The Affiliated Jiangyin Hospital of Southeast University Medical School

Chengjiang, China

The Affiliated Jiangyin Hospital of Southeast University Medical School

Chengjiang, China
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Shen N.,The Affiliated Jiangyin Hospital of Southeast University Medical School | Ruan Y.,Renji Orthopedics Hospital | Lu Y.,Jiangyin No 3 Peoples Hospital | Jiang X.,The Affiliated Jiangyin Hospital of Southeast University Medical School | And 4 more authors.
Oncotarget | Year: 2017

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic destructive inflammation in synovial joints. To date, many studies explored the associations between tumor necrosis factor alpha inducible protein 3 (TNFAIP3) gene rs6920220, rs2230926, and rs5029937 polymorphisms and the risk of rheumatoid arthritis (RA), but with contradictory results. We therefore conducted a comprehensive meta-analysis to address the associations. We searched in the databases of PubMed and Embase. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by the Stata 11.0 software. A total of 21 case-control studies for these three single nucleotide polymorphisms (SNPs) were included in this meta-analysis. Meta-analysis indicated that TNFAIP3 gene rs6920220, rs2230926, and rs5029937 polymorphisms were associated with the increased risk of RA. Stratification analysis of ethnicity found that rs6920220 and rs5029937 polymorphisms increased the risk of RA among Caucasians, while rs2230926 polymorphism increased the risk of RA among Asians. In summary, this meta-analysis confirms that TNFAIP3 gene polymorphisms may play important roles in the pathogenesis of RA.


Zhang Y.,Jiangyin No 3 Peoples Hospital | Zhang J.,Nanjing Southeast University | Shen N.,The Affiliated Jiangyin Hospital of Southeast University Medical School | Ren K.,The Affiliated Jiangyin Hospital of Southeast University Medical School
International Journal of Clinical and Experimental Medicine | Year: 2016

The epidermal growth factor (EGF) pathway stimulates the proliferation and differentiation of epidermal and epithelial tissues, and plays an important role in tumorigenesis, including the initiation and development of hepatocellular carcinoma (HCC). Since the association between EGF rs4444903A/G polymorphism and the risk of HCC is still controversial and ambiguous, this meta-analysis aimed to evaluate and confirm this relationship. We conducted a literature search in the PubMed and WanFang databases, covering all papers published by July 10, 2014. Overall, 9 case-control studies comprising 1,874 patients and 2,302 healthy controls were retrieved based on the search criteria for HCC susceptibility related to the rs4444903A/G polymorphism. Odds ratio (OR) and 95% confidence interval (CI) were used to assess the strength of this association. We found that in the overall analysis, EGF rs4444903A/G polymorphism decreased HCC risk (A-allele vs. G-allele, OR = 0.93, 95% CI = 0.88-0.98, Pheterogeneity = 0.118). However, this finding was not observed in Chinese individuals, who carried the A allele (AA+AG vs. GG, OR = 0.93, 95% CI = 0.88-0.99, Pheterogeneity = 0.249). This trend was observed in both hospital-based and population-based subgroups. Our study showed that the A allele of EGF rs4444903 was a poor protective factor of HCC risk in Chinese individuals. © 2016, E-Century Publishing Corporation. All rights reserved.


Liu P.,The Affiliated Jiangyin Hospital of Southeast University Medical School | Chen S.,The Affiliated Jiangyin Hospital of Southeast University Medical School | Wu W.,University of California at San Diego | Liu B.,The Affiliated Jiangyin Hospital of Southeast University Medical School | And 4 more authors.
Japanese Journal of Clinical Oncology | Year: 2012

Objective: Oesophageal squamous cell carcinoma is one of the deadliest malignancies worldwide. Contactin-1, a neural adhesion molecule, is implicated in tumour invasion and metastasis. The purpose of this study was to investigate the expression of CNTN-1 in normal and cancerous oesophageal tissue, and the potential relevance to clinicopathological features. Methods: Thirty normal oesophageal tissue samples and 82 primary oesophageal squamous cell carcinoma tissue samples were included in this study. The expression levels of CNTN-1, VEGF-C and HIF-1α messenger RNA were determined using reverse transcriptase-polymerase chain reaction and quantitative real-time polymerase chain reaction. The expression of the CNTN-1 protein was measured using immunohistochemistry. Results: The expression of CNTN-1 messenger RNA was significantly increased in the tumour tissue compared with the normal oesophageal tissue (P = 0.001). The oesophageal squamous cell carcinoma tissue consistently showed higher CNTN-1 protein levels. The CNTN-1 expression correlated with the oesophageal squamous cell carcinoma stage (P = 0.006), lymph node metastasis (P = 0.018) and lymphatic invasion (P = 0.035). The messenger RNA level of CNTN-1 correlated significantly with those of VEGF-C and HIF-1α. Conclusions: The expression of CNTN-1 is upregulated in the oesophageal squamous cell carcinoma tissue and related to stage, lymph node metastasis and lymphatic invasion. Thus, CNTN-1 may be involved in the progression and pathogenesis of oesophageal squamous cell carcinoma. © The Author 2012. Published by Oxford University Press. All rights reserved.


Xiang B.,The Affiliated Jiangyin Hospital of Southeast University Medical School | Mi Y.-Y.,Nantong University | Li T.-F.,The Affiliated Jiangyin Hospital of Southeast University Medical School | Liu P.-F.,The Affiliated Jiangyin Hospital of Southeast University Medical School
Asian Pacific Journal of Cancer Prevention | Year: 2012

Objective: The p53 tumor suppressor pathway plays an important role in gastric cancer (GC) development. Auto-regulatory feedback control of p53 expression is critical to maintaining proper tumor suppressor function. So far, several studies between p53 Arg72Pro polymorphism and GC have generated controversial and inconclusive results. Methods: To better assess the purported relationship, we performed a meta-analysis of 19 publications. Eligible studies were identified by searching the Pubmed database. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess any link. Results: Overall, a significant association was detected between the p53 Arg72Pro polymorphism and GC risk (Pro-allele vs. Arg-allele: OR = 1.05, 95%CI = 1.01-1.08; Pro/Pro vs. Arg/Arg: OR = 1.13, 95%CI = 1.04-1.22). Moreover, on stratified analysis by race, significantly increased risk was found for Asian populations (Pro-allele vs. Arg-allele: OR = 1.06, 95%CI = 1.02-1.10; Pro/Pro vs. Arg/Arg: OR = 1.16, 95%CI = 1.07-1.26; Pro/Pro+Pro/Arg vs. Arg/Arg: OR = 1.58, 95%CI = 1.09-2.27). Conclusions: Our study provided evidence that the p53 72Pro allele may increase GC risk in Asians. Future studies with larger sample size are warranted to further confirm this association in more detail.


Hou X.-H.,The Affiliated Jiangyin Hospital of Southeast University Medical School | Huang Y.-M.,Nanjing Medical University | Mi Y.-Y.,Nantong University
Asian Pacific Journal of Cancer Prevention | Year: 2012

Objective: Methylenetetrahydrofolate reductase (MTHFR) catalyzes the metabolism of folate and nucleotides needed for DNA synthesis and repair. Variations in MTHFR functions likely play roles in the etiology of lung cancer (LC). So far, several studies between MTHFR C677T polymorphism and LC provide controversial or inconclusive results. Methods: To better assess the purported relationship, we performed a meta-analysis of 14 publications. Eligible studies were identified by searching the Pubmed, Embase, Web of Science and Google Scholar databases. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association. Results: Overall, no significant association was detected between the MTHFR C677T polymorphism and LC risk, the same as in race subgroup. However, in the stratified analysis by histological type, significantly increased non-small-cell lung cancer (NSCLC) risk was indicated (T-allele vs. C-allele: OR = 1.11, 95%CI = 1.03-1.19; TT vs. CC: OR = 1.24, 95%CI = 1.09-1.41; TC vs. CC: OR = 1.11, 95%CI = 1.03-1.20 and TT+TC vs. CC: OR = 1.09, 95%CI = 1.03-1.15). At the same time, ever-smokers who carried T-allele (TT+TC) had a 10% decreased LC risk compared with CC genotype carriers. Conclusions: Our study provided evidence that the MTHFR 677T null genotype may increase NSCLC risk, however, it may protect ever-smokers against LC risk. Future studies with large sample sizes are warranted to further evaluate this association in more detail.


PubMed | Nanjing Medical University, Nantong University and The Affiliated Jiangyin Hospital of Southeast University Medical School
Type: | Journal: Scientific reports | Year: 2015

Previous studies have investigated the association between osteopontin (OPN) gene polymorphisms, rs17524488 (-156 GG/G), rs11730582 (-443 T/C), and rs9138 (C/A) and cancer risk in the Chinese population. However, the results are controversial and indefinite. We therefore carried out a meta-analysis to derive a more precise estimation of these associations. The PubMed database was systematically searched to identify potentially eligible reports. Crude odds ratios (OR) and 95% confidence intervals (CI) were used to assess the strength of associations between 3 OPN gene polymorphisms and cancer risk in a Chinese population. A total of 10 articles involving 2,391 cases and 3,007 controls were evaluated. The pooled OR indicated that OPN rs17524488 (-156 GG/G) polymorphism was significantly associated with cancer risk in Chinese population. In a stratified analysis by source of control, significant associations were also observed among rs17524488 (-156 GG/G) and rs11730582 (-443 T/C) polymorphisms and cancer. In addition, a stronger association was observed between rs9138 (C/A) polymorphism and cancer risk. In conclusion, this meta-analysis suggests that OPN rs17524488 (-156 GG/G), rs11730582 (-443 T/C), and rs9138 (C/A) polymorphisms may be associated with cancer susceptibility in the Chinese population. Nevertheless, further investigation on a larger population covering different ethnicities are warranted.


PubMed | Nanjing Medical University and The Affiliated Jiangyin Hospital of Southeast University Medical School
Type: Journal Article | Journal: Biochemical and biophysical research communications | Year: 2016

The mitogenic effects of periodic mechanical stress on nucleus pulpous cells have been studied extensively but the mechanisms whereby nucleus pulpous cells sense and respond to mechanical stimulation remain a matter of debate. We explored this question by performing cell culture experiments in our self-developed periodic stress field and perfusion culture system. Under periodic mechanical stress, rat nucleus pulpous cell proliferation was significantly increased (p<0.05 for each) and was associated with increases in the phosphorylation and activation of EGFR, Rac1, and ERK1/2 (p<0.05 for each). Pretreatment with the ERK1/2 selective inhibitor PD98059 reduced periodic mechanical stress-induced nucleus pulpous cell proliferation (p<0.05 for each), while the activation levels of EGFR and Rac1 were not inhibited. Proliferation and phosphorylation of ERK1/2 were inhibited after pretreatment with the Rac1 inhibitor NSC23766 in nucleus pulpous cells in response to periodic mechanical stress (p<0.05 for each), while the phosphorylation site of EGFR was not affected. Inhibition of EGFR activity with AG1478 abrogated nucleus pulpous cell proliferation (p<0.05 for each) and attenuated Rac1 and ERK1/2 activation in nucleus pulpous cells subjected to periodic mechanical stress (p<0.05 for each). These findings suggest that periodic mechanical stress promotes nucleus pulpous cell proliferation in part through the EGFR-Rac1-ERK1/2 signaling pathway, which links these three important signaling molecules into a mitogenic cascade.


PubMed | the Affiliated Jiangyin Hospital of Southeast University Medical School
Type: Journal Article | Journal: Scandinavian journal of rheumatology | Year: 2014

Signal transducer and activator of transcription 4 (STAT4) transmits signals induced by the cytokines interleukin (IL)-12, IL-23, and interferon (IFN)-, which play an important role in the development of rheumatoid arthritis (RA). Studies have shown conflicting results concerning the association between the rs7574865 G/T polymorphism in the STAT4 gene and RA in an Asian population. We have performed a meta-analysis to examine this relationship.We searched PubMed and WanFang databases for all papers published up to 5 October 2013. Eight case-control studies with 6029 cases and 4685 controls were retrieved based on the search criteria for RA susceptibility related to the STAT4 rs7574865 G/T polymorphism. Risk ratios (RRs) and 95% confidence intervals (CIs) were used to assess the strength of this association. Publication bias was assessed using Beggs test.A significant association was found between the STAT4 rs7574865 G/T polymorphism and RA risk (e.g. GG+GT vs. TT: RR 0.96, 95% CI 0.95-0.97; GG+TT vs. GT: RR 0.94, 95% CI 0.91-0.97). Subgroup analysis of rheumatoid factor (RF) status revealed a protective relationship between the STAT4 rs7574865 G/T polymorphism and RF(+)/RF(-) RA risk. A similar relationship was detected in the anti-cyclic citrullinated peptide (CCP) status subgroup. No clear evidence of publication bias was detected in the overall analysis.Our study indicates that the STAT4 rs7574865 G/T polymorphism was significantly associated with a decreased RA risk in an Asian population.


PubMed | the Affiliated Jiangyin Hospital of Southeast University Medical School
Type: Journal Article | Journal: Asian Pacific journal of cancer prevention : APJCP | Year: 2012

The p53 tumor suppressor pathway plays an important role in gastric cancer (GC) development. Auto-regulatory feedback control of p53 expression is critical to maintaining proper tumor suppressor function. So far, several studies between p53 Arg72Pro polymorphism and GC have generated controversial and inconclusive results.To better assess the purported relationship, we performed a meta-analysis of 19 publications. Eligible studies were identified by searching the Pubmed database. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess any link.Overall, a significant association was detected between the p53 Arg72Pro polymorphism and GC risk (Pro-allele vs. Arg-allele: OR=1.05, 95%CI=1.01-1.08; Pro/Pro vs. Arg/Arg: OR=1.13, 95%CI=1.04-1.22). Moreover, on stratified analysis by race, significantly increased risk was found for Asian populations (Pro-allele vs. Arg-allele: OR=1.06, 95%CI=1.02-1.10; Pro/Pro vs. Arg/Arg: OR=1.16, 95%CI=1.07-1.26; Pro/Pro+Pro/Arg vs. Arg/Arg: OR=1.58, 95%CI=1.09-2.27).Our study provided evidence that the p53 72Pro allele may increase GC risk in Asians. Future studies with larger sample size are warranted to further confirm this association in more detail.


PubMed | the Affiliated Jiangyin Hospital of Southeast University Medical School
Type: Journal Article | Journal: Asian Pacific journal of cancer prevention : APJCP | Year: 2012

Methylenetetrahydrofolate reductase (MTHFR) catalyzes the metabolism of folate and nucleotides needed for DNA synthesis and repair. Variations in MTHFR functions likely play roles in the etiology of lung cancer (LC). So far, several studies between MTHFR C677T polymorphism and LC provide controversial or inconclusive results.To better assess the purported relationship, we performed a meta-analysis of 14 publications. Eligible studies were identified by searching the Pubmed, Embase, Web of Science and Google Scholar databases. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association.Overall, no significant association was detected between the MTHFR C677T polymorphism and LC risk, the same as in race subgroup. However, in the stratified analysis by histological type, significantly increased non-small-cell lung cancer (NSCLC) risk was indicated (T-allele vs. C-allele: OR=1.11, 95%CI=1.03-1.19; TT vs. CC: OR=1.24, 95%CI=1.09-1.41; TC vs. CC: OR=1.11, 95%CI=1.03-1.20 and TT+TC vs. CC: OR=1.09, 95%CI=1.03-1.15). At the same time, ever-smokers who carried T-allele (TT+TC) had a 10% decreased LC risk compared with CC genotype carriers.Our study provided evidence that the MTHFR 677T null genotype may increase NSCLC risk, however, it may protect ever-smokers against LC risk. Future studies with large sample sizes are warranted to further evaluate this association in more detail.

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