Lack of association of the cyclin D1 G870A variation with oral carcinoma risk: Evidence from 2,404 subjects.

Evidence implicates cyclin D1 (CCND1) G870A polymorphisms as risk factors for various cancers. An increasing number of investigations have been conducted on the association of CCND1 G870A polymorphisms with susceptibility to oral carcinoma, and have yielded inconclusive results. The aim of the present study was to derive a more precise estimation of the correlation. Meta-analyses examining the association between CCND1 G870A polymorphisms and oral carcinoma were performed. Separate analyses on ethnicity, smoking status and control sources were also implemented. Eligible studies were identified prior to February 2012. From the overall data from 1,128 cases and 1,276 controls, no associations of CCND1 G870A polymorphisms with oral carcinoma were observed [AA vs. GG: odds ratio (OR)=1.06; 95% confidence interval (CI), 0.62-1.82; dominant model: OR=1.04; 95% CI, 0.76-1.43; recessive model: OR=1.06; 95% CI, 0.70-1.59]. In the subgroup analysis by ethnicity, smoking status and control sources, no significant associations of CCND1 G870A polymorphisms and oral cancer were observed for the three genetic models. Collectively, the data failed to suggest CCND1 G870A polymorphism as a low-penetrant risk factor for developing oral carcinoma. Additional studies with large sample sizes concerning different ethnicities in different areas are required.

NAT2 polymorphisms with oral carcinoma susceptibility: a meta-analysis.

Published data have implicated NAT2 polymorphisms as risk factors for various cancers. A number of studies have focused on the association of NAT2 polymorphisms with susceptibility to oral carcinoma and have yielded inconclusive results. The aim of the present study was to derive a more precise estimation of the relationship. We first carried out a deliberate search in the databases without a language limitation, covering all papers published up to Dec 2011. A total of seven case-control studies including 1,379 cases and 1,868 controls were selected and the relevant data were extracted for systematic meta-analyses. No significant association was found for the overall data (OR: 1.04, 95 % CI: 0.79-1.39). In subgroup analyses according to ethnicity, slow acetylators might increase oral cancer risk among Asians (OR: 1.38, 95 % CI: 1.04-1.82) but not Caucasians or Mixed races. The data suggested that NAT2 polymorphisms might be a low-penetrant risk factor for oral carcinoma in Asians.

Assessment of the relationship between Helicobacter pylori and lung cancer: a meta-analysis.

BACKGROUND AND AIMS: Helicobacter pylori infection has been thought to play a critical role in gastric carcinoma tumorigenesis and progression. Several studies have been devoted to the relationship between H. pylori infection and lung cancer risk and have generated inconclusive results. In this study we aimed to evaluate the potential association of H. pylori infection with lung cancer risk. METHODS: We conducted a search in Medline, OVID, EMBASE and CNKI, covering all published papers until October 2008. The relevant published papers were deliberately selected according to the established inclusion criteria for publications. Essential data were then extracted from the included studies and further analyzed by a systematic meta-analysis. RESULTS: A total of 98 papers were identified. Of these, four case-control studies met the inclusion criteria and thus were finally selected. Lung cancer risk for H. pylori infection was 3.24-fold (95% CI=1.11-9.47) (Z=2.15, p<0.05) compared with the controls. CONCLUSIONS: The pooled data suggest infection of H. pylori as a potential risk factor for lung cancer.

TP53 codon 72 polymorphism contributes to nasopharyngeal cancer susceptibility: a meta-analysis.

BACKGROUND AND AIMS: Previously, TP53 codon 72 polymorphisms have been implicated as risk factors for various cancers. Several studies have been conducted on the association of TP53 codon 72 polymorphisms with susceptibility to nasopharyngeal carcinoma (NPC) and have yielded inconclusive results. The aim of the present study was to assess possible associations of NPC risk with TP53 codon 72 polymorphisms. METHODS: We conducted a search in Medline, EMBASE, OVID, ScienceDirect, and Chinese National Knowledge Infrastructure (CNKI) without a language limitation, covering all papers published until November 2008. The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications. RESULTS: Consequently, five studies including 394 cases and 606 controls met the included criteria and thus were selected. Ultimately, relevant data were extracted and further analyzed using systematic meta-analyses. The results showed that individuals carrying wild homozygote Arg/Arg genotype have a decreased risk of NPC compared with those carrying Pro/Pro genotype (OR: 0.46, 95% CI: 0.30-0.70). For Pro allele, no evidence indicated that individuals with a combined Pro genotype (Arg/Pro+Pro/Pro) have a significant risk of NPC compared with those with Arg/Arg genotype (OR: 0.81, 95% CI: 0.62-1.07). For Arg allele, individuals with a combined Arg genotype (Arg/Pro+Arg/Arg) have a marked decreased susceptibility to NPC relative to those with homozygote Pro/Pro genotype. CONCLUSIONS: Results of the present study suggest that TP53 codon 72 polymorphisms may be a risk factor for NPC. Homozygote Pro/Pro genotype could significantly increase susceptibility to NPC, whereas Arg allele markedly decreases NPC risk.

Association studies of CYP1A1 and GSTM1 polymorphisms with esophageal cancer risk: evidence-based meta-analyses.

BACKGROUND AND AIMS: Previous studies have implicated cytochrome P450 1A1 (CYP1A1) and glutathione S-transferase M1 (GSTM1) polymorphisms as risk factors for various cancers. A number of studies have been devoted to the association of CYP1A1 or GSTM1 polymorphism with susceptibility to esophageal carcinoma and have yielded conflicting results. We undertook this study to assess possible associations of esophageal cancer risk with CYP1A1 genetic variation and GSTM1 null genotype, respectively. METHODS: We conducted a search in MEDLINE, EMBASE and Chinese National Knowledge Infrastructure (CNKI) without a language limitation, covering all papers published until May 2008. The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications. RESULTS: Ultimately, 26 studies met the included criteria and thus were selected. Relevant data were extracted and further analyzed using systematic meta-analyses. Results showed that the overall OR for CYP1A1 Msp1 polymorphism was 1.24 (95% CI = 0.84-1.83). Restricting analyses to ethnic groups and histological groups, data failed to show a correlation between CYP1A1 Msp1 polymorphism and esophageal cancer risk. Overall OR for CYP1A1 exon7 polymorphism was 1.37 (95% CI = 1.06-1.77), and subgroup analyses showed that CYP1A1 exon7 polymorphism increases esophageal cancer risk in Asians but not in Caucasians. As for GSTM1 deficiency, the overall OR was 1.20 (95% CI = 0.96-1.49), and further subgroup analyses failed to show a marked association of GSTM1 deletion with esophageal cancer. CONCLUSIONS: Results of the present study suggest that CYP1A1 exon7 polymorphisms may be a risk factor for esophageal cancer in Asians but not in Caucasians, whereas neither CYP1A1 Msp1 nor GSTM1 polymorphism was associated with increased susceptibility to esophageal cancer.

Polymorphisms of CYP1A1 and GSTM1 and laryngeal cancer risk: evidence-based meta-analyses.

PURPOSE: Previous evidence implicates CYP1A1 and GSTM1 polymorphisms as risk factors for various cancers. A number of studies have been devoted to the association of CYP1A1 or GSTM1 polymorphism with susceptibility to laryngeal carcinoma, with the results inconsistent and inconclusive. The aim of the present study was to assess the possible associations of laryngeal cancer risk with CYP1A1 genetic variation and GSTM1 null genotype respectively. METHODS: The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications, then the extracted data were further analyzed using systematic meta-analyses. RESULTS: The results showed that the overall odds ratio (OR) was 1.32 (95% CI = 1.08-1.61) for CYP1A1 Mspl polymorphism. Using subgroup analysis, the pooled ORs were 1.38 (95% CI = 0.98-1.95) in Asians and 1.29 (95% CI = 1.01-1.65) in Caucasians. For CYP1A1 exon7 polymorphism, the overall OR was 1.38 (95% CI = 0.98-1.95). The overall OR was 1.24 (95% CI = 1.03-1.49) for GSTM1 polymorphism and the pooled ORs were 1.36 (95% CI = 0.75-2.48) in Asians, 1.16 (95% CI = 0.94-1.44) in Caucasians and 1.52 (95% CI = 1.05-2.19) in Turkey population. CONCLUSIONS: The data suggest CPY1A1 MspI polymorphism as a risk factor for laryngeal cancer in Caucasians but not in Asians. However, the results suggest a marked correlation of GSTM1 polymorphism with laryngeal cancer risk in Turkey population but not Caucasians and Asians.

Study on TP53 codon 72 polymorphisms with oral carcinoma susceptibility.

BACKGROUND AND AIMS: Previous published data have implicated TP53 codon 72 polymorphisms as risk factors for various cancers. Growing bodies of studies have been conducted on the association of TP53 codon 72 polymorphisms with susceptibility to oral carcinoma and have yielded inconclusive results. The aim of the present study was to derive a more precise estimation of this relationship. METHODS: We conducted a search in the relevant databases without a language limitation, covering all papers published until May 2009. The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications. RESULTS: Nine studies including 1990 cases and 2074 controls were selected. Data were extracted and further analyzed using systematic meta-analyses. Results showed that no significant differences of oral cancer risk were found between individuals carrying homozygote Arg/Arg genotype and those carrying Pro/Pro genotype (OR: 0.96, 95% CI: 0.78-1.19). Likewise, no evidence indicated that individuals with Arg/Arg genotype have a significant risk of oral cancer compared with those with a combined Pro genotype (Arg/Pro+Pro/Pro) (OR: 0.98, 95% CI: 0.85-1.12). Similarly, individuals with a combined Arg genotype (Arg/Pro+Arg/Arg) do not have a marked increased or decreased susceptibility to oral cancer relative to those with homozygote Pro/Pro genotype (OR: 1.00, 95% CI: 0.83-1.21). Moreover, when stratifying for race, results were similar among Asians or Caucasians. In addition, TP53 codon 72 polymorphisms may not associate with oral cancer risks in smokers and HPV infection status. CONCLUSIONS: No evidence suggests that TP53 codon 72 polymorphisms may be a risk factor for oral carcinoma.

Possible association of Helicobacter pylori infection with laryngeal cancer risk: an evidence-based meta-analysis.

BACKGROUND: Infection with Helicobacter pylori (H. pylori) is a major cause of various gastric diseases and has been reported to play a role in the process of tumorigenesis and progression of gastric carcinoma. However, whether H. pylori infection increases susceptibilities to other cancers is not fully understood. Several studies have been devoted to the relationship between H. pylori infection and laryngeal cancer risk and have yielded conflicting results. In this study, we aimed to evaluate the possible association of H. pylori infection with laryngeal cancer risk. METHODS: The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications. Extracted data were further analyzed by a systematic meta-analysis. RESULTS: A total of 15 papers were identified. Of these, five case-control studies were selected. Laryngeal cancer risk for H. pylori infection was 2.03-fold (95% CI=1.28-3.23) (Z=3.00, p<0.01) compared with the controls. CONCLUSIONS: The pooled data suggest infection with H. pylori as a possible risk factor for laryngeal cancer.

Is the application of prostaglandin E1 effective for the treatment of sudden hearing loss? An evidence-based meta-analysis.

Microvascular dysfunction in the cochlea has been considered the major cause of sudden hearing loss (SHL). For some time, prostaglandin E(1) (PGE(1)), an effective vasodilator, has been used to treat patients with SHL, however the benefits of this therapy remain unclear. The present study assessed the efficacy of PGE(1) on SHL via a quantitative meta-analysis of 13 randomized controlled studies. The pooled odds ratio was 1.95 (95% confidence interval: 1.53, 2.50) and the test for overall effect (Z-value) was 5.31 (P < 0.00001), suggesting that PGE(1) is an effective and promising strategy for the treatment of SHL.

Adenoviral-mediated up-regulation of Otos, a novel specific cochlear gene, decreases cisplatin-induced apoptosis of cultured spiral ligament fibrocytes via MAPK/mitochondrial pathway.

Previous reports have implicated Otos, a novel specific gene expressed by spiral ligament fibrocytes (SLFs) with unclear functions, as a protective gene for cochlea. However, whether Otos gene could protect SLFs against cisplatin (DDP)-induced apoptosis remains largely unknown. In the present study, we utilized Adenoviral-mediated gene transfection to up-regulate Otos expression in cultured SLFs and further assessed the cell viability and apoptosis as well as possible MAPK and mitochondrial pathways. As expected, the data showed that Otos up-regulation significantly decreased apoptosis of SLFs induced by DDP possibly through activation of ERK and partial inhibition of JNK and mitochondrial pathway but not p-38 pathway, suggesting Otos as a potential protective gene for cochlea and raising the possibility of Otos up-regulation as a promising approach to DDP-induced deafness therapy.

Short interfering RNA directed against TWIST, a novel zinc finger transcription factor, increases A549 cell sensitivity to cisplatin via MAPK/mitochondrial pathway.

Previous reports have implicated epithelial-mesenchymal transition (EMT) as a major cause of cancer. TWIST, a novel zinc finger transcription factor, was suggested to be an important inducer of EMT and therefore be involved in different phases of tumorigenicity. However, whether TWIST suppression could increase chemosensitivity of cancer cells to chemotherapeutic agent remains unclear. In the present study, we utilized RNA interference to knockdown TWIST expression in A549 cells and further assessed the cell viability and apoptosis as well as possible MAPKs and mitochondrial pathways. The data showed that TWIST depletion significantly sensitized A549 cells to cisplatin by inducing activation of JNK/mitochondrial pathway but not ERK and p-38 pathways, suggesting critical roles of TWIST in A549 cell chemoresistance to cisplatin and raising the possibility of TWIST depletion as a promising approach to lung cancer therapy.