Survivin蛋白与食管癌关系的系统评价

目的系统评价Survivin蛋白表达水平与食管癌的关系。方法计算机检索CochraneLibrary（2011年第1期）、PubMed、CNKI等数据库,并辅以手工检索,按照纳入与排除标准选择病例对照试验。评价质量及提取资料后,采用STATAll．0软件对数据库进行系统评价。结果共纳入15个研究,包括950例食管癌患者,617例正常对照。Meta分析结果显示：Survivin在食管癌组及正常对照组f比值比（OR）=39．98,95％可信区间（CI）15．08-106．021的表达差异具有统计学意义（P〈0．05）。临床病理检测的Survivin在食管癌低分化组与中高分化组（OR=1．47,95％CI0．59-3．68）的表达差异无统计学意义（P〉0．05）。Survivin在食管癌L-T4期与T1-T：期（OR=2．82,95％CI1．35-5．90）、临床分期Ⅲ-Ⅳ期与Ⅰ-Ⅱ期（OR=2．99,95％C12．03。4．41）、淋巴结转移组与非淋巴结转移组（OR=4．11,95％CI2．79-6．05）的表达差异均有统计学意义（均P〈0．05）。Spearman等级相关分析显示,Survivin与缺氧诱导因子一lα（HIF—lα）表达具有相关性（r=0．542,P〈0．005）。结论Survivin在食管癌中高表达,增加了其恶性行为的发生危险,同时Survivin与HIF－1α在食管癌的表达也有一定的相关性。     

Association between GSTP1 Ile105Val polymorphism and oxaliplatin-induced neuropathy: a systematic review and meta-analysis

Background and aims

The association between glutathione-S-transferase P1 (GSTP1) Ile105Val polymorphism and oxaliplatin-induced neuropathy has been investigated in a number of published studies. However, most of these studies were based on small sample sizes and the results remained inconsistent. To assess the relationship between GSTP1 gene Ile105Val polymorphism and its susceptibility to oxaliplatin-induced neuropathy, a meta-analysis of previous studies was conducted.

Methods

Two investigators independently searched studies published up to December 2012 from the databases of PubMed, EMBASE and The Cochrane Library. The pooled effect was calculated as odds ratio (OR) and corresponding 95 % confidence intervals (CIs) using fixed-effect or random-effect model.

Results

Twelve prospective trials and two retrospective clinical trials involving 2,191 participants met the inclusion criteria. Combined analyses of these studies showed no significant associations between GSTP1 Ile105Val polymorphism and oxaliplatin-induced neuropathy, yielding OR of 1.08 (95 %CI 0.67–1.74, P = 0.754) in dominant model. Similar results were also obtained in recessive model (OR = 1.67, 95 %CI 0.56–4.93, P = 0.357) and allelic analysis (OR = 1.22, 95 %CI 0.67–2.24, P = 0.513). Since significant heterogeneity across studies, the pooled effects were calculated by random-effect model. No evidence of publication biases was identified in this meta-analysis.

Conclusion

This meta-analysis did not support the hypothesis that GSTP1 Ile105Val polymorphism was related to the occurrence of neurotoxicity in oxaliplatin-treated patients. Given the limited number of studies and potential bias, large-scale and well-designed clinical trials should be needed to confirm these hypotheses.     

Link between CFTR mutations and ABPA: a systematic review and meta-analysis

Summary There is a biological plausibility on the link between cystic fibrosis transmembrane conductance regulator (CFTR) mutations and allergic bronchopulmonary aspergillosis (ABPA). The aim of the systematic review was to investigate this link by determining the frequency of CFTR mutations in ABPA. We searched the PubMed and EmBase databases for studies reporting CFTR mutations in ABPA. We pooled the odds ratio (OR) and 95% confidence intervals (CI) from individual studies using both fixed and random effects model. Statistical heterogeneity was evaluated using the I(2) test and the Cochran-Q statistic. Publication bias was assessed using both graphical and statistical methods. Our search yielded four studies (79 ABPA, 268 controls). The odds of encountering CFTR mutation was higher in ABPA compared with the control group (OR 10.39; 95% CI, 4.35-24.79) or the asthma population (OR 5.53; 95% CI 1.62-18.82). There was no evidence of statistical heterogeneity or publication bias. There is a possible pathogenetic link between CFTR mutations and ABPA. However, because of the small numbers of patients, further studies are required to confirm this finding. Future studies should adopt a uniform methodology and should screen for the entire genetic sequence of the CFTR gene.     

Obesity as a risk factor for triple-negative breast cancers: a systematic review and meta-analysis

Triple-negative breast cancer (TNBC) is a subtype of breast tumor with unique characteristics in terms of clinical?pathological presentation, prognosis, and response to therapy. Epidemiological investigations focusing on the identification of risk factors involved in the onset and progression of TNBCs have identified unique demographic, anthropometric, and reproductive characteristics involved in the etiopathogenesis of this subtype of breast tumors. This systematic review and meta-analysis evaluates the association between TNBCs and obesity and menopause status. Eligible articles were identified through three databases and secondary reference analysis. The search was conducted from the first record to February 2012. Eleven original articles meeting a priori established inclusion criteria were incorporated in the quantitative analysis. Case?case and case–control comparisons were performed. In addition, a case–case comparison was conducted before and after stratification according to menopausal status. Based on the level of between-study heterogeneity, pooled odds ratio (OR) and 95 % confidence interval were calculated using fixed or random models. The case?case comparison showed a significant association between TNBC and obesity (OR: 1.20; 95 % CI: 1.03?1.40). These results were confirmed by the case–control comparison (OR: 1.24; 95 % CI: 1.06?1.46). Once stratification based on menopausal status was applied to the case–case analysis, significant results were observed only in the pre-menopausal group (OR: 1.43; 95 % CI: 1.23?1.65). According to this analysis, obese women are at a greater risk of presenting with a TNBC than non-obese women, and menopause status may be a mitigating factor. If validated, these findings should be taken into consideration for the development of targeted preventive programs.     

Association between glutathione S-transferases M1 and T1 gene polymorphisms and prostate cancer risk: a systematic review and meta-analysis

Genetic polymorphisms in glutathione S-transferases M1 (GSTM1) and T1 (GSTT1) genes have been widely reported and considered to have a significant effect on prostate cancer (PCa) risk, but the results are inconsistent. To evaluate the impact of the GSTM1 and GSTT1 polymorphism on PCa risk, we conducted a comprehensive meta-analysis based on 18 eligible studies. A total of 18 studies, including 7,119 subjects for GSTM1 and 6,454 subjects for GSTT1 between 1999 and 2012 were identified through researching MEDLINE, PubMed, Web of Science, EMBASE, Chinese National Knowledge Infrastructure database, and Chinese Biomedical Literature database. A meta-analysis was performed to obtain summary-estimated odd ratios and 95 % confidence intervals of GSTM1 and GSTT1 polymorphisms for PCa, with attention to study quality and publication bias. Overall, there is a significant association between GSTM1 (odds ratio (OR)?=?1.407, 95 % confidence intervals (95 % CI)?=?1.147–1.727, I ²?=?73.2 %, P?= 0.001) genotypes and PCa susceptibility. Significant associations were also observed in subgroups of Caucasian populations (OR?=?1.262, 95 % CI?=?1.055–1.511, I ²?=?48.7 %, P?=?0.011) and Asian populations (OR?=?1.776, 95 % CI?=?1.134–2.781, I ²?=?83.4 %, P?=?0.012). However, no significant association was found (OR?=?1.776, 95 % CI?=?1.134–2.781, P?=?0.243) in African-American populations when stratified by ethnicity. While, there was no significant association seen between GSTT1 (OR?=?1.003, 95 % CI?=?0.823–1.298, I ²?=?68.8 %, P?=?0.778) genotypes and PCa risk. However, no significant associations were observed in subgroups of Caucasian populations (OR?=?1.086, 95 % CI?=?0.801–1.471, I ²?=?72.1 %, P?=?0.597) and Asian populations (OR?=?0.961, 95 % CI?=?0.644–1.434, I ²?=?73.0 %, P?=?0.846), and similar result was found among African-American populations (OR?=?0.802, 95 % CI?=?0.194–3.321, P?=?0.761) when stratified by ethnicity. Our results suggest that the GSTM1 gene polymorphism contributes to PCa susceptibility, while GSTT1 gene polymorphism is not associated with PCa in our study.     

The association between physical activity and renal cancer: systematic review and meta-analysis

Background:

Physical activity may decrease renal cancer risk by reducing obesity, blood pressure, insulin resistance, and lipid peroxidation. Despite plausible biologic mechanisms linking increased physical activity to decreased risk for renal cancer, few epidemiologic studies have been able to report a clear inverse association between physical activity and renal cancer, and no meta-analysis is available on the topic.

Methods:

We searched the literature using PubMed and Web of Knowledge to identify published non-ecologic epidemiologic studies quantifying the relationship between physical activity and renal cancer risk in individuals without a cancer history. Following the PRISMA guidelines, we conducted a systematic review and meta-analysis, including information from 19 studies based on a total of 2 327 322 subjects and 10 756 cases. The methodologic quality of the studies was examined using a comprehensive scoring system.

Results:

Comparing high vs low levels of physical activity, we observed an inverse association between physical activity and renal cancer risk (summary relative risk (RR) from random-effects meta-analysis=0.88; 95% confidence interval (CI)=0.79–0.97). Summarising risk estimates from high-quality studies strengthened the inverse association between physical activity and renal cancer risk (RR=0.78; 95% CI=0.66–0.92). Effect modification by adiposity, hypertension, type 2 diabetes, smoking, gender, or geographic region was not observed.

Conclusion:

Our comprehensive meta-analysis provides strong support for an inverse relation of physical activity to renal cancer risk. Future high-quality studies are required to discern which specific types, intensities, frequencies, and durations of physical activity are needed for renal cancer risk reduction.     

The association between physical activity and bladder cancer: systematic review and meta-analysis

Background:

Physical activity may protect against bladder cancer through several biologic pathways, such as enhanced immune function and decreased chronic inflammation. Physical activity may also indirectly prevent bladder cancer by reducing obesity. A sizeable number of epidemiologic studies have examined the association between physical activity and bladder cancer, but the available evidence has not yet been formally summarised using meta-analysis.

Methods:

We performed a systematic literature review and meta-analysis of English-language studies published from January 1975 through November 2013. We followed the PRISMA guidelines and used a random effects model to estimate the summary risk estimates for the association between physical activity and bladder cancer.

Results:

A total of 15 studies with 5 402 369 subjects and 27 784 bladder cancer cases were included. High vs low levels of physical activity were related to decreased bladder cancer risk (summary relative risk (RR)=0.85, 95% confidence interval (CI)=0.74–0.98; I²=83% P-value for heterogeneity across all studies<0.001). Results were similar for cohort studies (RR=0.89, 95% CI=0.80–1.00; I²=64%) and case–control studies (RR=0.71, 95% CI=0.43–1.16; I²=87% P-value for difference=0.108) and they were comparable for women (RR=0.83, 95% CI=0.73–0.94; I²=0%) and men (RR=0.92, 95% CI=0.82–1.05; I²=67; P-value for difference=0.657). Findings were also comparable for recreational (RR=0.81, 95% CI=0.66–0.99; I²=77%) and occupational physical activity (RR=0.90, 95% CI=0.76–1.0; I²=76% P-value for difference=0.374), and they were largely consistent for moderate (RR=0.85, 95% CI=0.75–0.98; I²=76%) and vigorous activity (RR=0.80, 95% CI=0.64–1.00;I²=87% P-value for difference=0.535).

Conclusions:

Physical activity is associated with decreased risk of bladder cancer. Further studies are required to assess the relations of intensity, frequency, duration, and timing in life of physical activity to bladder cancer risk.     

Significant association between CYP1A1 T3801C polymorphism and cervical neoplasia risk: a systematic review and meta-analysis

Recently, many studies have been published to evaluate the correlation between the cytochrome P450 1A1 (CYP1A1) T3801C polymorphism and cervical neoplasia risk. However, the results remain inconclusive. To clarify this possible association, we conducted a systematic review and meta-analysis of published studies. Data were collected from the following electronic databases: PubMed, Embase, Ovid, ISI Web of Knowledge, Google Scholar, and Chinese Biomedical Database databases. The pooled odds ratio (OR) and its 95 % confidence interval (95 % CI) were used to assess the strength of this association. The pooled ORs were performed for the allele model (C vs. T), the homozygote model (CC vs. TT), the dominant model (CC/CT vs. TT), and the recessive model (CC vs. TT/CT), respectively. Finally, a total of 12 independent studies including a total of 3,724 subjects (1,912 cases/1,812 controls) were eligible for meta-analysis. Overall, there was a significant association between the CYP1A1 T3801C polymorphism and cervical neoplasia susceptibility (C vs. T, OR 1.32, 95 % CI 1.04–1.68, P?=?0.02; CC vs. TT, OR 1.99, 95 % CI 1.19–3.35, P?=?0.01; CC/CT vs. TT, OR 1.36, 95 % CI 1.02–1.81, P?=?0.02; CC vs. TT/CT, OR 1.57, 95 % CI 1.23–2.02, P?<?0.01). Meta-analysis of the ten studies on cervical cancer suggested a significant association between the CYP1A1 T3801C polymorphism and cervical cancer risk (C vs. T, OR 1.38, 95 % CI 1.05–1.82, P?=?0.02; CC vs. TT, OR 2.06, 95 % CI 1.15–3.70, P?=?0.02; CC/CT vs. TT, OR 1.45, 95 % CI 1.03–2.02, P?=?0.03; CC vs. TT/CT, OR 1.56, 95 % CI 1.20–2.03, P?<?0.01). In the stratified analysis by ethnicity, significant associations were also detected in some genetic models. This meta-analysis demonstrates a significant association between the CYP1A1 T3801C polymorphism and cervical neoplasia susceptibility.     

The prevalence of pituitary adenomas: a systematic review

BACKGROUND: Pituitary adenomas display an array of hormonal and proliferative activity. Once primarily classified according to size (microadenomas, < 1 cm; macroadenomas, > or = 1 cm), these tumors are now further classified according to immunohistochemistry and functional status. With these additional classifications in mind, the goals of the current study were to determine the prevalence of pituitary adenomas and to explore the clinical relevance of the findings. METHODS: The authors conducted a metaanalysis of all existing English-language articles in MEDLINE. They used the search string (pituitary adenoma or pituitary tumor) and prevalence and selected relevant autopsy and imaging evaluation studies for inclusion. RESULTS: The authors found an overall estimated prevalence of pituitary adenomas of 16.7% (14.4% in autopsy studies and 22.5% in radiologic studies). CONCLUSIONS: Given the high frequency of pituitary adenomas and their potential for causing clinical pathologies, the findings of the current study suggest that early diagnosis and treatment of pituitary adenomas should have far-reaching benefits.     

Association between the GSTP1 Ile105Val polymorphism and prostate cancer risk: a systematic review and meta-analysis

Many studies have reported the role of glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism with prostate cancer (PCa) risk. However, these studies have yielded conflicting results. Hence, we performed this meta-analysis to investigate the association between GSTP1 Ile105Val polymorphism and PCa in different inheritance models. A total of 13 eligible studies were pooled into this meta-analysis. There was significant association between the GSTP1 Ile158Val variant genotypes and PCa for Ile/Ile vs Val/Val comparison [odds ratio (OR)?=?0.705; I ²?=?63.7 %; 95 % confidence interval (95 % CI)?=?0.508–0.977], Ile/Val vs Val/Val comparison (OR?=?0.736; I ²?=?8.0 %; 95 % CI?=?0.613–0.883), and dominant model (OR?=?0.712; I ²?=?45.5 %; 95 % CI?=?0.555–0.913). However, no associations were detected for other genetic models. In the stratified analysis by ethnicity, significant associations between GSTP1 Ile105Val polymorphism and PCa risk were also found among Caucasians (Ile/Ile vs Val/Val comparison OR?=?0.818, I ²?=?0.0 %, 95 % CI?=?0.681–0.982; Ile/Val vs Val/Val comparison OR?=?0.779, I ²?=?0.0 %, 95 % CI?=?0.651–0.933; and dominant model OR?=?0.794, I ²?=?0.0 %, 95 % CI?=?0.670–0.941), while there were no associations found for other genetic models. However, no associations were found in Asians and African-Americans for all genetic models when stratified by ethnicity. In conclusion, our meta-analysis indicates that GSTP1 Ile105Val polymorphisms contributed to the PCa susceptibility. However, a study with the larger sample size is needed to further evaluate gene–environment interaction on GSTP1 Ile105Val polymorphisms and PCa risk.     

Adiponectin and cancer: a systematic review

Recent studies have demonstrated that obesity is a significant risk factor for the development of several malignancies, but the mechanisms underlying this relationship remain to be fully elucidated. Adiponectin, an adipocyte secreted endogenous insulin sensitizer, appears to play an important role not only in glucose and lipid metabolism but also in the development and progression of several obesity-related malignancies. In this review, we present recent findings on the association of adiponectin with several malignancies as well as recent data on underlying molecular mechanisms that provide novel insights into the association between obesity and cancer risk. We also identify important research questions that remain unanswered.     

HIF-1: an oxygen and metal responsive transcription factor

Normal development and function of metazoan organisms depend on oxygen availability. The level of oxygen can be sensed by individual cells, which respond to reduced oxygenation (hypoxia) largely through activation of hypoxia-inducible factor-1 (HIF-1). At the organism level the response to hypoxia involves an increase in red blood cell production. Within tissues, HIF activation increases the blood supply and blood vessel growth. At the individual cell level it is manifested as an increase in anaerobic metabolism in order to sustain basic cellular functions. Iron is central to the oxygen sensing mechanism, and sensitivity to other metals, namely cobalt and nickel, is a distinctive feature of the HIF system; in fact, this is often used as an initial way of implicating HIF-1 in a biological response. Historically, the fact that nickel or cobalt mimicked hypoxia provided an important clue as to the nature of the oxygen sensing mechanism. It also raises the possibility that nickel or cobalt exposure may have important toxic and pathological effects mediated by HIF activation. Here we review the implications of the metal sensitivity of the HIF-1 system, and examine the hypothesis that HIF-1 activation may play an important role in metal induced carcinogenesis.     

Association between NSAIDs use and breast cancer risk: a systematic review and meta-analysis

The association between non-steroidal anti-inflammatory drugs (NSAIDs) use and breast cancer has remained controversial. Therefore, an overall quantitative estimate of the association needs to be studied. A systematic review and meta-analysis was executed to explore the pooled estimate for relative risk (RR) and 95% confidence interval (CI) using random or fixed effects models based on heterogeneity analysis. Overall 26 studies with 528,705 participants were included. The RR of NSAIDs use and the incidence of breast cancer was 0.94 (95% CI: 0.88–1.00) with random effects model. A slight reduction of breast cancer by taking aspirin and ibuprofen was both observed with pooled RR of 0.91 (95% CI: 0.83–0.98) and 0.81 (95% CI: 0.67–0.97), respectively. Our results indicate that NSAIDs use is associated with a slight decrease for the development of breast cancer with a marginally statistical significant difference. The associations are slightly more obvious in aspirin and ibuprofen use.