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In previous studies, we found that B7 homolog 3 (B7-H3) was highly expressed in lung adenocarcinoma (LUAD) and promoted epithelial-to-mesenchymal transition (EMT) of LUAD cells. However, the underlying molecular mechanism is unclear. This study is aimed at evaluating the role of Ets-like protein 1 (ELK1) as a transcriptional regulator of B7-H3 for mediating the development and progression of LUAD in vitro and in vivo. We confirmed that ELK1 is highly expressed in LUAD and is associated with poor patient prognosis. ELK1 was found to promote proliferation, invasion, migration, and EMT of LUAD cells through in vivo and in vitro experiments. In terms of mechanism, ELK1 binds to the B7-H3 promoter region and induces the upregulation of B7-H3 in LUAD. Our data suggest that ELK1 plays an important role in the development of LUAD and could be used as a prognostic marker and therapeutic target for LUAD.

To explore the effect of Shenmai Injection (SMI) on the long-term prognosis of patients with chronic heart failure (CHF).The Hospital Information System was used to extract data of CHF patients, and the retrospective cohort study was conducted for analysis. In non-exposed group, standardized Western medicine treatment and Chinese patent medicine or decoction were applied without combination of SMI while in the exposed group, SMI were applied for more than 7 days. Evaluation indicators are followed with New York Heart Association functional classification (NYHA classification), left ventricular ejection fraction (LVEF), N-terminal brain natriuretic peptide precursor (NT-ProBNP), cardiogenic death and heart failure (HF) readmission. Statistical analysis includes Kaplan-Meier analysis and Cox regression which are used to explore the relationship between SMI and outcome events.A total of 1,211 eligible CHF patients were involved and finally 1,047 patients were followed up successfully. After treatment, the cases of NYHA classification decline in the exposed and non-exposed groups accounted for 64.30% and 43.45%, respectively; the improvement values of LVEF were 8.89% and 7.91%, respectively; the improvement values of NT-ProBNP were 909 pg/mL and 735 pg/mL, respectively. After exposure on SMI, the rates of cardiogenic death and HF readmission reduced from 15.43% to 10.18% and 38.93% to 32.37%. According to Kaplan-Meier analysis, the log-rank P value of SMI and cardiogenic death was 0.014, while the counterpart of SMI and HF readmission was 0.025. Cox regression analysis indicated that for cardiogenic death, age, cardiomyopathy, diabetes, and NYHA classification were risk factors while β-blockers, aldosterone receptor antagonists, Chinese patent medicine/decoction and SMI were protective factors. Likewise, for HF readmission, age, cardiomyopathy, and NYHA classification were risk factors while SMI was a protective factor.Combination with SMI on the standardized Western medicine treatment can effectively reduce cardiogenic mortality and readmission rate in CHF patients, and thereby improve the long-term prognosis.

The aim of the present study was to explore the underlying mechanisms involved in gastric cancer (GC) formation using data‐independent acquisition (DIA) quantitative proteomics analysis. We identified the differences in protein expression and related functions involved in biological metabolic processes in GC. Totally, 745 differentially expressed proteins (DEPs) were found in GC tissues vs. gastric normal tissues. Despite enormous complexity in the details of the underlying regulatory network, we find that clusters of proteins from the DEPs were mainly involved in 38 pathways. All of the identified DEPs involved in oxidative phosphorylation were down‐regulated. Moreover, GC possesses significantly altered biological metabolic processes, such as NADH dehydrogenase complex assembly and tricarboxylic acid cycle, which is mostly consistent with that in KEGG analysis. Furthermore the higher expression of UQCRQ, NDUFB7 and UQCRC2 were positively correlated with a better prognosis, implicating these proteins may as novel candidate diagnostic and prognostic biomarkers.

Background It has been documented that transient receptor potential melastatin 7 (TRPM7) plays a pivotal role in the development of multiple cancers. However, the role of TRPM7 in human colorectal cancer (CRC) is poorly understood. Therefore, the aim of this study was to investigate the expression and significance of TRPM7 in CRC. Methods In this study, TRPM7 expression was first investigated in Gene Expression Omnibus (GEO), and then validated it with the data from our medical center. CCK-8, colony survival, transwell, and flow cytometry assays were employed to evaluate the effects of TRPM7 knockdown on the CRC cell proliferation, migration, and invasion, as well as cell cycle and apoptosis. Results We observed markedly increased TRPM7 expression in CRC tissues. CRC patients with high expression of TRPM7 suggested deeper tumor infiltration, positive lymph node metastasis, distant metastasis, and advanced clinical stage. In addition, TRPM7 was also overexpressed in CRC cell lines. Downregulated TRPM7 in vitro suppressed CRC cell proliferation, migration, and invasion, as well as triggered cell cycle arrest at the G0/G1 phase, reduced the S phase, and promoted apoptosis. Importantly, decreased TRPM7 in CRC cells reversed the epithelial-mesenchymal transition (EMT) status, accompanied by downregulation of N-cadherin and upregulation of E-cadherin. Conclusion Our study indicated that the expression of TRPM7 was positively correlated with tumor infiltration, lymph node metastasis, distant metastasis and clinical stage of CRC. Besides, decreased TRPM7 in vitro inhibited CRC cell proliferation, migration and invasion by modulating EMT.

Objective Recent studies have shown that Chondroitin polymerizing factor (CHPF) is abnormally expressed in malignant tumors, however, the expression of CHPF in lung adenocarcinoma (LUAD) has not been reported. In this study, the relationship of CHPF and LUAD will be explored. Methods Differential genes present in LUAD were screened by bioinformatics analysis. The expression status of CHPF in LUAD tissues and cell lines were deteced by Western blotting or Real-time Quantitative Polymerase Chain Reaction Detecting System (qPCR), and the relationship between CHPF and prognosis of LUAD patients was analyzed. CHPF was effectively silenced in LUAD cell lines by lentivirus- mediated methods. The effect of CHPF on proliferation, cell cycle progression and apoptosis of cancer cells was assessed. We further determined the role of CHPF in tumor growth in vivo by using xenograft LUAD tumor models. Western blotting assay was performed to assess the expression changes of MAPK signaling pathway. Results We found that CHPF is highly expressed in LUAD tissues and cell lines. In vitro experiments, CHPF knockdown in LUAD cells can effectively inhibit proliferation and promote apoptosis of cancer cell. In vivo experiment, tumor growth was markedly inhibited by CHPF knockdown in the xenograft model of LUAD. Notably, CHPF also could promote tumor progression by regulating MAPK pathway. Conclusion CHPF can promote the proliferation and antiapoptosis of LUAD cells, which is promising to become a potential target for LUAD treatment.

The ammunition safety problem is particularly prominent when the storage and transportation launch box is airdropped and landed. A safety evaluation method of rocket air drop based on propellant damage evaluation is proposed. Based on the theory of fracture mechanics and the evaluation method of structural integrity of rocket engine, established a local finite element model of rocket engine with initial damage, the crack propagation analysis is carried out by using the propagation finite element method (XFEM). The results show that when the landing impact overload is 30g (25ms) that the airdrop equipment should be able to withstand, the modified double base propellant has produced the phenomenon of crack instability propagation. When the initial crack direction and load direction are 120 °, the propagation is the most serious and there are safety problems; when the solid propellant is airdropped, it is necessary to increase the buffer to reduce the overload.

Accumulating studies have identified that microRNAs (miRNAs) are novel regulators acting as tumor suppressors or oncogenes in tumor progression. The aim of the study is to investigate the functional roles of miR-138-5p in breast cancer (BC) cells and explore the underlying mechanisms by identifying its target gene. Our results first showed that miR-138-5p expression was remarkably decreased in BC tissues and cells using quantitative real-time PCR analysis. Forced expression of miR-138-5p significantly suppressed cell migration and invasion ability of BC using transwell assay. Moreover, miR-138-5p overexpression suppressed cell epithelial–mesenchymal transition (EMT) phenomenon of BC by upregulating E-cadherin expression, but downregulating N-cadherin and Vimentin expression. More importantly, rhomboid domain-containing protein 1 (RHBDD1) was predicted as the direct target of miR-138-5p by TargetScan and miRanda, which was subsequently confirmed by luciferase reporter assay in BC cells. RHBDD1 was up-regulated in BC tissues and negatively correlated with miR-138-5p expression. Furthermore, forced expression of miR-138-5p could down-regulate the expression of RHBDD1, but overexpression of RHBDD1 reversed the suppressive effects of miR-138-5p in BC cell migration, invasion and EMT. Our findings revealed the tumor-suppressive role of miR-138-5p in regulating BC migration by targeting RHBDD1, suggesting that miR-138-5p negatively regulating EMT might be a therapeutic target in BC.

The sonic hedgehog (SHH) morphogen regulates cell differentiation and controls a number of genes during renal morphogenesis. To date, the effects of SHH on fibroblast growth factors (Fgfs) in embryonic kidney development remain unclear. In the present study, explants of BALB/c mouse embryonic kidney tissues were used to investigate the role of exogenous SHH on Fgf8 and Fgf10 expression levels ex vivo. Ureteric bud branches and epithelial metanephric derivatives were used to determine the renal morphogenesis with Dolichos biflorus agglutinin or hematoxylin‑eosin staining. mRNA expression levels were determined using reverse transcription‑quantitative polymerase chain reaction, while the protein expression levels were examined using immunohistochemistry and western blot analysis. During the initial stages of metanephric development, low levels of SHH, Fgf8, and Fgf10 expression were observed, which were found to increase significantly during more advanced stages of metanephric development. In addition, exogenous SHH protein treatment increased the number of ureteric bud branches and enhanced the formation of nephrons. Exogenous SHH reduced the Fgf8 mRNA and protein expression levels, whereas cyclopamine (an SHH‑smoothened receptor inhibitor) interfered with SHH‑mediated downregulation of Fgf8 expression. By contrast, exogenous SHH protein was not found to modulate Fgf10 mRNA and protein expression levels. In conclusion, these results indicate that the modulatory effects of SHH on BALB/c mouse metanephric explant cultures may involve the regulation of Fgf8 expression but not Fgf10 expression, which provides evidence for the functional role of Fgf proteins in renal morphogenesis.

Lactate dehydrogenase A (LDH-A) is a key enzyme during glycolysis, which increases the synthesis of related proteins and has elevated activity in cancer cells. The role of LDH-A in lung adenocarcinoma (LUAD) progression was investigated in the present study. Expression levels of LDH-A were assessed in LUAD samples, and the relationship between LDH-A expression status and the prognosis of LUAD patients was confirmed. The effect of LDH-A on proliferation, invasion, migration, and colony formation of cancer cells was assessed. We further determined the role of LDH-A in tumor growth in vivo by using xenograft LUAD tumor models. The potential mechanism of LDH-A promotion in LUAD progression was explored. LDH-A showed an abnormally high expression in LUAD, which is closely associated with poor prognosis in patients with LUAD. In in vitro experiments, silencing LDH-A expression in LUAD cells could effectively inhibit proliferation, invasion, migration, and colony formation of cancer cells. In in vivo experiments, tumor growth was markedly inhibited by LDH-A silencing in a xenograft model of LUAD. Notably, LDH-A could also promote tumor progression by regulating epithelial–mesenchymal transition (EMT)-related molecules. LDH-A can promote the malignant biological behaviors of LUAD cells, and thus can be a potential target for LUAD treatment.

Purpose: The aim of the present study was to explore the role of CHPF in non-small-cell lung cancer (NSCLC) and to develop an shRNA vector-based therapy to repress the expression of CHPF gene in NSCLC cell lines. Methods: In this study, we used immunohistochemical staining to verify the expression of CHPF in NSCLC tissue. Then, we determined the expression of CHPF gene in different NSCLC cell lines with RT-PCR and Western blotting. Specific CHPF shRNA was used to knockdown the expression of CHPF. Celigo image cytometry, cell cycle analysis, and flow cytometry assay were performed. Results: The results showed that expression level of CHPF was higher in NSCLC tissues than normal lung tissues. Further, we established that CHPF expression knockdown in NSCLC cells could substantially restrain the cell proliferation, apoptosis, and cell cycle in vitro. Conclusion: On the basis of these results, we concluded that CHPF expression has an important role in the progression of human NSCLC cells. Therefore, its interference could possibly be used as a potential therapeutic target against NSCLC.

Fascin-1 is a cytoskeletal protein and it can specifically bind to F-actin, it can be abnormally expressed in a variety of solid tumors. Fascin-1 was identified as a factor for poor prognosis in non-small cell lung cancer (NSCLC). However, the relevant molecular mechanisms are not yet fully understood. In this study, the fascin-1 knockdown cells were produced by lentivirus infection, and then cell proliferation, invasion and cell migration assay were used to investigate the role of fascin-1 in NSCLC cells. The MAPK pathway related proteins were determined by western blot. In the current study, lentivirus-mediated fascin-1 knockdown significantly decreased the proliferation of NSCLC cells. Furthermore, fascin-1 silencing partly inhibited cell invasion and migration. Inhibition of fascin-1 decreased the activity of the MAPK pathway. Therefore, targeting fascin-1 may inhibit the growth and metastasis of NSCLC cells, which is a potentially effective therapeutic strategy for treating NSCLC.

bHLH transcript factor superfamily members involve in various bio-events in mice. According to existing researches, there are six members of bHLH superfamily likely to participate in the uterine development during early pregnancy in mice. Expression of six members of bHLH superfamily Hes6, Tcf23, Twist1, Twist2, Mitf and Tead4 in mouse uterus in early pregnancy was detected by RT-qPCR. All the six genes were expressed in early pregnancy mouse uterus, and expression pattern of each one was different from others. In situ hybridization results showed that Tead4 was expressed in decidual tissues of the 8th day pregnancy mouse. Tead4 might be involved in the regulation of embryo implantation in mice.

The oxides adsorbent of NiO-ZnO/-Al2O3-SiO2 was prepared by co-precipitation method. SEM, XRD and BET studies were performed to understand the structural properties of the adsorbent. And the adsorbent can be used for the desulfurization of thiophene in n-hexane as model gasoline. Removal rate of thiophene increased with increasing reaction time. Removal rate of thiophene in equilibrium decreases with increasing the initial concentration of thiophene. The extent of adsorption in adsorbent increased with increasing the initial concentration of thiophene. The removal rate of thiophene increases with increasing reaction temperature, it showed that the desulfurization is a chemical process not a physical process.

Neural stem cells (NSCs), as therapeutic agents, play the key role in the treatment of central nervous system (CNS) disorders. It is a researching tendency for promote proliferation and differentiation of neural stem cells by using tissue engineering. It is discovered that joint use neural stem cells and NSCs-seeded scaffold may increase the cell survival state and better control cellular microenvironment. We find suitable material include natural biological materials, synthetic materials, compound materials, bio-derived materials and 3D-materials of neural stem cells tissue engineering by analyzing and summing up of the research which combine tissue engineering with NSCs transplant in past several years. It hold out a hope of the possibility of utilizing the treatment of neural stem cells transplantation with tissue engineering, and there has been a great quantity of achievements on the research of it to treat CNS disorders by promote proliferation and differentiate.

A kind of digital pressure control project is put forward to solve the problem of pressure fluctuation inside the carriage by using the experience of airplane's pressure control system. Based on the pressure difference monitored between the inside and outside of the carriage, the control signal is output to the actuator by the controller, according to the control program set in it, in order to stabilize the pressure in the carriage. After the mathematical models of the main parts of the control system are found, a mathematical model of the whole system is established. Fuzzy control technology is applied in the new control system. The fuzzy controller is designed by using the matlab software, and then the simulation system is constructed. It is proved practical by the simulation result.

The presence forms of sulfur in High-sulfur petroleum coke and high temperature transfer was studied in this paper. It was found that a part of sulfur escape in the form of gaseous compounds through heating coke without air. The present structure of sulfide is inferred to be thiophene according to XPS spectra. The scientific calculation for amount of high sulfur petroleum coke can be continued according to the sulfur content of petroleum coke, sulfur transfer agent and permissible content of sulfur in the coke. The gaseous sulfur caused by the high sulfur petroleum coke which is directly used as boiler fuel and coal blending can be recycled through the original sulfur purification recovery system, meanwhile, the purification load rises.

Rice hull (designated with RH) was activated by phosphoric acid to prepare an adsorbent for the removal of sulfur-containing compounds from diesel fuel. Adsorption tests for both, a 300 µg.g-1 dibenzothiophene (DBT)-containing n-octane solution using as model oil and a commercial hydro-treated diesel fuel, were performed to elucidate the effect of varying phosphoric acid to RH ratio, treating temperature and the removal of silica from the adsorbent on the combination of the textural structure, surface chemical property and adsorption capacity. It was indicated that high surface area and micro-pore volume of the adsorbent favored the adsorption of DBT and its derivatives. Richening of oxygen-containing compounds on the adsorbent surface was advantageous to the adsorption and removal of DBTs. At a phosphoric acid and RH weight ratio of 3:1 by using a two-step treatment, a satisfactory adsorbent with an adsorption capacity of 28.89 mg S/g was successfully prepared. If the silica in the adsorbent was further removed, the product exhibited the highest performance, reaching 30.43 mg S/g for the model oil and 21.79 mg S/g for the commercial diesel fuel. Both the textural structure and the surface chemical property like acidic groups of a RH-based adsorbent play important roles in its adsorption behaviors, and the formation of donor-acceptor complexes between surface acidic groups and DBT may probably benefit DBT adsorption capacity.

To examine the expression of osteopontin (OPN) in patients with advanced non-small cell lung cancer (NSCLC), and to analyze the correlation of the expression level of OPN with response to platinum-based chemotherapy and the prognosis of NSCLC patients.This retrospective study enrolled 92 patients with advanced NSCLC. All of the patients received platinum- based regimens as first-line chemotherapy. The expression of OPN in advanced NSCLC tissue was detected by immunohistochemistry. The associations between OPN expression with response to chemotherapy and the prognosis were analyzed by SPSS 17.0 statistical software.The positive expression rate of OPN in advanced NSCLC tissue was 36.9% (34/92). The positive expression rate of OPN was higher in patients ≥70 years old (65.2%;15/23) vs those aged70 years (27.5%;19/69; p0.05), which was also higher in patients with distant metastasis (51.9%;28/54) than that in patients without metastasis 15.8% (6/38) , the difference with statistically significant (p0.05). Pearson's correlation analysis results showed that OPN expression was significantly correlated with age (r=0.338, p=0.001) , distant metastasis (r=0.368, p0.001), curative effect of platinum-based regimen (r=0.403, p0.001), progression-free survival/PFS (r=-0.486, p0.001) and overall survival/OS (r=-0.552, p0.001). Furthermore, the OPN expression was an independent predictor of PFS and OS for patients with advanced NSCLC after receiving platinum-based first-line chemotherapy (p0.001).OPN expression is an independent predictor of response to platinum-based first-line chemotherapy and of the prognosis of patients with advanced NSCLC.

Vasohibin-1 (VASH1) is a newly discovered angiogenesis inhibitor that is specifically expressed in human vascular endothelial cells in response to vascular endothelial growth factor and fibroblast growth factor-2. This study aimed to evaluate the expression of VASH1 in non-small cell lung cancer (NSCLC) and correlates its expression with the clinicopathological parameters and prognosis of the disease. Immunohistochemical analysis was used to determine the expression of VASH1 in NSCLC tissue and adjacent normal tissue from 84 patients. The relationship between VASH1 expression and clinicopathological indicators was examined with the chi-squared test. Moreover, the survival rate was calculated with the Kaplan–Meier survivor curve. Finally, the correlation between the indicators and patient survival was estimated with Cox analysis. VASH1 was high expressed in 63.1 % of NSCLC tissues versus 21.4 % of adjacent tissues (P < 0.01). High VASH1 expression in NSCLC tissue was correlated with clinicopathological features including lymph node status (P = 0.024) and TNM stage (P = 0.036). The Kaplan–Meier curve indicated that the patients with high VASH1 expression had significantly shorter survival than those with low VASH1 expression. In the multivariate Cox regression model, high VASH1 expression was identified as an independent prognostic factor for patients with NSCLC. High VASH1 expression is predictive of poor prognosis of NSCLC, implying that VASH1 may be a promising new target for targeted therapies for NSCLC.

To investigate the association of Osteopontin (OPN) expression in tumor tissue with clinicopathological features of non-small cell lung carcinoma (NSCLC) patients. Publications assessing the clinicopathological characteristics and prognostic significance of OPN in expression NSCLC were identified up to March 2014. A meta-analysis of eligible studies was performed using standard statistical methods to clarify the association between OPN expression and these clinical parameters. A total of eleven studies met the inclusion criteria, and included 1536 cases of NSCLC tumor tissue and 340 cases of normal lung tissue. The OPN expression rate in NSCLC tissue was higher than normal tissue [Odds ratio (OR) 6.427; 95% confidence interval (CI) 4.689-8.808; P = 0.000]. Simultaneously, we also found that OPN expression was positively associated with stage (OR 0.332; 95% CI 0.250-0.440; P = 0.000), lymph node metastasis (OR 3.094; 95% CI 2.295-4.172; P = 0.000), tumor size (tumor size3 cm vs. ≥3 cm; OR 0.484; 95% CI 0.303-0.773; P = 0.002) and pathology (OR 0.611; 95% CI 0.466-0.800; P = 0.000). It was unrelated that OPN expression in NSCLC tissue with and degree of differentiation and other clinical features (P0.05). Experimental findings indicate that, OPN plays a crucial role in the development of NSCLC.

Paired box2 (Pax2) gene plays a crucial role in kidney development and is expressed in the nephric duct, mesenchyme of pronephrons, mesonephrons, and metanephrons with special spatial and temporal characteristic. Research in animals indicate that Pax2 can interact with many important transcription factors such as Gdnf, Ret, SHH, Wnt4, and Fgf to organize the nephric linage specification, pro/mesonephric tubule formation and descent, emergence of the ureteric bud, branching morphogenesis, and nephron induction. Pax2 is associated with various congenital renal and ureter malformations, and the mutation is easist to detected in Renal-coloboma syndrome. In renal cell carcinoma, Wilms tumor and many acquired kidney diseases Pax2 is expressed abnormally, whose diagnose and therapy value will be the focus of further research. This paper reviews the molecular structure, expression and regulation of Pax2 in kidney development and diseases.

Xiao-Ling Ling,* Tao Zhang,* Xiao-Ming Hou, Da Zhao Department of Oncology, The First Hospital of Lanzhou University (The Branch Hospital of Donggang), Lanzhou, Gansu Province, People’s Republic of China *These authors contributed equally tothis work Purpose: Fascin-1 promotes the formation of filopodia, lamellipodia, and microspikes of cell membrane after its cross-linking with F-actin, thereby enhancing the cell movement and metastasis and invasion of tumor cells. This study explored the fascin-1 protein’s expression in non-small cell lung cancer (NSCLC) tissues and its relationship with clinical pathology and prognostic indicators.Methods: Immunohistochemical analysis was used to determine the expression of fascin-1 in NSCLC tissues. We used quantitative real-time polymerase chain reaction and western blot analysis to further verify the results. The fascin-1 expression and statistical method for clinical pathological parameters are examined by χ2. Kaplan–Meier method is used for survival analysis. Cox’s Proportional Hazard Model was used to conduct a combined-effect analysis for each covariate.Results: In 73 of the 128 cases, NSCLC cancer tissues (57.0%) were found with high expression of fascin-1, which was significantly higher than the adjacent tissues (35/128, 27.3%). The results suggested that the high expression of fascin-1 was significantly correlated with lymph node metastasis (P=0.022) and TNM stage (P=0.042). The high fascin-1 expression patients survived shorter than those NSCLC patients with low fascin-1 expression (P

Tao Zhang,1,* Dong-ming Zhang,2,* Da Zhao,1 Xiao-ming Hou,1 Shou-cheng Ma,1 Xiao-jun Liu1 1Department of Oncology, The First Hospital of Lanzhou University, The Branch Hospital of Donggang, Lanzhou, 2Department of Oncology, The Second People's Hospital of Pingliang, Pingliang, People's Republic of China *These authors contributed equally to this work Background: The xeroderma pigmentosum complementary group D (XPD) gene has been linked to the development of colorectal cancer (CRC) through disruption of DNA repair. Several studies have suggested that the XPD polymorphism Lys751Gln is associated with an increased risk of developing CRC. However, previous results remain inconclusive. Herein, we performed a meta-analysis to evaluate the potential for this relationship. Methods: Relevant studies were retrieved from the PubMed database. Strict selection and exclusion criteria were determined, and the odds ratio with a 95% confidence interval was used to assess the strength of associations. The fixed or random effects model was selected on the basis of heterogeneity tests among studies. Publication bias was estimated using funnel plots and Egger's regression test. Results: The meta-analysis included 2,961 cases and 4,539 controls from eleven studies. The results indicated that the XPD Lys751Gln polymorphism had no association with CRC risk for all genetic models (Gln-Gln versus Lys-Lys, P=0.477; Lys-Gln versus Lys-Lys, P=0.283; Lys-Gln + Gln-Gln versus Lys-Lys, P=0.562), even when compared within subgroups based on ethnicity and source of controls. Conclusion: Based on the results of our meta-analysis, there is no evidence of a link between the XPD Lys751Gln polymorphism and risk of CRC. Keywords: XPD Lys751Gln polymorphism, colorectal cancer risk, meta-analysis