distribution and intensity of COX-2, p53 and Ki-67 expression in both cancerous and non-cancerous tissues from patients with sporadic and ulcerative colitis (UC)-associated colorectal cancer. We selected 21 colorectal cancer specimens, obtained by surgical resection or colonoscopic biopsy, from 21 patients, including 3 with UC (13 men and 8 women; aged 42–78 years). Histological examination of hematoxylin and eosin-stained specimens revealed that 9 were well differentiated; 11, moderately differentiated; and 1 was a poorly differentiated adenocarcinoma. We used anti-COX-2, p53, and Ki-67 antisera to perform immunohistochemical staining by the labelled streptavidin biotin method and then assessed and graded the staining intensity and distribution. COX-2 staining was more intense in cancer tissue than in non-cancerous areas. Colorectal cancers associated with UC were not stained intensely. COX-2, p53, and Ki-67 positivity rates in were 38.1%, 38.1%, and 47.6%, respectively. There were no relationships among the distributions or intensities of COX-2, p53, and Ki-67 expression. Our results indicate that colorectal cancer tissues overexpress COX-2, but that there are no relationships between COX-2, p53, and Ki-67 expression, suggesting that COX-2 expression may not be related to cell proliferation or to the grade of malignancy. However, it is necessary to determine whether COX-2 in cancer tissue is involved in carcinogenesis or whether it is simply a product of cancer. (Received: July 7, 1998; accepted: Oct. 23, 1998)     

Overexpression of cyclooxygenase-2 correlates with advanced stages of colorectal cancer

OBJECTIVE: We aimed to investigate the associations of cyclooxygenase-2 (COX-2) with pathological features and survival in patients with colorectal cancer. METHODS: The expression of COX-2 was examined by immunohistochemistry in 112 primary colorectal cancers, with 64 samples from the corresponding normal mucosa and 16 metastases in the regional lymph nodes of patients with colorectal cancer. The associations of COX-2 expression with clinicopathological features, including survival, were analyzed. RESULTS: The frequency and intensity of COX-2 staining were remarkably increased from the normal samples (17%) to the primary tumors (72%) and to the metastases (100%). Expressions of COX-2 were 25%, 74%, 78%, and 67% in Dukes' A, B, C, and D tumors, respectively (p = 0.005), and positively related to proliferative activity (p = 0.003). COX-2 expressions were 80% in colonic tumors and 60% in rectal tumors (p = 0.03). The expression of COX-2 was positively related to the better differentiated tumors in the colon (p = 0.04). We were unable to find any relationship of COX-2 with patient age, sex, tumor growth pattern, apoptosis, and patient survival (p > 0.05). CONCLUSION: We found that the expression of COX-2 was upregulated from normal cells to primary tumors and to metastases, and related to proliferative activity, tumor location, Dukes' stage, and differentiation. These results further support the evidence that COX-2 may be involved in tumorigenesis and development of colorectal cancer.     

结肠癌组织P57kip2和Ki67表达对侵袭性的影响

目的:研究结肠癌中P57kip2与Ki67的表达与肿瘤的发生和发展的关系．方法:采用免疫组化技术ABC法检测P57kip2与Ki67抗原在正常结肠粘膜10例、结肠良性肿瘤10例和结肠癌69例组织中的表达．结果:正常结肠黏膜组织和结肠良性肿瘤组织中P57kip2和Ki67的表达没有统计学差异．结肠癌组织中P57kip2抗原表达的标志指数(labeling index,LI)较正常结肠黏膜组织和结肠良性肿瘤明显降低(P=0．0001);Ki67抗原表达LI较正常结肠黏膜组织和结肠良性肿瘤明显升高(P=0．0001)．不同性别、年龄结肠癌患者癌组织中P57kip2和Ki67的表达没有统计学差异．P57kip2在结肠癌低分化腺癌组织中的表达较在中高分化腺癌组织中的表达明显降低(P=0．032)．Ki-67在结肠癌低分化腺癌组织中的表达较在中高分化腺癌组织的表达明显升高(P=0．0226)．P57kip2在有淋巴管浸润的结肠癌组织中的表达较在无淋巴管浸润的结肠癌组织中的表达明显降低(P=0．0001)．Ki-67在有淋巴管浸润的结肠癌组织中的表达较在无淋巴管浸润的结肠癌组织中的表达明显升高(P=0．0001)．P57kip2在结肠癌Duke’s A期和B期的癌组织中的表达较在C期和D期癌组织中的表达明显升高(P=0．0002)．Ki-67在A期和B期的癌组织中的表达较在C期和D期癌组织中的表达明显降低(P=0．0006)．P57kip2在结肠癌T1,T2期的癌组织中的表达较在T3,T4期癌组织中的表达明显升高(P=0．0311)．Ki-67在T1, T2期的癌组织中的表达较在T3,T4期癌组织中的表达明显降低(P=0．0235)．P57kip2与Ki-67在结肠癌组织中的表达呈现明显的负相关(r= -0．847,P=0．0001)．结论:P57kip2表达下调,Ki67抗原表达上调在结肠癌的发生发展和转移过程中发挥着重要作用．