The Eighty First Hospital Of Peoples Liberation Army

Nanjing, China

The Eighty First Hospital Of Peoples Liberation Army

Nanjing, China
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PubMed | Operating Room of Peoples Hospital of Zhucheng, Nanjing Medical University, The Eighty First Hospital of Peoples Liberation Army and Maternal and Children Healths Hospital
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Published studies showed controversial findings about the relationship between glutathione S-transferase M1 (GSTM1) null genotype and clinical outcomes of patients with colorectal cancer. We performed a meta-analysis to quantitatively assess the association between GSTM1 null genotype and prognosis of patients with colorectal cancer. We systematically searched Pubmed, Embase, and Web of Science to identify prospective or retrospective cohort studies assessing the association of GSTM1 null genotype with overall survival (OS) or disease-free survival (DFS) in colorectal cancer. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) were used to assess the association of GSTM1 null genotype with OS or DFS. Finally, 15 studies from 14 publications with 4326 colorectal cancer patients were included into the meta-analysis. There was no heterogeneity in the meta-analysis relating OS (I (2)=0%) and DFS (I (2)=0%). Overall, GSTM1 null genotype was significantly associated with poor OS in patients with colorectal cancer (HR=1.18, 95% CI 1.07-1.30, P=0.001). In addition, GSTM1 null genotype was also significantly associated with poor DFS in patients with colorectal cancer (HR=1.15, 95% CI 1.03-1.28, P=0.015). No obvious risk of publication bias was observed. GSTM1 null genotype is significantly associated with poor OS and DFS in patients with colorectal cancer, which suggests that GSTM1 null genotype confers poor effect on the prognosis of colorectal cancer.


PubMed | Jiangsu University, Nanjing Medical University, The Eighty First Hospital of Peoples Liberation Army and Nantong University
Type: | Journal: BioMed research international | Year: 2014

To investigate the role and mechanism of miR-15b in the proliferation and apoptosis of glioma.The miR-15b mimics were transfected into human glioma cells to upregulate the miR-15b expression. Cyclin D1 was determined by both western blotting analysis and luciferase reporter assay. Methylthiazol tetrazolium (MTT) and flow cytometry were employed to detect the cell proliferation, cell cycle, and apoptosis.Overexpression of miR-15b inhibits proliferation by arrested cell cycle progression and induces apoptosis, possibly by directly targeting Cyclin D1. Both luciferase assay and bioinformatics search revealed a putative target site of miR-15b binding to the 3-UTR of Cyclin D1. Moreover, expression of miR-15b in glioma tissues was found to be inversely correlated with Cyclin D1 expression. Enforced Cyclin D1 could abrogate the miR-15b-mediated cell cycle arrest and apoptosis.Our findings identified that miR-15b may function as a glioma suppressor by targeting the Cyclin D1, which may provide a novel therapeutic strategy for treatment of glioma.


Yan S.,Nanjing Medical University | Yan S.,The Eighty First Hospital Of Peoples Liberation Army | Yan S.,Weifang Medical University | Wang Z.,Maternal And Children Healths Hospital | And 5 more authors.
Tumor Biology | Year: 2016

Published studies showed controversial findings about the relationship between glutathione S-transferase M1 (GSTM1) null genotype and clinical outcomes of patients with colorectal cancer. We performed a meta-analysis to quantitatively assess the association between GSTM1 null genotype and prognosis of patients with colorectal cancer. We systematically searched Pubmed, Embase, and Web of Science to identify prospective or retrospective cohort studies assessing the association of GSTM1 null genotype with overall survival (OS) or disease-free survival (DFS) in colorectal cancer. The hazard ratios (HRs) and 95 % confidence intervals (95 % CIs) were used to assess the association of GSTM1 null genotype with OS or DFS. Finally, 15 studies from 14 publications with 4326 colorectal cancer patients were included into the meta-analysis. There was no heterogeneity in the meta-analysis relating OS (I2 = 0 %) and DFS (I2 = 0 %). Overall, GSTM1 null genotype was significantly associated with poor OS in patients with colorectal cancer (HR = 1.18, 95 % CI 1.07–1.30, P = 0.001). In addition, GSTM1 null genotype was also significantly associated with poor DFS in patients with colorectal cancer (HR = 1.15, 95 % CI 1.03–1.28, P = 0.015). No obvious risk of publication bias was observed. GSTM1 null genotype is significantly associated with poor OS and DFS in patients with colorectal cancer, which suggests that GSTM1 null genotype confers poor effect on the prognosis of colorectal cancer. © 2016, International Society of Oncology and BioMarkers (ISOBM).


Yan S.,The Eighty First Hospital Of Peoples Liberation Army | Yan S.,Nanjing Medical University | Xu D.,Nanjing Medical University | Jiang T.,The Eighty First Hospital Of Peoples Liberation Army | And 13 more authors.
Tumor Biology | Year: 2014

Cluster of differentiation 24 (CD24) has been implicated in the development of cancer. Several single nucleotide polymorphisms (SNPs) in CD24 gene are reported to exert diverse effect on cancer risk. However, the association between CD24 SNPs and cancer risk remains unclear due to contradictory published findings. We performed a meta-analysis by pooling all available published studies on the susceptibility of CD24 rs52812045 and rs3838646 polymorphisms to cancer. The pooled odds ratios (ORs) with 95 % confidence intervals (95 % CIs) were calculated. There were five independent case–control studies with 5,539 cases and 10,241 controls included into the present study. The pooled results showed that no appreciable relationship was identified between any of the SNPs of CD24 and cancer risk. Interestingly, a protective role of the CD24 rs3838646 polymorphism was found in the risk of breast cancer, but lack of statistical significance (del allele vs. TG allele: OR = 0.89; 95 % CI, 0.79–1.01; POR = 0.063; del/del vs. TG/TG: OR = 0.70; 95 % CI, 0.44–1.12; POR = 0.135; del/TG vs. TG/TG: OR = 0.91; 95 % CI, 0.80–1.04, POR = 0.180; del/del + del/TG vs. TG/TG: OR = 0.90; 95 % CI, 0.79–1.03; POR = 0.123; del/del vs. TG/TG + del/TG: OR = 0.69; 95 % CI, 0.44–1.08, POR = 0.105). Our study firstly provides the evidence that SNPs (rs52812045 and rs3838646) of CD24 may not modify the risk of cancer. Nonetheless, more individual studies with high quality are needed for further elucidation. © 2014, International Society of Oncology and BioMarkers (ISOBM).


PubMed | The Eighty First Hospital of Peoples Liberation Army, Nanjing Medical University, Peoples Hospital of Rizhao and Qingdao University
Type: | Journal: Mediators of inflammation | Year: 2015

SUA is a potent antioxidant and thus may play a protective role against cancer. Many epidemiological studies have investigated this hypothesis but provided inconsistent and inconclusive findings. We aimed to precisely elucidate the association between SUA levels and cancer by pooling all available publications. Totally, 5 independent studies with 456,053 subjects and 12 with 632,472 subjects were identified after a comprehensive literature screening from PubMed, Embase, and Web of Science. The pooled RRs showed that individuals with high SUA levels were at an increased risk of total cancer incidence (RR = 1.03, 95% CI 1.01-1.05, P = 0.007). Positive association between high SUA levels and total cancer incidence was observed in males but not females (for men: RR = 1.05, 95% CI 1.02-1.08, P = 0.002; for women, RR = 1.01, 95% CI 0.98-1.04, P = 0.512). Besides, high SUA levels were associated with an elevated risk of total cancer mortality (RR = 1.17, 95% CI 1.04-1.32, P = 0.010), particularly in females (RR = 1.25, 95% CI 1.07-1.45, P = 0.004). The study suggests that high SUA levels increase the risk of total cancer incidence and mortality. The data do not support the hypothesis of a protective role of SUA in cancer.


Wang B.J.,The Eighty first Hospital of Peoples Liberation Army | Zhang B.,The Eighty first Hospital of Peoples Liberation Army | Yan S.S.,The Eighty first Hospital of Peoples Liberation Army | Li Z.C.,The Eighty first Hospital of Peoples Liberation Army | And 7 more authors.
Diseases of the Esophagus | Year: 2016

Currently published studies on the relationship between hormonal and reproductive factors and esophageal cancer (EC) risk in women have yielded contradictory findings. For a better understanding of this relationship, we first performed this meta-analysis by pooling all available publications. Sixteen independent studies were retrieved after a comprehensive search in PubMed and Embase databases. The pooled relative risks (RRs) with 95% confidence intervals (95% CIs) were calculated. The pooled RRs implicated that hormone replacement therapy was negatively associated with the risk of EC (RR = 0.72, 95% CI 0.60–0.86, P < 0.001) and esophageal squamous cell carcinoma (RR = 0.68, 95% CI 0.48–0.97, P = 0.031). Menopausal women were at an increased risk of EC (RR = 1.47, 95% CI 1.07–2.03, P = 0.018), particularly esophageal squamous cell carcinoma (RR = 1.66, 95% CI 1.12–2.48, P = 0.012). Additionally, decreased risk of EC (RR = 0.79, 95% CI 0.68–0.92, P = 0.003) and esophageal adenocarcinoma (RR = 0.66, 95% CI 0.53–0.82, P < 0.001) was demonstrated among women with breast-feeding history. Moreover, such associations were more significant among Caucasians, but not Asians. Our study suggests that menopause is an independent risk factor for EC, while hormone replacement therapy and breast-feeding history play a protective role against EC, particularly among Caucasians. All results are consistent with the hypothesis that effects of estrogen may lower the risk of EC in women. © 2015 International Society for Diseases of the Esophagus


PubMed | The Eighty first Hospital of Peoples Liberation Army
Type: Journal Article | Journal: Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus | Year: 2016

Currently published studies on the relationship between hormonal and reproductive factors and esophageal cancer (EC) risk in women have yielded contradictory findings. For a better understanding of this relationship, we first performed this meta-analysis by pooling all available publications. Sixteen independent studies were retrieved after a comprehensive search in PubMed and Embase databases. The pooled relative risks (RRs) with 95% confidence intervals (95% CIs) were calculated. The pooled RRs implicated that hormone replacement therapy was negatively associated with the risk of EC (RR = 0.72, 95% CI 0.60-0.86, P < 0.001) and esophageal squamous cell carcinoma (RR = 0.68, 95% CI 0.48-0.97, P = 0.031). Menopausal women were at an increased risk of EC (RR = 1.47, 95% CI 1.07-2.03, P = 0.018), particularly esophageal squamous cell carcinoma (RR = 1.66, 95% CI 1.12-2.48, P = 0.012). Additionally, decreased risk of EC (RR = 0.79, 95% CI 0.68-0.92, P = 0.003) and esophageal adenocarcinoma (RR = 0.66, 95% CI 0.53-0.82, P < 0.001) was demonstrated among women with breast-feeding history. Moreover, such associations were more significant among Caucasians, but not Asians. Our study suggests that menopause is an independent risk factor for EC, while hormone replacement therapy and breast-feeding history play a protective role against EC, particularly among Caucasians. All results are consistent with the hypothesis that effects of estrogen may lower the risk of EC in women.

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