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Background: Several studies have reported a possible association of miR-146a rs2910164 polymorphism with Breast Cancer (BC) development. However, the correlation between this polymorphism and susceptibility to BC is under debate. The current meta-analysis was designed and performed to more conclusively evaluate the miR-146a rs2910164 polymorphism and its potential link to BC. Methods: Our team has selected eligible studies (published up to October 2, 2020) from several electronic databases, including Web of Science, PubMed, Scopus and Google Scholar. A total number of 9,545 BC cases and 10,030 controls extracted from 26 eligible articles were included in this study. We utilized pooled Odds Ratios (ORs) as well as 95% confidence intervals (95% CIs) under five genetic models for quantitative estimation of any possible association between miR-146a rs2910164 polymorphism and BC. Results: Based on this meta-analysis, our findings suggest that there is no significant association between miR-146a rs2910164 polymorphism and BC risk. However, stratified analysis revealed that the rs2910164 polymorphism significantly increased the risk of BC in hospital-based studies using the homozygous genetic model (OR=1.37, 95%CI=1.01-1.86, p=0.043, CC vs. GG). Neither Asian nor Caucasian populations showed any significant association between rs2910164 polymorphism and BC susceptibility. Conclusion: In summary, our findings suggest that BC development is not associated with miR-146a rs2910164 polymorphism. However, larger ingenious future investigations might be needed for a more precise estimation of any association between miR-146a rs2910164 polymorphism and BC.

Introduction Programmed cell death-1 (PD-1) and its ligands (PD-L1 and PD-L2) play a critical role as a regulator of immune-system cells, including T cell, natural killer T (NKT), monocytes, dendritic cells (DC), and B cells. Objective This study aimed to find a possible association between PD-1 (rs11568821, rs2227981, rs2227982), and PD-L1 (rs4143815, rs2890658) variants and Breast Cancer (BC) risk in a sample of southeast Iranian women. Method The case-control study consisted of 520 individuals, including 260 histologically confirmed BC patients and 260 non-cancer age-matching healthy women as the control group. The Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) and Tetra-Primer Amplification Refractory Mutation System-Polymerase Chain Reaction (T-ARMS-PCR) methods were used for genotyping of PD-1 (rs11568821, rs2227981, rs2227982), and PD-L1 (rs4143815, rs2890658) polymorphisms. Results and conclusion Our findings indicated that the PD-L1 rs4143815 (G/C) variant meaningfully reduced the risk of BC. However, the PD-L1 rs2890658 variant increased the BC risk in the AC genotype as well as the A allele. Furthermore, we could not find a meaningful association between PD-1 rs11568821, PD-1 rs2227981, PD-1 rs2227982, and BC. Our team examined the possible association between variants and clinicopathological characteristics, including age, size of tumour, lymph node, histology, grade of tumour, estrogen and progesterone receptors status as well as human growth factor receptor 2 (HER2). Our findings demonstrated that PD-L1 rs4143815, PD-L1 rs2890658, PD-1 rs2227982 had a significant association with age. Additionally, we found a significant relation between PD-1 rs2227982 variant and tumour size. Statistical analyzes of PD-1 rs2227981 and PD-1 rs11568821 variants showed a meaningful relation between tumour grade and tumour stage (p=0.006), respectively. .

Bladder cancer (BC) is considered the sixth prevalent malignancy in men and the ninth leading cause of malignancy-related worldwide. Superoxide dismutase (SOD) is an antioxidant enzyme in the defense system against oxidative stress. Hence, we aimed to investigate whether the 50 bp Insertion/Deletion(Ins/Del) polymorphism of the SOD1 associated with the risk of BC. The study was conducted on 158 BC patients and 153 age-matched healthy subjects. Genomic DNA from all individuals was screened for the 50-bp SOD1 promoter deletion using PCR assay. Our results demonstrated an association between SOD1 Ins/Del (45% vs. 32%) genotype and risk of BC and this genotype elevated the susceptibility to BC (OR = 1.80, 95% CI: (1.10-2.90)

Neuroblastoma (NB), a neuroendocrine tumour, is one of the most prevalent cancers in children. The link between LMO1 polymorphisms and NB has been investigated by several groups, rendering inconclusive results. Here, with this comprehensive systematic review and up‐to‐date meta‐analysis, we aim to distinctively elucidate the possible correlation between LMO1 polymorphisms and NB susceptibility. Eligible studies were systematically researched and identified using PubMed, Web of Science and Scopus databases up to 10 February 2019. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the strength of the associations. Our findings revealed that rs110419 and rs2168101 polymorphisms were significantly associated with a decreased risk of NB in all genetic models. In addition, the rs4758051 variant appeared protective against NB in homozygous, dominant and allele genetic models, whereas the rs10840002 variant markedly decreased the risk of NB in the allele model. In contrast, the rs204938 polymorphism showed a positive association with NB susceptibility in allele genetic models. In summary, our meta‐analysis is the first to provide clear evidence of an association between specific polymorphisms of LMO1 and susceptibility to NB. Of note, additional larger well‐designed studies would be helpful to further evaluate and confirm this association.

Introduction MicroRNAs (miRNAs) play an essential role in the susceptibility and development of cancer cells. Objective Examining the dependency of breast cancer risk with genetic polymorphisms of miR-1307, miR-1269, and miR-3117 in a sample of Iranian women (southeast region). Methods The case-control study consisted of 520 individuals (260 diagnosed BC patients, 260 healthy individuals). The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used for genotyping of miR-1307 rs7911488, miR-1269 rs73239138, and miR-3117 (rs4655646 and rs7512692) polymorphisms. Results and conclusion This study provided evidence that miR-1307 rs7911488 polymorphism significantly reduced the risk of BC in heterozygous AG genotype, as well as dominant (AG+GG) genotype and G allele. A significant correlation was found between dominant (AA+AG) genotype, the A allele and protection against BC due to miR-1269 rs73239138 in the sample of study. In contrast, our findings suggested that AG genotype and G allele of miR-3117 rs4655646 polymorphism could increase BC's susceptibility among the southeastern Iranian females. The miR-3117 rs7512692 variant also increased the risk of BC in codominant, dominant and recessive models, as well as the T allele. The possible dependency of miR-1307, miR-1269, and miR-3117 variants with patients' clinicopathological characteristics and BC was also studied. It was concluded that there is a correlation between miR-3117 rs7512692 variant and tumor grade (p=0.031); also, a correlation between miR-1269 rs73239138 variant and progesterone receptor status (p=0.006). The current investigation revealed that miR-1307, miR-1269, and miR-3117 polymorphisms might play a crucial role in the Iranian population's vulnerability to BC. .

Fibroblast growth factor receptor 4 (FGFR4) is a cell surface receptor tyrosine kinases (RTKs) for FGFs. Several studies have focused on the association between FGFR4 polymorphisms and cancer development. This meta-analysis aimed to estimate the association between FGFR4 rs351855 (Gly388Arg), rs1966265 (Val10Ile), rs7708357, rs2011077, and rs376618 polymorphisms and cancer risk. Eligible studies were identified from electronic databases. All statistical analyses were achieved with the STATA 14.0 software. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to quantitatively estimate the association. Overall, no significant association was found among rs351855, rs2011077, and rs376618 polymorphisms with the risk of overall cancer. The rs1966265 polymorphism significantly decreased the risk of cancer in recessive (OR = 0.87, 95% CI = 0.78–0.97, P=0.009, TT vs CT+CC) genetic model. Whereas the rs7708357 polymorphism was positively associated with cancer risk in dominant (OR = 1.17, 95% CI = 1.02–1.36, P=0.028) genetic model. Stratified analysis revealed that rs351855 variant significantly increased the risk of prostate cancer in heterozygous (OR = 1.16, 95% CI = 1.02–1.32, P=0.025 AG vs GG), dominant (OR = 1.20, 95% CI = 1.06–1.35, P=0.004, AG+AA vs GG), and allele (OR = 1.22, 95% CI = 1.06–1.41, P=0.005, A vs G) genetic models. In summary, the findings of this meta-analysis indicate that rs1966265, rs7708357, and rs351855 polymorphisms are correlated to cancer development. Further well-designed studies are necessary to draw more precise conclusions.

Several recent investigations show that HOX transcript antisense intergenic RNA (HOTAIR) play an important role in the pathogenesis of different cancers. HOTAIR polymorphisms has been widely studied in the context of association between with the risk of cancer pathogenesis. However, there is no certain conclusion about the role of HOTAIR polymorphisms in different cancer initiation and progression. Our team has selected eligible studies up to 1 May 2019, from several electronic databases, including Web of Science, PubMed, Scopus, and Google Scholar databases. We have included total number of 102 case-control investigations extracted from 41 eligible articles for the current meta-analysis. We calculated pooled odds ratio (ORs) with their corresponding 95% confidence intervals (CIs) using either fixed-effect or random-effect models for quantitative evaluation of the strength for the association between HOTAIR gene polymorphisms and the risk of cancer. Our current meta-analysis investigation showed that HOTAIR rs4759314 polymorphism particularly increased the overall risk of cancer in different models including homozygous, recessive and allele genetic. HOTAIR rs920778 significantly raised the cancer risk only in recessive genetic model. HOTAIR rs12826786 polymorphism was associated with cancer development in heterozygous, homozygous, dominant, recessive and allele genetic models. Also, an increase in cancer risk was observed with rs874945 polymorphism of HOTAIR gene in heterozygous, dominant and allele genetic models. The rs12427129 polymorphism showed correlation with cancer susceptibility only in recessive model. Subgroup analysis based on cancer type suggested that rs4759314 polymorphism significantly increased the risk of gastric and cervical cancers, and the rs920778 polymorphism increased the risk of gastrointestinal, cervical and gastric cancers. In summary, this study found that HOTAIR polymorphisms are significantly associated with cancer development.

Long noncoding RNA (lncRNA) H19, a well-known oncogenic lncRNA, is overexpressed in various cancers. Several studies have investigated the association between polymorphisms in lncRNA H19 and the risk of various cancer types; however, the findings were inconsistent. In this study, we performed a meta-analysis to identify the precise association between H19 polymorphisms and cancer risk. Appropriate studies were retrieved from searching Web of Science, PubMed, Scopus, and Google scholar databases, updated 25 November 2018. The pooled odds ratios (ORs with 95% confidence intervals (CIs) were calculated to estimate the strength of the association between H19 polymorphisms and cancer risk. Our findings revealed that the H19-rs217727 C>T polymorphism is significantly associated with an increased risk of overall cancer in homozygous codominant (OR=1.28, 95% CI=1.04-1.57, P =0.020, TT vs CC), dominant (OR=1.20, 95% CI=1.04-1.37, P =0.010, CT+TT vs CC), recessive (OR=1.21, 95% CI=1.00-1.46, P =0.048, TT vs CT+CC), and allele (OR=1.16, 95% CI=1.05-1.28, P =0.003, T vs C) genetic models. No significant correlations were observed between H19: rs2839698 G>A, rs2107425 C>T, rs2735971 C>T, rs3024270 G>C, rs3741219 T>C, rs2839701 C>G, rs2735469 C>T, rs17658052 G>A, and rs3741216 T>A polymorphisms and overall cancer risk. Stratified analysis by cancer type proposed that the rs217727 variant is associated with increased risk of oral squamous cell carcinoma (OSCC) and lung cancer, whereas the rs2839698 variant is associated with increased risk of gastrointestinal cancer. Taken together, these findings support an association between H19 rs217727, and rs2839698 polymorphisms and cancer susceptibility. Larger and well-designed studies are necessary to further confirm these findings in detail.

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68&ndash, 0.99, p = 0.04, TT vs. CT+CC, OR = 0.79, 95% CI = 0.67&ndash, 0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70&ndash, 0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02&ndash, 1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41&ndash, 0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50&ndash, 0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60&ndash, 0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63&ndash, 0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.

As a complex disease, various factors are implicated in breast cancer (BC) etiopathogenesis. Mounting evidence indicating that cytokines are one of the crucial elements of carcinogenesis. Interleukin (IL)-1a is a key regulatory cytokine involved in inflammation, immune system activities, and several human diseases, including BC. Eventually, polymorphisms of the IL1A gene can alter IL-1a expression and function. The present study explored the possible relationship between rs3783553as a functional polymorphism in the 3′ untranslated region of IL1A and BC risk. This case-control study was completed on 190 BC patients and 200 age-matched healthy female subjects. Genotyping for rs3783553 was done by mismatched polymerase chain reaction-restriction fragment length polymorphism. The results showed that rs3783553 was not associated with BC risk in any hereditary models (OR = 0.75, 95%CI = 0.50–1.13, p = 0.18, ins/del vs ins/ins and OR = 0.92, 95%CI = 0.29–2.95, p = 0.99, del/del vs ins/ins for codominant; OR = 0.77, 95%CI = 0.51–1.14, p = 0.22, ins/del + del/del vs ins/ins for dominant; OR = 1.05, 95%CI = 0.33–3.32, p = 0.99, del/del vs ins/ins + ins/del for recessive) as well as allele frequency (OR = 0.85, 95%CI = 0.62–1.16, p = 0.33, del vs ins). Our finding indicated the lack of association between rs3783553 and susceptibility to BC in a sample from southeast of Iran. Further studies in other ethnic groups with a larger study population should be done to elucidate the exact association of rs3783553 and BC susceptibility.

Breast cancer (BC) is one of the most prevalent cancers in females, which causes significant mortality. The immune system and inflammation are linked to the pathogenesis of BC. IFNAR1 is an essential part of the immune response in human. To date, no study evaluated the association between IFNAR1 polymorphism and BC susceptibility. This study was aimed to investigate the correlation between IFNAR1 gene polymorphism (rs17875871) and susceptibility to BC, for the first time. This case-control study was done on 192 BC patients and 201 age-matched healthy subjects. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The results revealed that rs17875871 polymorphism was significantly associated with lower risk of BC in heterozygous (OR = 0.40, 95%CI = 0.23–0.68, p = .001), homozygous (OR = 0.25, 95%CI = 0.11–0.53, p