Search

We utilize the lepton number violation signal process $p\, e^- \to \tau^+ jjj$ to search for heavy Majorana neutrinos at future proton-electron colliders. The LHeC (FCC-eh) is considered to run with an electron beam energy of 60 GeV, a proton beam energy of 7 (50) TeV and an integrated luminosity of 1 (3) ab$^{-1}$. We apply detector configurations and simulate signal and related SM background events for both hadronic $\tau_h$ and leptonic $\tau_\ell$ final states. After preselection, multivariate analyses are performed to reject the background. The strategy to measure the heavy neutrino mass is developed and distributions of reconstructed mass are presented. Upper limits on parameter $|V_{\tau N}|^2 |V_{eN}|^2 / ( |V_{\tau N}|^2 + |V_{eN}|^2 )$ for the heavy neutrino mass between 10 and 1000 GeV are predicted. At the 95\% confidence level, the best limit is $\sim 4.4\,\,(1.7) \times 10^{-6}$ at the LHeC (FCC-eh) when $m_N \sim 100$ GeV for the hadronic $\tau_h$ final state. Limits for the leptonic $\tau_\ell$ final state are found to be weaker than those for the hadronic $\tau_h$ final state. We also derive the limits on mixing parameters from electroweak precision data (EWPD) and DELPHI experiment. Assuming $|V_{\tau N}|^2 = |V_{eN}|^2 = |V_{\ell N}|^2$, sensitivity bounds from the LHeC and FCC-eh experiments are found to be stronger than those from EWPD for almost all the mass range, and also stronger than those from DELPHI when $m_N \gtrsim 60$ GeV. Constraints are also interpreted and compared in the $|V_{\tau N}|^2$ vs. $|V_{e N}|^2$ plane. Compared with current limits from EWPD, DELPHI, and LHC experiments, future $pe$ experiments can probe large additional regions in the parameter space formed by $|V_{\tau N}|^2$ and $|V_{e N}|^2$, and thus enhance the constraints significantly in the $|V_{\tau N}|^2$ vs. $|V_{e N}|^2$ plane., Comment: 18 pages, 16 figures, 6 tables. arXiv admin note: substantial text overlap with arXiv:2201.12997

We utilize the lepton number violation signal process $p\, e^- \to τ^+ jjj$ to search for heavy Majorana neutrinos at future proton-electron colliders. The LHeC (FCC-eh) is considered to run with an electron beam energy of 60 GeV, a proton beam energy of 7 (50) TeV and an integrated luminosity of 1 (3) ab$^{-1}$. We apply detector configurations and simulate signal and related SM background events for both hadronic $τ_h$ and leptonic $τ_\ell$ final states. After preselection, multivariate analyses are performed to reject the background. The strategy to measure the heavy neutrino mass is developed and distributions of reconstructed mass are presented. Upper limits on parameter $|V_{τN}|^2 |V_{eN}|^2 / ( |V_{τN}|^2 + |V_{eN}|^2 )$ for the heavy neutrino mass between 10 and 1000 GeV are predicted. At the 95\% confidence level, the best limit is $\sim 4.4\,\,(1.7) \times 10^{-6}$ at the LHeC (FCC-eh) when $m_N \sim 100$ GeV for the hadronic $τ_h$ final state. Limits for the leptonic $τ_\ell$ final state are found to be weaker than those for the hadronic $τ_h$ final state. We also derive the limits on mixing parameters from electroweak precision data (EWPD) and DELPHI experiment. Assuming $|V_{τN}|^2 = |V_{eN}|^2 = |V_{\ell N}|^2$, sensitivity bounds from the LHeC and FCC-eh experiments are found to be stronger than those from EWPD for almost all the mass range, and also stronger than those from DELPHI when $m_N \gtrsim 60$ GeV. Constraints are also interpreted and compared in the $|V_{τN}|^2$ vs. $|V_{e N}|^2$ plane. Compared with current limits from EWPD, DELPHI, and LHC experiments, future $pe$ experiments can probe large additional regions in the parameter space formed by $|V_{τN}|^2$ and $|V_{e N}|^2$, and thus enhance the constraints significantly in the $|V_{τN}|^2$ vs. $|V_{e N}|^2$ plane., 18 pages, 16 figures, 6 tables. arXiv admin note: substantial text overlap with arXiv:2201.12997

The relationship between cyclin D1 (CCND1) rs9344 G>A polymorphism and colorectal cancer (CRC) risk is still ambiguous. To obtain a precise estimation of the relationship, we performed an extensive meta-analysis based on the eligible studies. Crude odds ratios with their 95% confidence intervals were harnessed to determine the strength of correlation between CCND1 rs9344 G>A polymorphism and CRC risk under the allele, the homozygote, the dominant, and the recessive genetic models, respectively (28 studies with 5,784 CRC cases and 7,858 controls). Our results indicated evidence of the association between CCND1 rs9344 G>A polymorphism and the increased risk of CRC in four genetic models: A vs G, AA vs GG, AA+GA vs GG, and AA vs GA+GG. In a stratified analysis by cancer type of CRC, there was an increased risk of sporadic CRC found in three genetic models: A vs G, AA vs GG, and AA+GA vs GG. In a stratified analysis by ethnicity, there was an increased CRC risk found among Asians in allele comparison genetic models, as well as Caucasians in two genetic models: AA+GA vs GG and A vs T. In summary, this meta-analysis demonstrates that CCND1 rs9344 G>A polymorphism may be a risk factor for CRC.

Coronary artery disease (CAD) is a complex disease resulting from a combination of environmental and genetic factors. We hypothesized that polymorphisms hsa-mir-499 rs3746444 T/C, IRAK1 rs3027898 C/A and RANKL rs7984870 C/G might contribute to CAD susceptibility.We studied the association between the three polymorphisms and the risk of CAD in a Chinese population using 435 CAD patients and 480 controls. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) was used to perform the genotyping, and the differences were analysed.When the hsa-mir-499 rs3746444 TT homozygote genotype was used as the reference group, the TC, CC or TC/CC genotypes were associated with a significantly increased risk of CAD [TC vs. TT: adjusted odds ratio (OR) 1.41, 95% confidence interval (CI) 1.02-1.94, p = 0.04; CC vs. TT: adjusted OR 3.14, 95% CI 1.77-5.56, p0.001; CC/TC vs. TT: adjusted OR 1.68, 95% CI 1.25-2.26, p0.001). In the recessive model, when the hsa-mir-499 rs3746444 TT/TC genotypes were used as the reference group, the CC homozygote genotype was associated with a significantly increased risk of CAD (adjusted OR 2.87, 95% CI 1.63-5.04, p0.001). Risk factors such as diabetes mellitus (DM), hypertension, smoking and low high-density ipoprotein cholesterol (HDL-c) were also associated with a significantly increased risk for CAD. Logistic regression analyses revealed that IRAK1 rs3027898 C/A and RANKL rs7984870 C/G polymorphisms were not associated with risk of CAD.These findings suggested that the functional polymorphism hsa-mir-499 rs3746444 T/C is associated with CAD susceptibility.

Hao Qiu,1,* Chengguo Cheng,2,* Yafeng Wang,3 Mingqiang Kang,4 Weifeng Tang,4,5 Shuchen Chen,4 Haiyong Gu,6 Chao Liu,5 YuChen7,8 1Department of Immunology, School of Medicine, Jiangsu University, 2Department of Pulmonary Medicine,Affiliated Hospital of JiangsuUniversity, Zhenjiang, 3Department of Cardiology, The People’s Hospital of Xishuangbanna Dai Autonomous Prefecture, Jinghong, 4Department of Thoracic Surgery, Affiliated Union Hospital, Fujian Medical University, Fuzhou, 5Department of Cardiothoracic Surgery, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, 6Department of Thoracic Surgery, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai, 7Department of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Cancer Hospital, 8Fujian Provincial Key Laboratory of Translational Cancer Medicine, Fuzhou, People’s Republic of China *These authors contributed equally tothis work Abstract: The relationship between cyclin D1 (CCND1) rs9344 G>A polymorphism and colorectal cancer (CRC) risk is still ambiguous. To obtain a precise estimation of the relationship, we performed an extensive meta-analysis based on the eligible studies. Crude odds ratios with their 95% confidence intervals were harnessed to determine the strength of correlation between CCND1 rs9344 G>A polymorphism and CRC risk under the allele, the homozygote, the dominant, and the recessive genetic models, respectively (28 studies with 5,784CRC cases and 7,858 controls). Our results indicated evidence of the association between CCND1 rs9344 G>A polymorphism and the increased risk of CRC in four genetic models: Avs G, AA vs GG, AA+GA vs GG, and AA vs GA+GG. In a stratified analysis by cancer type of CRC, there was an increased risk of sporadic CRC found in three genetic models: A vs G, AA vs GG, and AA+GA vs GG. In a stratified analysis by ethnicity, there was an increased CRC risk found among Asians in allele comparison genetic models, as well as Caucasians in two genetic models: AA+GA vs GG and A vs T. In summary, this meta-analysis demonstrates that CCND1 rs9344 G>A polymorphism may be a risk factor for CRC. Keywords: polymorphism, CCND1, colorectal cancer, susceptibility, meta-analysis

Several studies have focused on the correlation between the programmed death-1 (PD-1) rs2227981 C > T polymorphism and the risk of cancer; however, the results of such studies remain conflicting. To address this gap, we performed this meta-analysis to identify the potential association. Search strategies were performed in PubMed and EMBASE using appropriate terms. In total, 2,977 cancer cases and 2,642 controls from seven publications were recruited in our study. According to the seven eligible publications, the odds ratios (ORs) and 95% confidence intervals (CIs) on the risk of cancer for the TT vs. CC and TT vs. CT+CC genotypes were 0.67 and 0.50-0.91 and 0.65 and 0.47-0.90, respectively. In a subgroup analysis by cancer type, PD-1 rs2227981 C > T polymorphism was associated with a significantly decreased risk of breast cancer (OR, 0.82; 95% CI, 0.71-0.95; P = 0.009 for T vs. C and OR, 0.76; 95% CI, 0.63-0.92; P = 0.005 for TT+CT vs. CC) and of other cancer (OR, 0.58; 95% CI, 0.36-0.92; P = 0.004 for TT vs. CT+CC). In a subgroup analysis by ethnicity, a significant decreased cancer risk was identified among Asians (OR, 0.74; 95% CI, 0.63-0.86; P < 0.001 for T vs. C and OR, 0.71; 95% CI, 0.59-0.87; P = 0.001 for TT+CT vs. CC) and among Caucasians (OR, 0.66; 95% CI, 0.44-0.99; P = 0.047 for TT vs. CT+CC). These findings highlight the fact that the T allele of PD-1 rs2227981 C > T polymorphism modestly decreases the susceptibility of cancer. Nevertheless, further large and well-designed studies are needed to enrich the evidence of this association.

Methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms are associated with many types of cancers. The purpose of our study was to evaluate the effect of MTHFR single nucleotide polymorphisms (SNPs) on gastric cardia adenocarcinoma (GCA). We conducted a hospital-based case-control study. Three hundred and thirty cases with GCA and 608 controls were recruited. The ligation detection reaction (LDR) method was used to determine genotypes. The genotype MTHFR rs1801133 TT was significantly more frequent in cases than in controls (adjusted odds ratio (OR) = 1.46, 95% confidence interval (CI) = 1.04-2.05, P = 0.029) in a recessive model, after adjusting for age, sex and smoking and alcohol use. The haplotype MTHFR Grs4845882Ars4846048Trs1801133Crs9651118Ars3753584 was more frequent in cases than in controls (crude OR = 5.32, 95% CI = 2.34-12.10, P < 0.001). No association between other genotypes and haplotypes was observed. Our results suggest that the genotype MTHFR rs1801133 TT and the MTHFR Grs4845882Ars4846048Trs1801133Crs9651118Ars3753584 haplotype may be associated with susceptibility to GCA. Further studies are needed to confirm these findings.

Studies examining the association between the cyclin D1 (CCND1) A870G (rs9344 G>A) polymorphism and esophageal squamous cell carcinoma (ESCC) have yielded inconsistent results. Here, we conducted a hospital-based case-control study in a Chinese Han population to assess the association between the CCND1 A870G polymorphism and ESCC. We then performed a meta-analysis to further investigate this association. We recruited 629 patients with ESCC and 686 cancer-free controls. Genotyping was performed with the polymerase chain reaction-ligase detection reactions (PCR-LDR) method. The meta-analysis was performed with the STATA 12.0 software. The case-control study showed no significant difference between the ESCC cases and controls in the allele frequencies or genotype distributions of the CCND1 A870G polymorphism. To obtain a more precise estimate of this relationship, we performed a meta-analysis of seven case-control studies involving a total of 2080 ESCC cases and 2833 controls. The meta-analysis suggested that the CCND1 A870G polymorphism is not associated with a risk of ESCC. A further subgroup analysis based on ethnicity also detected no association. This study suggests that the CCND1 A870G polymorphism is not associated with the risk of ESCC.