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Background Circular RNAs (circRNAs) have gained attention as novel biomarkers for cancer diagnosis and prognosis. Aberrant expression of circRNAs is widely involved in cancer development, whereas the function and mechanism of novel circRNAs in colorectal cancer (CRC) remain unclear. Methods CircZFR was identified both in CRC tissues from the GEO database and in serum exosomes by competing endogenous RNA (ceRNA) microarray. The expression of circZFR was evaluated in CRC tissues and serum by qRT-PCR and in tissue microarray (TMA) by FISH. The functional roles were confirmed using a series of in vitro assays and tumor xenografts and pulmonary/hepatic metastasis mouse models. The mechanisms of circZFR were assessed through circRNA pulldown, RNA immunoprecipitation (RIP), dual-luciferase reporter assays and rescue experiments. Lastly, TCP1-CD-QDs nanocarrier was used to carry circZFR siRNA (si-circZFR) to exam the therapeutic potential of circZFR in patient-derived xenograft (PDX) models. Results CircZFR was upregulated in cancer tissues and serum exosomes of CRC patients and its level was positively associated to advanced TNM stages and poor prognosis. Serum circZFR was indicative of CRC incidence, advanced-stages and metastasis. Functional experiments demonstrated that circZFR promoted CRC proliferation and metastasis but inhibited apoptosis in vitro and in vivo, exosomes with upregulation of circZFR facilitated growth and migration of cocultured CRC cells. Mechanistically, the generation of circZFR could be improved by epithelial splicing regulatory protein 1 (ESRP1) in CRC cells. CircZFR bound to BCL2-associated transcription factor 1 (BCLAF1) and inhibited its ubiquitinated degradation. Moreover, circZFR sponged miR-3127-5p to increase the expression of rhotekin 2 (RTKN2). Our TCP1-CD-QDs nanocarrier was able to carry si-circZFR and delivered them to the vasculature of CRC tissues and cells, resulting in suppressive tumor growth without obvious adverse effects in PDX models. Conclusions Our findings indicate that ESRP1-mediated circZFR exerts oncogenic effects on CRC development and spread through suppressing BCLAF1 degradation and regulating the miR-3127-5P/RTKN2 axis. CircZFR is a promising serum biopsy marker for CRC diagnosis and an attractive target for further therapy.

Background Circular RNAs (circRNAs) have gained attention as novel biomarkers for cancer diagnosis and prognosis. Aberrant expression of circRNAs is widely involved in cancer development, whereas the function and mechanism of novel circRNAs in colorectal cancer (CRC) remain unclear. Methods CircZFR was identified both in CRC tissues from the GEO database and in serum exosomes by competing endogenous RNA (ceRNA) microarray. The expression of circZFR was evaluated in CRC tissues and serum by qRT-PCR and in tissue microarray (TMA) by FISH. The functional roles were confirmed using a series of in vitro assays and tumor xenografts and pulmonary/hepatic metastasis mouse models. The mechanisms of circZFR were assessed through circRNA pulldown, RNA immunoprecipitation (RIP), dual-luciferase reporter assays and rescue experiments. Lastly, TCP1-CD-QDs nanocarrier was used to carry circZFR siRNA (si-circZFR) to exam the therapeutic potential of circZFR in patient-derived xenograft (PDX) models. Results CircZFR was upregulated in cancer tissues and serum exosomes of CRC patients and its level was positively associated to advanced TNM stages and poor prognosis. Serum circZFR was indicative of CRC incidence, advanced-stages and metastasis. Functional experiments demonstrated that circZFR promoted CRC proliferation and metastasis but inhibited apoptosis in vitro and in vivo, exosomes with upregulation of circZFR facilitated growth and migration of cocultured CRC cells. Mechanistically, the generation of circZFR could be improved by epithelial splicing regulatory protein 1 (ESRP1) in CRC cells. CircZFR bound to BCL2-associated transcription factor 1 (BCLAF1) and inhibited its ubiquitinated degradation. Moreover, circZFR sponged miR-3127-5p to increase the expression of rhotekin 2 (RTKN2). Our TCP1-CD-QDs nanocarrier was able to carry si-circZFR and delivered them to the vasculature of CRC tissues and cells, resulting in suppressive tumor growth without obvious adverse effects in PDX models. Conclusions Our findings indicate that ESRP1-mediated circZFR exerts oncogenic effects on CRC development and spread through suppressing BCLAF1 degradation and regulating the miR-3127-5P/RTKN2 axis. CircZFR is a promising serum biopsy marker for CRC diagnosis and an attractive target for further therapy.

Anastomotic stenosis is a common complication of colorectal cancer surgery with anastomosis. Transanal minimally invasive surgery is a novel approach to the treatment of anastomotic stenosis.This study aimed to evaluate the efficacy and safety of transanal minimally invasive surgery for anastomotic stenosis treatment.This was a retrospective study.This study was conducted at a comprehensive cancer center.This study included patients with rectal anastomotic stenosis who after undergoing colorectal surgery were admitted to the Sir Run Run Shaw Hospital between September 2017 and June 2019.The primary outcome was the operative success rate. The secondary outcomes were intraoperative variables, postoperative complications, stoma closure conditions, and stenosis recurrence risks.Nine patients, aged 52 to 80 years, with a history of colorectal cancer with end-to-end anastomosis underwent transanal minimally invasive surgery for anastomotic stenosis. The distance between the stenosis and the anal verge ranged from 5 to 12 cm. The mean stenosis diameter was 0.3 cm. Four patients had completely obstructed rectal lumens. Eight of 9 patients successfully underwent transanal minimally invasive surgery radial incision and cutting. The average operation time was 50 minutes. After the procedure, 1 patient had symptomatic procedure-associated perforations but recovered with conservative treatment. No perioperative mortality occurred. One patient underwent transverse colostomy 1 month after transanal minimally invasive surgery because of proximal colon ischemia induced by primary rectal surgery. Eight patients underwent protective loop ileostomy. After transanal minimally invasive surgery, stoma closure was performed in 88% of patients with no stenosis recurrence or obstruction at follow-up (21-42 mo).This study was limited by its small sample size and single-center design.Transanal minimally invasive surgery provides an excellent operative field, good maneuverability, and versatile instrumentation and is a safe and effective treatment for rectal anastomotic stenosis, especially for severe fibrotic stenosis or complete obstruction. See Dynamic Article Video at http://links.lww.com/DCR/B965 .

Background: Colorectal cancer (CRC) is associated with high mortality rates. Some studies have attempted to elucidate the molecular mechanisms underlying CRC, and few CRC biomarkers are now used in clinical practice. Methods: Herein our aim was to identify a new potential prognostic biomarker of CRC, while providing further theoretical basis for studying the pathogenesis of CRC. Results: PYCR2 expression was to be much higher in CRC tissues than in corresponding non-cancerous tissues, and the prognosis of patients with high PYCR2 expression was significantly poorer than that of those with low PYCR2 expression. Further, PYCR2 showed a high correlation with TRMT61B and CDC23 expression. We found that gene mutations had a significant influence on the prognosis of CRC. PYCR2 siRNA transfection decreased and inhibited the ability of migration and invasion in CRC cells. Conclusions: To summarize, our findings provide novel insights to facilitate better diagnosis as well as treatment of CRC.

Background: Sigmoid colon cancer is a common type of colon cancer; it refers to tumor lesions occurring in the segment approximately 16 cm to 50 cm from the anal margin. Currently, surgical resection is the most effective treatment for non-metastatic sigmoid colon cancer. Therefore, to more accurately standardize colon cancer surgery, we classified the sigmoid colon into distal and proximal segments. This study compares and analyzes the intraoperative situation, postoperative pathology and safety of radical resection of sigmoid cancer in different locations from different aspects. Result: The patients with sigmoid colon tumor can be divided into distal group (16-30cm from the anus) and proximal group (31-50cm from the anus) according to the distance between the tumor and the anal margin. Conclusion: The patients in the distal group using stapler for intestinal anastomosis and anal decompression tube were significantly more than those in the proximal group. For the ligation of the inferior mesenteric artery, high ligation was usually used or the left colic artery was usually preserved in the distal group, and the superior rectal artery was usually retained in the proximal group. The incidence of postoperative complications in the distal group was higher than that in the proximal group, but there was no significant difference between the two groups.

Ly6/Plaur domain‑containing 8 (LYPD8) contributes to the segregation of intestinal microbiota and intestinal epithelia and is critical for the prevention of intestinal inflammation. However, its relevance in cancer biology remains to be fully elucidated. The present study aimed to clarify the biological effects of LYPD8 on colon cancer tissue from patients and colorectal cancer (CRC) cells. The results revealed that the expression of LYPD8 was significantly reduced in the CRC tissue compared with that in precancerous tissue and normal tissue, particularly in stage III tissue. The results also revealed increased levels of P65 and signal transducer and activator of transcription 3 (STAT3) phosphorylation and increased secretion of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) in CRC tissue compared with levels in precancerous tissue. Supporting these findings, the levels of secreted TNF‑α and IL‑6 were significantly reduced when LYPD8 was overexpressed in human CRC cells, and the secretion of TNF‑α and IL‑6 were positively associated with the phosphorylation of STAT3 and P65. However, this trend was restored upon supplementation with TNF‑α and IL‑6 in CRC cells. Furthermore, the overexpression of LYPD8 in CRC cells significantly inhibited CRC cell proliferation and migration. Overall, the LYPD8‑mediated tumor‑inhibiting role involves a direct effect on the secretion of IL‑6/TNF‑α in CRC cells by reducing the phosphorylation of STAT3 and P65.

Background: 5-Fluorouracil (5-Fu) is the first-line chemotherapeutic drug in the treatment of colorectal cancer. The efficiency of 5-Fu is limited by drug resistance in colorectal cancer patients. This study was aimed to define the functions of tissue inhibitor metalloproteinases 2 (TIMP-2) in the 5-Fu resistance to colorectal cancer and investigate its potential mechanism.Methods: Cytokine array, ELISA and RT-qPCR were performed to detect cytokine expression levels. Western blot and immunohistochemistry were used to show the differential expression of proteins. In addition, cell viability was detected by CCK-8.Results: We established that there is an up-regulation in the expression of the TIMP-2 in colorectal cancer patients. This up-regulation in TIMP-2 expression was evident in 5-Fu resistant colorectal cancer patients and resulted in a poor prognosis. Besides, in vivo, clinical studies and patient-derived xenograft (PDX) models confirmed that TIMP-2 was highly expressed in the 5-Fu-resistant colorectal cancer. We deduced an autocrine mechanism through which elevated TIMP-2 protein levels sustained colorectal cancer cell resistance to 5-Fu by constitutively activating the ERK/MAPK signaling pathway via an autocrine mechanism. The 5-Fu resistance could overcome by the inhibition of TIMP-2 by anti-TIMP-2 antibody or ERK/MAPK by U0126.Conclusion: Our findings identify a TIMP-2-ERK/MAPK mediated 5-Fu resistance mechanism in colorectal cancer. Moreover, we recommend the use of an ERK/MAPK signal pathway inhibitor or TIMP-2-mediated immunotherapy for 5-Fu resistant colorectal cancer.

Rationale: A co-delivery system that can transport chemotherapeutic drugs and nucleotide drugs to distinct targets in tumors is an attractive strategy for cancer therapy. In this study, well-defined targeted quantum dot (QD)-based multifunctional nanocarriers were developed through self-assembly driven by host-guest interactions. 5-fluorouracil (5-FU) and microRNA-34a mimics (miR-34a(m)) were co-administered to achieve synergistic effects for colorectal cancer (CRC) therapy for the first time. Furthermore, the CRC patient-derived tumor xenograft (PDX) model, which closely mimics human CRC tumor pathological properties, was used for evaluating the therapeutic effect in this research. Methods: Multiple β-cyclodextrin (CD)-attached QD nanoparticles were used as host molecules. An adamantane (ADA)-modified TCP1 peptide-targeting ligand (TCP1) was used as the guest molecule. 5-FU and miR-34a(m) were loaded into TCP1-CD-QD nanocarriers, which were used to treat CRC in vitro and in vivo. In addition, the CRC PDX model was used to evaluate the treatment efficacy of this co-delivery system. Results: 5-FU and miR-34a(m) can be efficiently encapsulated into TCP1-CD-QD nanocarriers and delivered into CRC cells, which led to the inhibition of the proliferation and migration of CRC cells in vitro and suppression of tumor growth in a CRC cell-derived tumor xenograft model. The obtained data further suggested that co-delivery of 5-FU and miR-34a(m) could achieve synergistic effects for CRC therapy. Notably, targeted therapy via the co-delivery of 5-FU and miR-34a(m) by TCP1-CD-QD nanocarriers significantly inhibited the growth of PDX tumors. Conclusions: These studies strongly indicate that such a nanocarrier-based co-delivery system is a promising combined therapeutic strategy that utilizes chemotherapeutic drugs and nucleotide drugs for enhancing colorectal cancer targeting and synergistic therapy.

Introduction: Primary colorectal angiosarcoma is a highly rare malignant tumor. There is no standard treatment method for this disease. No treatment of rectal angiosarcoma with apatinib has been reported so far. Case Presentation: In the current study, an 87-year-old male presented with the symptoms of frequent defecation for more than one month in Hangzhou, China, in 2018. The patient was initially diagnosed with a rectal stromal tumor. The patient underwent ultrasound-guided transrectal mass puncture in the next treatment. However, immunohistochemical examinations confirmed the initial diagnosis of rectal angiosarcoma. The patient had advanced age and rectal angiosarcoma with metastasis; he had no surgical indications, and we tried to use apatinib 250 mg/d treatment to control the progression of the lesion. Then, he received apatinib, a novel tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2). The patient has been stable to apatinib with a dose of 250 mg daily by now. Conclusions: Apatinib may play an important role in the treatment of unresectable angiosarcoma.

Purpose5-Fluorouracil (5-Fu) is used as a conventional chemotherapy drug in chemotherapy for patients with advanced colorectal cancer, but many patients still suffer from treatment failure due to 5-Fu resistance. Emerging observations revealed the important role of chemokine (C-X-C motif) ligand 13 (CXCL-13) in tumor microenvironment and its relationship with prognosis in patients with colorectal cancer. This study is designed to reveal the important role of CXCL-13 in causing colorectal cancer resistance to 5-Fu.Materials and MethodsCXCL-13 levels of patient's serum or cell culture supernatants were measured separately by enzyme-linked immunosorbent assay. In cell assays, cell viability is detected by Cell Counting Kit-8. Therefore, the recombinant human CXCL-13 was used to simulate its high expression in cells while its antibody and siRNA were used to reduce CXCL-13 expression in cells.ResultsIn this study, we demonstrated that CXCL-13 is associated with 5-Fu resistance by culture medium exchange experiments and cytokine arrays of colorectal cancer resistant and nonresistant cells. Clinical studies showed that CXCL-13 is highly expressed in the serum of 5-Fu–resistant patients. High levels of serum CXCL-13 also predict a worse clinical outcome. The addition of recombinant CXCL-13 cytokine resulted in 5-Fu resistance, while its antibody overcame 5-Fu resistance, and knockdown of CXCL-13 expression by siRNA also reduced 5-Fu resistance, which can be saved by added recombination CXCL-13.ConclusionThese results not only identify a CXCL-13 mediated 5-Fu resistance mechanism but also provide a novel target for 5-Fu–resistant colorectal cancer in prevention and treatment strategies.

// Engeng Chen 1, 2 , Zhiru Zeng 3 , Bingjun Bai 1, 2 , Jing Zhu 1, 2 , Zhangfa Song 1, 2 1 Department of Colorectal Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, P.R. China 2 Key Laboratory of Biotherapy of Zhejiang Province, 310016, P.R. China 3 The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, P.R. China Correspondence to: Zhangfa Song, email: doctorsongzhangfa@163.com Keywords: CD133, CSCs, NSCLC, EGFR, meta-analysis Received: June 14, 2016 Accepted: July 19, 2016 Published: July 30, 2016 ABSTRACT The prognostic value of cancer stem cells (CSCs) marker CD133 in non-small-cell lung cancer (NSCLC) remains controversial. We performed this meta-analysis of 32 eligible studies to clarify the prognostic value of CD133 and provide evidence for CSCs hypothesis. We calculated pooled hazard ratio (HR) for survival outcomes and pooled odds ratio (OR) for clinical parameters associated with CD133 in total 3595 NSCLC patients by STATA. Our results showed that NSCLC patients with higher CD133 expression had shorter overall survival time only in Asian patients (HR = 3.80, 95% CI: 3.12–4.04, p < 0.001; I 2 = 32%) but not in Caucasian patients (HR = 1.15, 95% CI: 0.88–1.52, p = 0.307; I 2 = 0%), suggesting that differential prognostic value of CD133 in distinct ethnic group. We speculated that the intrinsic EGFR gene status of CSCs might be responsible for this racial difference. Additionally, we found that higher expression of CD133 was associated with poor differentiation (OR = 2.03, 95% CI: 1.32–3.14, p = 0.001) and lymph node metastasis (OR = 2.39, 95% CI: 1.62–3.52, p < 0.001) but there was no significant difference of CD133 expression between adenocarcinoma and squamous carcinoma (OR = 1.13, 95% CI: 0.93–1.38, p = 0.3) in NSCLC patients. These results may provide a new therapeutic perspective on the treatment of NSCLC patients according to the expression of CD133 in distinct ethnic group.

Great value in the early identification and treatment of adenomatous polyps or early canceration using colonoscopy has been recognized. A clear colonoscopic vision brought by good intestinal preparation will become crucial. Several studies have completed using the low-residue diet (LRD) versus a clear liquid diet (CLD) the day before colonoscopy that presenting contradictory results. Therefore, a more comprehensive and updated meta-analysis is needed to summarize the findings on the effects of LRD and CLD on intestinal preparation and the quality of coloscopy.The comprehensive search was performed in PubMed/MEDLINE, Scopus, Cochrane databases (February 2020). LRD vs CLD before colonoscopy were included in this study. Mantel-Haenszel or DerSimonian and Laird models with the relative risk (RR) to evaluate differences in intestinal preparation, tolerance, readiness to repeat preparation, detected of a polyp, and overall adverse reactions.Total 16 studies (N = 3413) were eligible. Patients with LRD compared with CLD indicated significantly better of tolerability (RR 0.92;95% CI,0.85-0.99; P .05).Patients with LRD the day before colonoscopy show better tolerance and willingness to repeat intestinal preparation, and no difference with adequate intestinal preparations compared with CLD, but the recommended level of evidence is weak. However, in terms of the detection rate of intestinal adenomas, the LRD group is not weaker than the CLD group, for its evidence level is high, and can significantly reduce the hunger experience of patients.

Fibroblasts have gained increasing attention in tissue desmoplasia, especially in tumors. Activated fibroblasts from various sources modulate matrix composition and stiffness associated with organ fibrosis as well as tumor progression. More importantly, cancer-associated fibroblasts (CAFs) interacts with both cancer cells and other stromal cells, providing a tumor-promoting microenvironment for tumor invasion and metastasis. However, CAF biology is not fully understood due to its heterogeneity. Here, we describe the main transforming cues that contribute to CAF activation and unveil the expanding CAF heterogeneity associated with tumor progression in multiple aspects. Finally, we summarize the prospective promising and challenging stroma-targeted anti-tumor strategies.

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The role of palliative primary tumor resection (PPTR) in improving survival in patients with synchronous unresectable metastatic colorectal cancer (mCRC) is controversial. In this study, we aimed to evaluate whether our novel scoring system could predict survival benefits of PPTR in mCRC patients.In this retrospective cohort study consecutive patients with synchronous mCRC and unresectable metastases admitted to Sir Run Run Shaw Hospital between January 2005 and December 2013 were identified. A scoring system was established by the serum levels of carcinoembryonic antigen (CEA), cancer antigen 19-9 (CA19-9), neutrophil/lymphocyte ratio (NLR), and lactate dehydrogenase (LDH). Patients with scores of 0, 1-2, or 3-4 were considered as being in the low, intermediate, and high score group, respectively. Primary outcome was overall survival (OS).A total of 138 eligible patients were included in the analysis, of whom 103 patients had undergone PPTR and 35 had not. The median OS of the PPTR group was better than that of the Non-PPTR group, with 26.2 and 18.9 months, respectively (P < .01). However, the subgroup of PPTR with a high score (3-4) showed no OS benefit (13.3 months) compared with that of the Non-PPTR group (18.9 months, P = .11). The subgroup of PPTR with a low score (52.1 months) or intermediate score (26.2 months) had better OS than that of the Non-PPTR group (P < .001, P = .017, respectively).A novel scoring system composed of CEA, CA19-9, NLR, and LDH values is a feasible method to evaluate whether mCRC patients would benefit from PPTR. It might guide clinical decision making in selecting patients with unresectable mCRC for primary tumor resection.

// Feifei Huang 1 , Bing Pan 1 , Jun Wu 1 , Engeng Chen 2 and Liying Chen 1 1 Department of Family Medicine, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, P.R. China 2 Department of Colorectal Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, P.R. China Correspondence to: Liying Chen, email: cly0906@163.com Keywords: PM2.5, lung cancer, mortality, incidence, meta-analysis Received: February 10, 2017 Accepted: April 04, 2017 Published: April 21, 2017 ABSTRACT We conducted a meta-analysis to examinine the relationship between exposure to PM2.5 and lung cancer incidence and mortality. In total, 17 studies met our inclusion criteria and provided information necessary to estimate the change in lung cancer risk per 10 μg/m 3 increase in exposure to PM2.5. The random-effects model was used to estimate the relative risk (RR) for specific PM2.5 values. The meta-estimate for lung cancer risk associated with PM2.5 was 1.11 for mortality (95% CI: 1.05, 1.18) and 1.08 (95% CI: 1.03, 1.12) for incidence. Analyses by continent showed that the meta-estimate for lung cancer mortality associated with PM2.5 was greatest in North America [1.15 (95% CI: 1.07, 1.24)], followed by Asia [1.12 (95% CI: 0.94, 1.35)], and then Europe [1.05 (95% CI: 1.01, 1.10)]. Lung cancer incidence associated with PM2.5 was greatest in Asia [1.09 (95% CI: 1.03, 1.15)], followed by North America [1.06 (95% CI: 1.01, 1.11)], and then Europe [1.03 (95% CI: 0.61, 1.75)]. In subgroup analyses of country, the mortality meta-estimate for developed countries was 1.14 (95% CI: 1.06, 1.23), and for developing countries was 1.03 (95% CI: 1.00, 1.07). The incidence meta-estimate for developed countries was 1.07 (95% CI: 0.96, 1.20), and was similar to that of developing countries, 1.07 (95% CI: 1.06, 1.09). In subgroup analyses of males and females, the meta-estimate for lung cancer mortality associated with PM2.5 was greater for males [1.26 (95% CI: 1.15, 1.40)] than for females [1.17 (95% CI: 0.98, 1.39)]. The meta-estimate for lung cancer incidence associated with PM2.5 was greater for males [1.23 (95% CI: 0.83, 1.81)] than for females [1.15 (95% CI: 1.12, 1.18)]. In subgroup analyses of smoking status, the meta-estimate for lung cancer mortality associated with PM2.5 for former smokers was 1.46 (95% CI: 0.84, 2.55), for current smokers was 1.33 (95% CI: 1.20, 1.49), and for never smokers was 1.16 (95% CI: 1.02, 1.33), respectively. The meta-estimate for lung cancer incidence associated with PM2.5 for former smokers was 1.19 (95% CI: 0.95, 1.50), for never smokers was 1.10 (95% CI: 0.76, 1.59), and for current smokers was 1.03 (95% CI: 0.87, 1.21). The relative risks of a relationship between PM2.5 and lung cancer incidence and mortality were 1.08 (95% CI: 1.03, 1.12) and 1.11 (95% CI: 1.05, 1.18), respectively. These findings will provide some evidence for policy makers and public health practitioners worldwide.

// Bingjun Bai 1, 2 , Xingxing Wang 1, 2 , Engeng Chen 1, 2 , Hongbo Zhu 1, 2 1 Department of Colorectal Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China 2 Key Laboratory of Biotherapy of Zhejiang province, Hangzhou, China Correspondence to: Hongbo Zhu, email: drzhuhongbo@yahoo.com Keywords: HCMV, colorectal cancer, viral DNA, tumor progression, meta-analysis Received: July 10, 2016 Accepted: October 03, 2016 Published: October 08, 2016 ABSTRACT Human cytomegalovirus infection (HCMV) has been recently considered as a factor for tumorigenesis. The current study used meta-analytical techniques to explore the prevalence of HCMV in tumor tissues and the relationship between human cytomegalovirus and colorectal cancer (CRC) risk. 11 studies detecting HCMV DNA in tumor tissues were included in meta-analysis. The prevalence rate and odds ratio (OR) were two main parameters. The overall prevalence of human cytomegalovirus DNA in tumor tissues were 27.5% (95% CI = 17.2%−37.8%). Binary logistic regression showed that the studies reported before 2010 involving formalin-fixed specimens from patients in developed region represented a lower proportion of HCMV. The tumor tissues had a significantly higher rate of virus infection compared with normal tissues (OR = 6.59, 95% CI = 4.48−9.69, I 2 = 0%, P = 0.71). Subgroup analysis revealed the prevalence of the virus didn’t differ in patients with different tumor stages, in tumor cells with different histologic grades, also in different kinds of specimen (polyp and adenocarcinoma). The results of current study suggested a statistically association between the virus infection and an increased risk of colorectal cancer.