Clinical significance of prostaglandin E synthase expression in gastric cancer tissue

Studies have linked microsomal prostaglandin E synthase (mPGES)-1 with gastric cancer. The purpose of this study was to determine mPGES-1, mPGES-2, and cytosolic PGES (cPGES) expression in gastric cancer and to evaluate the correlation between mPGES-1 and mPGES-2 expression and clinicopathological factors and cyclooxygenase-2 expression. PGES protein expression was examined by Western blot in gastric cancer cell lines and in biopsy samples from patients with gastric cancer. mPGES-1, mPGES-2, and cPGES protein localizations were examined immunohistochemically in 129 archival gastric cancer surgical resections. mPGES-1 protein expression was found in gastric cancer biopsies and cancer cell lines with differentiated or undifferentiated adenocarcinoma. There was no mPGES-1 expression in nonneoplastic biopsies. All cell lines and tissue samples expressed mPGES-2 and cPGES. Immunohistochemical analysis showed cancer cells expressed mPGES-1 in 47% of cases. mPGES-2 immunoreactivity was seen both in nonneoplastic glandular epithelium and cancer cells; however, cancer cell immunoreactivity was significantly more pronounced in 29% of cases. cPGES expression was constitutive both in nonneoplastic and neoplastic tissues, with no significant variation among cases. mPGES-1 and mPGES-2 expression correlated with cyclooxygenase-2 expression. mPGES-1 and mPGES-2 expression, and tumor-node-metastasis stage had independent prognostic significance under multivariate analysis in patients with gastric cancer overall and in patients with differentiated cancers. However, only tumor-node-metastasis stage and mPGES-2 expression retained independent prognostic significance in patients with poorly differentiated cancers. mPGES-1 and mPGES-2 correlate with clinicopathological factors and may be valuable prognostic factors in gastric cancer.     

Expression and regulation of prostaglandin E synthase isoforms in human myometrium with labour

Since the controversies regarding the use of non-steroidal anti-inflammatory drugs (NSAIDs) and selective cyclo-oxygenase (COX)-2 antagonists for the treatment of preterm labour (PTL), more emphasis has been placed on investigating the terminal synthases involved in the production of prostaglandins (PGs) to allow more targeted therapy in PTL. Prostaglandin E(2) (PGE(2)) is synthesized by one of three enzymes, cytosolic prostaglandin E synthase (cPGES), microsomal PGES-1 (mPGES-1) and microsomal PGES-2 (mPGES-2). We have determined (i) the immuno-localization of all three PGES enzymes in lower segment pregnant human myometrium, (ii) the expression of PGES and COX-2 mRNA expression at term and preterm gestation with and without labour and (iii) the effect of interleukin (IL)-1beta on COX-2 and PGES mRNA and protein expression in human myometrial smooth muscle (HMSM) cell cultures. We show mPGES-1 protein located predominantly in myometrial and vascular smooth muscle cells (SMCs), whilst mPGES-2 protein is largely in stromal cells surrounding the SMC and cPGES is diffusely located throughout the myometrium. Expression of mPGES-2 mRNA increased with term labour and PTL and expression of COX-2 and mPGES-1 mRNA with term labour, whereas cPGES expression did not change. IL-1beta stimulated release of PGE(2) by HMSM cells and increased COX-2 and mPGES-1 mRNA and protein expression. Thus, COX-2 expression and mPGES-1 expression are co-ordinately up-regulated in lower segment myometrium with term labour and with IL-1beta treatment in HMSM cells.     

Microsomal prostaglandin E synthase (mPGES)-1, mPGES-2 and cytosolic PGES expression in human gastritis and gastric ulcer tissue

Recently, three different prostaglandin E2 synthases have been identified: microsomal prostaglandin E synthase (mPGES)-1, cytosolic PGES (cPGES), and mPGES-2; however, their role and connection to cyclooxygenase (COX)-2 in the gastric ulcer repair process remain unknown. Therefore, we examined mPGES-1, cPGES, and mPGES-2 expression and localization in the stomach in vitro and in vivo. Tissues were obtained from Helicobacter pylori (H. pylori)-infected patients and consisted of surgical resections of gastric ulcers, or biopsies of gastric ulcers or gastritis. mPGES-1 mRNA and protein expression levels were examined by real-time polymerase chain reaction (PCR) and Western blot analysis, respectively. mPGES-1, cPGES, and mPGES-2 localization were analyzed immunohistochemically. Induction of PGES expression in response to interleukin (IL)-1beta was examined in vitro in the cultured human gastric fibroblast line Hs262.St. Real-time PCR analysis of mPGES-1 mRNA expression in biopsy samples showed significantly higher expression levels in open than in closed gastric ulcer tissue. Western blot analysis showed mPGES-1 protein expression limited to open ulcer tissue, while mPGES-2 and cPGES immunoreactivities were seen in both open and closed ulcer tissue. Immunohistochemical analysis showed strong mPGES-1 expression in fibroblasts and macrophages of the ulcer bed, paralleling COX-2 expression. cPGES and mPGES-2 expression levels were seen in both fibroblasts of the ulcer bed and in epithelial cells. Furthermore, stronger cPGES and mPGES-2 immunoreactivities were seen in scattered mast cell-like cells and neuroendocrine-like cells, respectively. Induction of mPGES-1 expression in response to IL-1beta was seen in cultured gastric fibroblasts in vitro, and double immunostaining showed mPGES-1 coexpression with COX-2 in fibroblasts of the ulcer bed in vivo. In conclusion, mPGES-1, cPGES, and mPGES-2 are all expressed in gastric ulcer tissue, but only mPGES-1 parallels COX-2 expression in mesenchymal and inflammatory cells of the ulcer bed, suggesting a key role for this enzyme in the ulcer repair process.     

Microsomal prostaglandin E synthase-1 (mPGES-1) is the primary form of PGES expressed by the primate periovulatory follicle

BACKGROUND: Prostaglandin E2 (PGE2) has been identified as the key ovulatory PG in the primate follicle. Follicular PGE2 levels increase just before the expected time of ovulation, suggesting that the midcycle LH surge induces the expression of enzymes involved in PGE2 synthesis. METHODS: To identify the specific form(s) of prostaglandin E synthase (PGES) expressed by the primate periovulatory follicle, we examined granulosa and theca cell expression of the three microsomal (m) and cytosolic (c) forms of PGES (mPGES-1, mPGES-2 and cPGES) identified to date. Monkey granulosa cells and whole monkey ovaries were obtained from animals receiving exogenous gonadotropins to stimulate multiple follicular development; monkeys then received an ovulatory dose of HCG to initiate periovulatory events. RESULTS: Expression of mPGES-1 mRNA and protein by granulosa cells of periovulatory follicles increased in response to HCG administration, peaking just before the expected time of ovulation. Immunocytochemistry showed that mPGES-1 protein was present in both granulosa and theca cells of monkey periovulatory follicles. Monkey granulosa cells also expressed mPGES-2 and cPGES mRNA, but mRNA levels did not change in response to HCG administration. Isolated monkey theca cells expressed both mPGES-1 and cyclooxygenase-2 mRNA, and produced PGE2 in vitro. Human granulosa-lutein cells obtained from women undergoing treatment for infertility expressed mRNAs for mPGES-1, mPGES-2 and cPGES. CONCLUSIONS: These data indicate that mPGES-1 is a gonadotropin-regulated PG synthesis enzyme expressed by granulosa cells of primate periovulatory follicles and suggest that mPGES-1 may be the primary PGES responsible for the increased follicular PGE2 levels necessary for primate ovulation.     

Expression of prostaglandin E synthases in periodontitis immunolocalization and cellular regulation

The inflammatory mediator prostaglandin E(2) (PGE(2)) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. The distribution of PGES in gingival tissue of patients with periodontitis and the contribution of these enzymes to inflammation-induced PGE(2) synthesis in different cell types was investigated. In gingival biopsies, positive staining for PGES was observed in fibroblasts and endothelial, smooth muscle, epithelial, and immune cells. To further explore the contribution of PGES to inflammation-induced PGE(2) production, in vitro cell culture experiments were performed using fibroblasts and endothelial, smooth muscle, and mast cells. All cell types expressed PGES and COX-2, resulting in basal levels of PGE(2) synthesis. In response to tumor necrosis factor (TNF-α), IL-1β, and cocultured lymphocytes, however, mPGES-1 and COX-2 protein expression increased in fibroblasts and smooth muscle cells, accompanied by increased PGE(2), whereas mPGES-2 and cPGES were unaffected. In endothelial cells, TNF-α increased PGE(2) production only via COX-2 expression, whereas in mast cells the cytokines did not affect PGE(2) enzyme expression or PGE(2) production. Furthermore, PGE(2) production was diminished in gingival fibroblasts derived from mPGES-1 knockout mice, compared with wild-type fibroblasts. These results suggest that fibroblasts and smooth muscle cells are important sources of mPGES-1, which may contribute to increased PGE(2) production in the inflammatory condition periodontitis.     

Expression and cellular localization of cyclooxygenases and prostaglandin E synthases in the hemorrhagic brain

Background  

Although cyclooxygenases (COX) and prostaglandin E synthases (PGES) have been implicated in ischemic stroke injury, little is known about their role in intracerebral hemorrhage (ICH)-induced brain damage. This study examines the expression and cellular localization of COX-1, COX-2, microsomal PGES-1 (mPGES-1), mPGES-2, and cytosolic PGES (cPGES) in mice that have undergone hemorrhagic brain injury.     

Microsomal prostaglandin E2 synthase-1 in breast cancer: a potential target for therapy

The anti-tumour actions of cyclooxygenases (COX) are thought to be mediated by inhibition of prostaglandin E(2) (PGE(2)) synthesis. However, COX-2 inhibition also alters cellular production of other prostaglandins such as prostacyclin (PGI(2)). The latter action is believed to be important for the development of adverse cardio-vascular events. Microsomal PGES (mPGES-1) is an enzyme downstream to COX-2 and affects PGE(2) production only. It is possible that targeting mPGES-1 could decrease PGE(2) production without affecting PGI(2) production. In order to assess the potential of mPGES-1 as a target for therapy, we analysed its expression in breast cell lines and normal and malignant breast tissues. The expression of mPGES-1 and COX-2 was correlated in tumour cells and vascular endothelium, and with prognostic parameters in breast cancer. Although not detectable in normal epithelial cells, expression was noted in areas of fibrocystic change and in situ carcinoma. mPGES-1 expression was noted in 79% of breast cancer tissues. Its expression did not correlate with COX-2 overexpression or with prognostic markers of breast cancer. Endothelial cells did not show mPGES-1 expression. Upregulation of mPGES-1 is therefore frequent in pre-malignant and malignant breast disease. In this study, coordinate over-expression of COX-2 and mPGES-1 was not observed, particularly in the endothelial cells of blood vessels. Targeting mPGES-1 might prove to be an alternative therapeutic strategy to inhibit PGE2 production.     

High expression of meningioma 1 is correlated with reduced survival rates in colorectal cancer patients

The identification of prognostic markers for colorectal cancer (CRC) has important clinical implications. However, the association between meningioma 1 (MN1) expression and clinical outcomes of CRC has not been fully investigated. The aim of this study was to investigate the expression of MN1 in the clinical context of CRC. We first used immunohistochemistry (IHC) staining to examine and compare MN1 expression between multiple human cancer tissues and normal tissues. Initial screening revealed that the expression of MN1 proteins was significantly higher in tumor tissues of the breast, colon, and liver than in normal tissues. In further testing conducted on 59 paired CRC samples, we observed that the expression of MN1 in CRC tissue samples was significantly higher than in adjacent normal tissues. Moreover, high MN1 expression was not significantly associated with clinicopathological characteristics. Kaplan-Meier survival analysis revealed that high expression of MN1 mRNA or MN1 protein was significantly associated with poor CRC prognosis. Furthermore, univariate Cox analysis revealed that a high MN1 score was significantly associated with prognostic factors. Multivariate Cox analysis further indicated that gender, histologic grade, tumor-node-metastasis (TNM) stage, and a high MN1 score were independent factors of overall CRC survival rates. Finally, MN1 and PCNA protein levels were positively correlated, which suggests that MN1 may be involved in the cell proliferation process during CRC formation. Our results, which confirm those of other studies, indicate that (1) high levels of MN1 expression contribute to poor CRC prognosis and (2) MN1 can serve as a novel potential biomarker in predicting the prognosis of CRC patients.     

Expression of proteins related to prostaglandin E<Subscript>2</Subscript> biosynthesis is increased in human gastric cancer and during gastric carcinogenesis

Prostaglandin E₂ (PGE₂) is related to carcinogenesis. Cyclooxygenase (COX) and prostaglandin E synthase (PGES) are involved in PGE₂ synthesis. However, overall situation of COX and microsomal PGES (mPGES) expression in gastric cancer has not been studied in detail. The expression of COX and mPGES was evaluated in 45 cases of gastric cancer (22 intestinal type and 23 diffuse type), 13 gastric dysplasia, 15 intestinal metaplasia, 18 Helicobacter pylori associated gastritis, and 10 normal gastric tissues by performing immunohistochemistry and Western blot analysis. COX-1 expression was higher in intestinal type cancers than diffuse ones. COX-2 and mPGES-1 were expressed more in cancers than in paired nonneoplastic adjacent tissues, and intestinal type cancers showed higher expression of COX-2 than diffuse ones. The expression of COX and mPGES was gradually increased with progression of gastric lesions and the highest in dysplasia. mPGES-1 was expressed not only in epithelial cells but also in stromal cells, whose phenotype was myofibroblast, endothelial cells and others. In conclusion, proteins related to PGE₂ biosynthesis affect both histogenesis and the carcinogenesis of human gastric cancer.     

Regulation of the microsomal prostaglandin E synthase-1 in polarized mononuclear phagocytes and its constitutive expression in neutrophils

PGs are potent mediators of pain and inflammation. PGE synthases (PGES) catalyze the isomerization of PGH(2) into PGE(2). The microsomal (m)PGES-1 isoform serves as an inducible PGES and is responsible for the production of PGE(2), which mediates acute pain in inflammation and fever. The present study was designed to investigate the regulation of expression of mPGES-1 in polarized phagocytes, which represent central, cellular orchestrators of inflammatory reactions. Here, we report that human peripheral blood monocytes did not express mPGES-1. Exposure to LPS strongly induced mPGES-1 expression. Alternatively activated M2 monocytes-macrophages exposed to IL-4, IL-13, or IL-10 did not express mPGES-1, whereas in these cells, IL-4, IL-13, and to a lesser extent, IL-10 or IFN-gamma inhibited LPS-induced, mPGES-1 expression. It is unexpected that polymorphonuclear leukocytes expressed high basal levels of mPGES-1, which was up-regulated by LPS and down-regulated by IL-4 and IL-13. Induction of mPGES-1 and its modulation by cytokines were confirmed at the protein level and correlated with PGE(2) production. Cyclooxygenase 2 expression tested in the same experimental conditions was modulated in monocytes and granulocytes similarly to mPGES-1. Thus, activated M1, unlike alternatively activated M2, mononuclear phagocytes express mPGES-1, and IL-4, IL-13, and IL-10 tune expression of this key enzyme in prostanoid metabolism. Neutrophils, the first cells to enter sites of inflammation, represent a ready-made, cellular source of mPGES-1.     

大肠癌中Bmi-1的表达及其临床病理意义

目的:研究大肠肿瘤组织中Bmi-1蛋白表达情况及其与大肠癌临床病理特征及预后的关系,并探讨Bmi-1蛋白在大肠癌中的表达与Ki67蛋白表达的关系。方法:采用免疫组织化学方法分别检测Bmi-1蛋白在60例大肠癌、30例大肠腺瘤及20例正常大肠黏膜组织3组中的表达情况及其与大肠癌临床病理特征及患者生存率的关系,并探讨大肠癌中Bmi-1 蛋白表达与Ki67蛋白的相关性。应用SPSS13.0软件包对结果进行统计学分析。结果:Bmi-1蛋白在大肠癌、大肠腺瘤及正常大肠黏膜组织中的表达率分别为25.0％、6.7％、0%, Bmi-1蛋白在大肠癌中表达明显高于腺瘤组及正常组（P＜0.05）,而在腺瘤组及正常组中的表达差异无显著（P＞0.05）;Bmi-1蛋白高表达与有无远处转移及TNM分期密切相关（P＜0.05）,而与患者性别、年龄、肿瘤大小、分布部位、分化程度、组织类型及淋巴结转移等临床病理特征无关（P＞0.05）;Kaplan-Meier生存分析显示Bmi-1蛋白高表达患者生存率明显低于低表达患者（P＜0.05）;大肠癌中Bmi-1蛋白高表达与Ki67蛋白表达无相关关系（P＞0.05）。结论:Bmi-1蛋白表达与大肠癌的发生、转移及预后关系密切,可作为评估患者侵润转移及预后的参考指标。     

结直肠癌中Keratin 17的表达及其临床预后价值

目的 分析角蛋白17(Keratin 17,KRT17)在结直肠癌(colorectal cancer,CRC)中的表达及其临床预后价值.方法 采用生物信息学方法分析KRT17在CRC数据库中的表达及预后价值;进一步,采用免疫组织化学技术检测KRT17蛋白在95对CRC临床样本组织中的表达水平,并分析其表达与患者临床病...     

ACTL8的表达与乳腺癌临床病理特征及预后的关系

目的:探讨肌动蛋白样蛋白8(ACTL8)在乳腺癌中的表达及其与乳腺癌临床病理特征及预后的关系。方法:采用Western blot方法检测人正常乳腺上皮细胞株MCF-10A和5种乳腺癌细胞株中ACTL8蛋白的表达;采用免疫组织化学方法检测6例乳腺癌标本及其对应的癌旁组织中ACTL8蛋白的表达;收集TCGA乳腺癌数据集,将488例乳腺标本纳入,分析ACTL8的mRNA表达水平与乳腺癌患者临床病理特征及预后的关系。结果:ACTL8蛋白在乳腺癌细胞株T47D、BT474、HCC1954和SKBR3中表达显著高于乳腺上皮细胞株MCF-10A;ACTL8蛋白在乳腺癌组织中的表达也显著高于癌旁组织;ACTL8 mRNA表达与乳腺癌患者年龄、肿瘤大小、临床TNM分期和淋巴结转移相关(P0.05)。ACTL8 mRNA高表达的乳腺癌患者5年内生存率低、预后差。结论:ACTL8在乳腺癌组织中高表达并与乳腺癌临床病理特征及预后密切相关,提示ACTL8可作为判断乳腺癌预后的标志物。     

Clinicopathological significance of PD-L1 expression in colorectal cancer: Impact of PD-L1 expression on pFOXO1 expression

ObjectiveThis study aimed to evaluate the clinicopathological significance of PD-L1 expression and its impact on phospho-Forkhead box O 1 (pFOXO1) expression in colorectal cancer (CRC).MethodsImmunohistochemical analysis for PD-L1 and pFOXO1 was performed on 265 human CRC tissues. PD-L1 expression was evaluated in the tumor and immune cells. The impact of PD-L1 expression on survival was investigated in relation to the pattern of pFOXO1 expression.ResultsPD-L1 was expressed in 25 (9.4%) and 41 (17.7%) patients in the tumor and immune cells of the 265 CRC tissues, respectively. PD-L1 expression in immune cells (I-PD-L1) was significantly correlated with less lymphatic invasion, lymph node metastasis, and distant metastasis and lower pT and pTNM stages. Additionally, there was a significant correlation between PD-L1 expression in tumor cells (T-PD-L1) and tumor location (right colon), but not the other clinicopathological characteristics. pFOXO1 expression was significantly lower in CRC with high I-PD-L1 expression than in CRC with low or negative I-PD-L1 expression. However, there was no significant correlation between pFOXO1 and T-PD-L1 expression in CRC. Patients with positive pFOXO1 and low or negative I-PD-L1 expression exhibited the worst survival among patients with CRC.ConclusionCollectively, our results indicate that I-PD-L1 expression was significantly correlated with favorable tumor behaviors and better survival. In addition, patients with high I-PD-L1 and low pFOXO1 expressions had a favorable prognosis than those with other I-PD-L1 and pFOXO1 expression patterns.     

Overexpression of UQCRC2 is correlated with tumor progression and poor prognosis in colorectal cancer

Ubiquinol-cytochrome c reductase complex core protein 2 (UQCRC2) is an important subunit of mitochondrial respiratory complex III. However, its role in tumorigenesis and tumor progression remains unknown, especially with regards to colorectal cancer (CRC). In this research, we measured the expression of UQCRC2 protein by immunohistochemistry assay in 89 paired paraffin-embedded tumor tissues and corresponding adjacent normal tissues from patients with colorectal adenocarcinoma and investigated possible correlations of UQCRC2 expression with clinicopathological parameters and prognosis. We found that UQCRC2 was significantly upregulated in CRC tissues compared with adjacent normal tissues, and immunohistochemical UQCRC2 status was correlated to the depth of invasion (T), lymph node metastasis (N), advanced TNM stage. Multivariate analysis indicated that UQCRC2 remained an independent prognostic factor for poorer overall survival. Furthermore, we determined the role of UQCRC2-knockdown in CRC cells (RKO and HCT116) using lentivirus-mediated small hairpin RNAs (shRNAs). The effects of UQCRC2 knockdown on CRC cells (RKO and HCT116) proliferation were analyzed by cell proliferation and colony formation assay, and cell cycle and apoptosis were assessed by flow cytometry. We found that silencing UQCRC2 suppressed cell proliferation and colony formation in RKO and HCT116 cells, led to a cell cycle arrest and induced cell apoptosis in vitro. These results provided novel insights into the potential role of UQCRC2 in the tumorigenesis and progression of CRC, and revealed that UQCRC2 may serve as a new prognostic and therapeutic target in CRC.     

STC-1在宫颈癌中的表达及其在预后判断中的价值

目的:研究宫颈癌中分泌蛋白斯坦尼钙调节蛋白1(stanniocalcin 1,STC-1)的表达情况及其与预后的关系.方法:Western印迹分析STC-1在宫颈癌细胞系的表达,免疫组织化学染色(immunochemistry,IHC)检测STC-1在宫颈癌和正常组织的表达,分析STC-1表达水平与宫颈患者临床病理特征之间关系,通过网上数据库初步探索STC-1表达与预后的关系.结果:宫颈正常上皮细胞Ect1/E6E7细胞株中几乎检测不到STC-1,宫颈癌细胞株中STC-1呈不同程度表达;IHC结果显示:STC-1主要在宫颈细胞的胞质和胞膜中表达,与匹配的癌旁正常组织相比,STC-1蛋白水平在宫颈癌组织中更高(P<0.05),并且与患者淋巴结转移正相关(P=0.038);另外,通过对数据库中宫颈癌患者的样本分析发现:高表达STC-1的宫颈癌患者预后更差(P<0.01).结论:STC-1表达与宫颈患者的总体存活负相关,STC-1可能具有预测宫颈癌患者预后生存时间的潜在价值.     

Prognostic significance of glucose-related protein 94 in colorectal cancer

AimsThe expression of glucose-related protein 94 (GRP94), a member of the heat shock protein 90 family, was correlated with a variety of clinicopathological factors and patient survival in a large colorectal cancer (CRC) cohort. We aimed to elucidate the role of GRP94 in the prognosis of CRC patients.MethodsTissue microarray blocks were generated from 709 CRC samples and immunohistochemically stained for GRP94.ResultsOf the 709 tumours, 164 (23.1%) and 545 (76.9%) were classified in the low and high expression groups, respectively. GRP94 expression was high in CRC cases with larger tumours (p = 0.005) and advanced pT stage (p = 0.021). GRP94 expression was higher in females than males (p = 0.024). In univariate and multivariate survival analyses, high GRP94 expression was unexpectedly associated with better overall survival in CRC patients younger than 65 years of age (p = 0.001)ConclusionOur conflicting results indicate that GRP94 has the ability to switch between oncogenic and tumour-suppressive roles depending on the conditions and microenvironment of the tumour cells. Furthermore, GRP94 could be a candidate biomarker to predict better prognosis in CRC patients.     

Does JC virus have a role in the etiology and prognosis of Egyptian colorectal carcinoma?

John Cunningham virus (JCV) encodes an oncogenic T‐antigen, which is capable of interacting with key growth regulatory pathways. JCV definite role as causal agent of human cancer, still awaits final confirmation. The present study was conducted to assess the possible role of JCV in Egyptian colorectal carcinoma (CRC) and correlate the expression with the clinicopathological features and survival. JCV in situ hybridization (ISH) signals and large T antigen immunoreactivity were examined in 87 colonic specimens. Positive glandular JCV ISH signals were detected in 20%, 25% and 40% of normal, adenoma and CRC cases respectively. Stromal JCV ISH signals were identified in 26% of CRC cases and 5% of adenoma however, normal mucosa did not show stromal positivity with significant difference (p = 0.03). Glandular JCV expression was significantly associated with high grade (p = 0.03), high mitotic index (p=0.02) and low apoptotic index (p = 0.00). Positive stromal signals were significantly associated with low apoptosis (p = 0.00). No positive nuclear immunostaining of JCV large T antigen was detected in all specimens. JCV stromal expression was the 2nd most powerful indicator of short survival and bad prognosis (p = 0.03) in CRC patients. JCV might play an etiological role in CRC tumorogenesis and short survival in Egyptian CRC patients.