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  1. Article ; Online: Genetic correlation and causal associations between psychiatric disorders and lung cancer risk.

    Shi, Jiajun / Wen, Wanqing / Long, Jirong / Gamazon, Eric R / Tao, Ran / Cai, Qiuyin

    Journal of affective disorders

    2024  Volume 356, Page(s) 647–656

    Abstract: Background: Patients with certain psychiatric disorders have increased lung cancer incidence. However, establishing a causal relationship through traditional epidemiological methods poses challenges.: Methods: Available summary statistics of genome- ... ...

    Abstract Background: Patients with certain psychiatric disorders have increased lung cancer incidence. However, establishing a causal relationship through traditional epidemiological methods poses challenges.
    Methods: Available summary statistics of genome-wide association studies of cigarette smoking, lung cancer, and eight psychiatric disorders, including attention deficit/hyperactivity disorder (ADHD), autism, depression, major depressive disorder, bipolar disorder, insomnia, neuroticism, and schizophrenia (range N: 46,350-1,331,010) were leveraged to estimate genetic correlations using Linkage Disequilibrium Score Regression and assess causal effect of each psychiatric disorder on lung cancer using two-sample Mendelian randomization (MR) models, comprising inverse-variance weighted (IVW), weighted median, MR-Egger, pleiotropy residual sum and outlier testing (MR-PRESSO), and a constrained maximum likelihood approach (cML-MR).
    Results: Significant positive correlations were observed between each psychiatric disorder and both smoking and lung cancer (all FDR < 0.05), except for the correlation between autism and lung cancer. Both univariable and the cML-MA MR analyses demonstrated that liability to schizophrenia, depression, ADHD, or insomnia was associated with an increased risk of overall lung cancer. Genetic liability to insomnia was linked specifically to squamous cell carcinoma (SCC), while genetic liability to ADHD was associated with an elevated risk of both SCC and small cell lung cancer (all P < 0.05). The later was further supported by multivariable MR analyses, which accounted for smoking.
    Limitations: Participants were constrained to European ancestry populations. Causal estimates from binary psychiatric disorders may be biased.
    Conclusion: Our findings suggest appropriate management of several psychiatric disorders, particularly ADHD, may potentially reduce the risk of developing lung cancer.
    MeSH term(s) Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/epidemiology ; Mendelian Randomization Analysis ; Mental Disorders/genetics ; Mental Disorders/epidemiology ; Genome-Wide Association Study ; Schizophrenia/genetics ; Schizophrenia/epidemiology ; Attention Deficit Disorder with Hyperactivity/genetics ; Attention Deficit Disorder with Hyperactivity/epidemiology ; Genetic Predisposition to Disease/genetics ; Autistic Disorder/genetics ; Autistic Disorder/epidemiology ; Bipolar Disorder/genetics ; Bipolar Disorder/epidemiology ; Risk Factors ; Sleep Initiation and Maintenance Disorders/genetics ; Sleep Initiation and Maintenance Disorders/epidemiology ; Depressive Disorder, Major/genetics ; Depressive Disorder, Major/epidemiology ; Neuroticism ; Causality ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/epidemiology ; Cigarette Smoking/epidemiology ; Cigarette Smoking/genetics ; Linkage Disequilibrium
    Language English
    Publishing date 2024-04-23
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 135449-8
    ISSN 1573-2517 ; 0165-0327
    ISSN (online) 1573-2517
    ISSN 0165-0327
    DOI 10.1016/j.jad.2024.04.080
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  2. Article ; Online: Drug-target Mendelian randomization revealed a significant association of genetically proxied metformin effects with increased prostate cancer risk.

    Sun, Xiaohui / Ping, Jie / Guo, Xingyi / Long, Jirong / Cai, Qiuyin / Shu, Xiao-Ou / Shu, Xiang

    Molecular carcinogenesis

    2024  Volume 63, Issue 5, Page(s) 849–858

    Abstract: The association between metformin use and risk of prostate cancer remains controversial, while data from randomized trials is lacking. We aim to evaluate the association of genetically proxied metformin effects with prostate cancer risk using a drug- ... ...

    Abstract The association between metformin use and risk of prostate cancer remains controversial, while data from randomized trials is lacking. We aim to evaluate the association of genetically proxied metformin effects with prostate cancer risk using a drug-target Mendelian randomization (MR) approach. Summary statistics for prostate cancer were obtained from the Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome Consortium (79,148 cases and 61,106 controls). Cis-expression quantitative trait loci (cis-eQTL) variants in the gene targets of metformin were identified in the GTEx project and eQTLGen consortium. We also obtained male-specific genome-wide association study data for type 2 diabetes, body mass index (BMI), total testosterone, bioavailable testosterone, estradiol, and sex hormone binding globulin for mediation analysis. Inverse-variance weighted (IVW) regression, weighted median, MR-Egger regression, and MR-PRESSO were performed in the main MR analysis. Multivariable MR was used to identify potential mediators and genetic colocalization analysis was performed to assess any shared genetic basis between two traits of interest. We found that genetically proxied metformin effects (1-SD HbA
    MeSH term(s) Male ; Humans ; Metformin/therapeutic use ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/genetics ; Genome-Wide Association Study ; Mendelian Randomization Analysis ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Testosterone ; Polymorphism, Single Nucleotide
    Chemical Substances Metformin (9100L32L2N) ; Testosterone (3XMK78S47O)
    Language English
    Publishing date 2024-03-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1004029-8
    ISSN 1098-2744 ; 0899-1987
    ISSN (online) 1098-2744
    ISSN 0899-1987
    DOI 10.1002/mc.23692
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  3. Article ; Online: Genetic correlation and causal associations between circulating C-reactive protein levels and lung cancer risk.

    Shi, Jiajun / Wen, Wanqing / Long, Jirong / Xue, Haoran / Yang, Yaohua / Tao, Ran / Pan, Wei / Shu, Xiao-Ou / Cai, Qiuyin

    Cancer causes & control : CCC

    2024  

    Abstract: Purpose: We aimed to characterize genetic correlations and causal associations between circulating C-reactive protein (CRP) levels and the risk of lung cancer (LC).: Methods: Leveraging summary statistics from genome-wide association studies of ... ...

    Abstract Purpose: We aimed to characterize genetic correlations and causal associations between circulating C-reactive protein (CRP) levels and the risk of lung cancer (LC).
    Methods: Leveraging summary statistics from genome-wide association studies of circulating CRP levels among 575,531 individuals of European ancestry, and LC risk among 29,266 cases and 56,450 controls, we investigated genetic associations of circulating CRP levels with the risk of overall lung cancer and its histological subtypes, by using linkage disequilibrium score (LDSC) regression and Mendelian randomization (MR) analyses.
    Results: Significant positive genetic correlations between circulating CRP levels and the risk of LC and its histological subtypes were identified from LDSC regression, with correlation coefficients ranging from 0.12 to 0.26, and all false discovery adjusted p < 0.05. Univariable MR demonstrated a nominal association between CRP levels and an increased risk of lung squamous cell carcinoma (SCC) (inverse variance-weighted OR = 1.15, 95% CI 1.01-1.30). However, this association disappeared when multivariable MR included cigarettes per day and/or body mass index. By using our recently developed constrained maximum likelihood-based MR method, we identified significant associations of CRP levels with the risk of overall LC (OR 1.06, 95% CI 1.03-1.09), SCC (OR 1.06, 95% CI 1.02-1.09), and small cell lung cancer (SCLC, OR 1.09, 95% CI 1.03-1.15). Moreover, most univariable and multivariable MR analyses also revealed consistent CRP-SCLC associations.
    Conclusion: There may be a genetic and causal association between circulating CRP levels and the risk of SCLC, which is in line with previous population-based observational studies.
    Language English
    Publishing date 2024-02-08
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1064022-8
    ISSN 1573-7225 ; 0957-5243
    ISSN (online) 1573-7225
    ISSN 0957-5243
    DOI 10.1007/s10552-024-01855-7
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  4. Article ; Online: Lifestyle factors, genetic susceptibility to obesity and their interactions on coronary artery disease risk: A cohort study in the UK Biobank.

    Choi, Jungyoon / Wen, Wanqing / Jia, Guochong / Tao, Ran / Long, Jirong / Shu, Xiao-Ou / Zheng, Wei

    Preventive medicine

    2024  Volume 180, Page(s) 107886

    Abstract: Objective: We aimed to evaluate potential modifying effects of genetic susceptibility to obesity on the association of lifestyle factors with coronary artery disease (CAD) risk.: Methods: A total of 328,606 participants (54% women) were included ... ...

    Abstract Objective: We aimed to evaluate potential modifying effects of genetic susceptibility to obesity on the association of lifestyle factors with coronary artery disease (CAD) risk.
    Methods: A total of 328,606 participants (54% women) were included using data from the UK Biobank. We evaluated the risk of developing CAD associated with obesity-related polygenic scores (PGSs) and healthy lifestyle scores (HLSs). HLSs were constructed using six lifestyle factors. Obesity PGSs were created using genetic variants identified by genome-wide association studies, including 941 variants for body mass index (BMI) and 457 for waist-to-hip ratio (WHR). Both HLSs and PGSs were categorized into three groups.
    Results: During a 9-year median follow-up, 14,541 participants developed CAD. An unhealthy lifestyle was significantly associated with an increased CAD risk (hazard ratio [HR] = 2.24, 95% confidence interval [CI] = 2.09-2.40). High BMI and WHR PGSs were each significantly associated with an increased CAD risk (HR
    Conclusions: While the observational nature of the study precludes the establishment of causality, our study provides supports for a causal association between obesity and CAD risk and the importance of lifestyle modification in the prevention of CAD.
    MeSH term(s) Humans ; Female ; Male ; Coronary Artery Disease/epidemiology ; Coronary Artery Disease/genetics ; Risk Factors ; Cohort Studies ; Genome-Wide Association Study ; Biological Specimen Banks ; UK Biobank ; Obesity/genetics ; Life Style ; Genetic Predisposition to Disease
    Language English
    Publishing date 2024-02-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 184600-0
    ISSN 1096-0260 ; 0091-7435
    ISSN (online) 1096-0260
    ISSN 0091-7435
    DOI 10.1016/j.ypmed.2024.107886
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    Zs.A 878: Show issues Location:
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  5. Article ; Online: Serum Lipid Profiles and Cholesterol-Lowering Medication Use in Relation to Subsequent Risk of Colorectal Cancer in the UK Biobank Cohort.

    Yuan, Fangcheng / Wen, Wanqing / Jia, Guochong / Long, Jirong / Shu, Xiao-Ou / Zheng, Wei

    Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

    2023  Volume 32, Issue 4, Page(s) 524–530

    Abstract: Background: Dyslipidemia is closely associated with metabolic syndrome, a known risk factor for colorectal cancer. However, the association of dyslipidemia with colorectal cancer risk is controversial. Most previous studies did not consider cholesterol- ... ...

    Abstract Background: Dyslipidemia is closely associated with metabolic syndrome, a known risk factor for colorectal cancer. However, the association of dyslipidemia with colorectal cancer risk is controversial. Most previous studies did not consider cholesterol-lowering medication use at the time of lipid measurements, which could bias findings.
    Methods: We analyzed data from 384,862 UK Biobank participants to disentangle the associations between blood lipids and colorectal cancer risk. Serum levels of total cholesterol, high- and low-density lipoprotein cholesterol (HDL-C, LDL-C), and triglyceride were measured at study baseline. Multivariable-adjusted Cox models were used to estimate HRs and 95% confidence intervals (CI).
    Results: During a median follow-up time of 8.2 years, 3,150 incident primary colorectal cancer cases were identified. Triglyceride levels were positively, while HDL-C levels were inversely associated with colorectal cancer risk (both Ptrend < 0.005). No significant associations were found for total cholesterol and LDL-C. However, among nonusers of cholesterol-lowering medications, a high total cholesterol level (> 6.7 mmol/L, HR = 1.11; 95% CI, 1.00-1.24) and LDL-C level (>4.1 mmol/L, HR = 1.11; 95% CI, 0.99-1.23) was associated with an increased colorectal cancer risk compared with the referent group (5.2-6.2 mmol/L and 2.6-3.4 mmol/L for total and LDL cholesterol, respectively). Compared with nonusers, cholesterol-lowering medication users had 15% increased colorectal cancer risk (HR = 1.15; 95% CI, 1.04-1.26).
    Conclusions: Circulating total cholesterol, LDL-C, HDL-C and triglyceride were modestly associated with colorectal cancer risk.
    Impact: Our findings call for careful consideration of cholesterol-lowering medication use in future studies of blood lipid-colorectal cancer associations.
    MeSH term(s) Humans ; Cholesterol, LDL ; Biological Specimen Banks ; Cholesterol ; Lipids ; Triglycerides ; Cholesterol, HDL ; Risk Factors ; Colorectal Neoplasms/etiology ; Colorectal Neoplasms/complications ; Dyslipidemias ; United Kingdom/epidemiology
    Chemical Substances Cholesterol, LDL ; Cholesterol (97C5T2UQ7J) ; Lipids ; Triglycerides ; Cholesterol, HDL
    Language English
    Publishing date 2023-02-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1153420-5
    ISSN 1538-7755 ; 1055-9965
    ISSN (online) 1538-7755
    ISSN 1055-9965
    DOI 10.1158/1055-9965.EPI-22-1170
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    Zs.A 3693: Show issues Location:
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  6. Article ; Online: Cis-regulation of antisense non-coding RNA at the JAZF1 locus in type 2 diabetes.

    Ding, Qiuju / Zhao, Weiwei / Long, Jirong / Alsafar, Habiba / Zhou, Qing / Chen, Huimei

    The journal of gene medicine

    2022  Volume 24, Issue 4, Page(s) e3407

    Abstract: Background: Several genomic loci of type 2 diabetes (T2D) nominated in genome-wide association studies (GWAS) have been suggested to regulate metabolism in muscle. However, a large portion of the genetic risk and the underlying regulation remain ... ...

    Abstract Background: Several genomic loci of type 2 diabetes (T2D) nominated in genome-wide association studies (GWAS) have been suggested to regulate metabolism in muscle. However, a large portion of the genetic risk and the underlying regulation remain unexplained. The present study aimed to localize the potentially functional regions or genes at juxtaposed with another zinc finger protein 1 (JAZF1) locus and interpret their possible biological mechanisms in the muscle of T2D.
    Methods: Seven GWAS datasets including 21,897 T2D patients and 32,710 healthy controls of 772 SNPs within JAZF1 locus were meta-analysed using unconditional logistic regression. The Sherlock and GTEx protal online algorithms were implemented to show the significant colocalizations. Multiple omics data were integrated to predict the potential biological functions of JAZF1-AS1 in muscle. The cis regulation of JAZF1-AS1 was analysed using in vitro cloning in Human skeletal muscle cells (HSkMC).
    Results: With a cross-population meta-analysis of seven GWAS, we identified a linkage disequilibrium (LD) block within intron 1 of JAZF1 that was significantly associated with T2D (false discovery rate < 0.05). The colocalization analysis showed a significant association between genetically determined expression of JAZF1 in skeletal muscle and T2D with a strong probability of colocalization (PP4 = 75.09%). This region also encodes the upstream regulatory region of the antisense non-coding RNA JAZF1-AS1. Expression-quantitative trait loci analysis detected a regulatory SNP within this LD block, rs864745, which is associated with the expression of JAZF1-AS1 and JAZF1. With in vitro cloning, we further reported the role of JAZF1-AS1 in cis-regulating JAZF1 by directly forming RNA double strands. Downregulation of JAZF1, caused by JAZF1-AS1 depletion, inhibited the glucose uptake and lipid oxidation in skeletal muscle.
    Conclusions: The present study proposes a strategy for identifying a novel T2D gene at the reported locus and generating a model in which polymorphisms at JAZF1 influence T2D risk through antisense-mediated gene regulation.
    MeSH term(s) Co-Repressor Proteins/genetics ; DNA-Binding Proteins/genetics ; Diabetes Mellitus, Type 2/genetics ; Genome-Wide Association Study ; Humans ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; RNA, Untranslated
    Chemical Substances Co-Repressor Proteins ; DNA-Binding Proteins ; JAZF1 protein, human ; RNA, Untranslated
    Language English
    Publishing date 2022-02-23
    Publishing country England
    Document type Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
    ZDB-ID 1458024-x
    ISSN 1521-2254 ; 1099-498X
    ISSN (online) 1521-2254
    ISSN 1099-498X
    DOI 10.1002/jgm.3407
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    Zs.A 5423: Show issues Location:
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  7. Article: Oral microbiome and ischemic stroke risk among elderly Chinese women.

    Wang, Cong / Yang, Yaohua / Cai, Qiuyin / Gao, Yutang / Cai, Hui / Wu, Jie / Zheng, Wei / Long, Jirong / Shu, Xiao-Ou

    Journal of oral microbiology

    2023  Volume 15, Issue 1, Page(s) 2266655

    Abstract: Background: Stroke, a leading cause of disability worldwide, has been associated with periodontitis. However, whether stroke risk is related to oral microbiota remains unknown. This study aims to evaluate the associations between the oral microbiome and ...

    Abstract Background: Stroke, a leading cause of disability worldwide, has been associated with periodontitis. However, whether stroke risk is related to oral microbiota remains unknown. This study aims to evaluate the associations between the oral microbiome and ischemic stroke risk.
    Methods: In a case-control study of 134 case-control pairs nested within a prospective cohort study, we examined pre-diagnostic oral microbiome in association with stroke risk via shotgun metagenomic sequencing. The microbial sub-community and functional profiling were performed using Latent Dirichlet Allocation and HUMAnN2. Associations of microbial diversity, sub-community structure, and individual microbial features with ischemic stroke risk were evaluated via conditional logistic regression.
    Results: Alpha and beta diversities differ significantly between cases and controls. One genus- and two species-level sub-communities were significantly associated with decreased ischemic stroke risk, with odds ratios (95% confidence intervals) of 0.52 (0.31-0.90), 0.51 (0.31-0.84), and 0.60 (0.36-0.99), respectively. These associations were potentially driven by the representative taxa in these sub-communities,
    Conclusion: Our study highlights the role of oral microbiota in the etiology of ischemic stroke and calls for further research.
    Language English
    Publishing date 2023-10-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2523919-3
    ISSN 2000-2297
    ISSN 2000-2297
    DOI 10.1080/20002297.2023.2266655
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  8. Article ; Online: Identification of target proteins for breast cancer genetic risk loci and blood risk biomarkers in a large study by integrating genomic and proteomic data.

    Jia, Guochong / Yang, Yaohua / Ping, Jie / Xu, Shuai / Liu, Lili / Guo, Xingyi / Tao, Ran / Long, Jirong / Zheng, Wei

    International journal of cancer

    2023  Volume 152, Issue 11, Page(s) 2314–2320

    Abstract: Genome-wide association studies (GWAS) have identified around 200 loci associated with breast cancer risk. However, protein targets for these loci remain largely unknown. Identifying protein targets and biomarkers can improve the understanding of cancer ... ...

    Abstract Genome-wide association studies (GWAS) have identified around 200 loci associated with breast cancer risk. However, protein targets for these loci remain largely unknown. Identifying protein targets and biomarkers can improve the understanding of cancer biology and etiology and identify high-risk individuals for cancer prevention. In this study, we investigated genetically predicted levels of 1142 circulating proteins with breast cancer risk in 133 384 cases and 113 789 controls of European ancestry included in the Breast Cancer Association Consortium (BCAC). We identified 22 blood protein biomarkers associated with the risk of overall breast cancer at a false discovery rate (FDR) <0.05, including nine proteins encoded by genes located at least 500 kb away from previously reported risk variants for breast cancer. Analyses focusing on 124 encoding genes located at GWAS-identified breast cancer risk loci found 20 proteins associated with overall breast cancer risk and one protein associated with triple-negative breast cancer risk at FDR <0.05. Adjustment for the GWAS-identified risk variants significantly attenuated the association for 13 of these proteins, suggesting that these proteins may be the targets of these GWAS-identified risk loci. The identified proteins are involved in various biological processes, including glutathione conjugation, STAT5 signaling and NF-κB signaling pathways. Our study identified novel protein targets and risk biomarkers for breast cancer risk.
    MeSH term(s) Humans ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Breast Neoplasms/genetics ; Proteomics ; Genetic Loci ; Genomics ; Polymorphism, Single Nucleotide
    Language English
    Publishing date 2023-02-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.34472
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  9. Article ; Online: Gut microbiome in association with chemotherapy-induced toxicities among patients with breast cancer.

    Nguyen, Sang M / Tran, Huong T T / Long, Jirong / Shrubsole, Martha J / Cai, Hui / Yang, Yaohua / Cai, Qiuyin / Tran, Thuan V / Zheng, Wei / Shu, Xiao-Ou

    Cancer

    2024  

    Abstract: Background: Little research has focused on the relationship between gut microbiome and chemotherapy-induced toxicity.: Methods: This prospective study involves 301 patients with breast cancer who had prechemotherapy stool samples collected. Gut ... ...

    Abstract Background: Little research has focused on the relationship between gut microbiome and chemotherapy-induced toxicity.
    Methods: This prospective study involves 301 patients with breast cancer who had prechemotherapy stool samples collected. Gut microbiome was sequenced by shotgun metagenomics; associations with chemotherapy-induced toxicities during first-line treatment by gut microbial diversity, composition, and metabolic pathways with severe (i.e., grade ≥3) hematological and gastrointestinal toxicities were evaluated via multivariable logistic regression.
    Results: High prechemotherapy α-diversity was associated with a significantly reduced risk of both severe hematological toxicity (odds ratio [OR] = 0.94; 95% CI, 0.89-0.99; p = .048) and neutropenia (OR = 0.94; 95% CI, 0.89-0.99; p = .016). A high abundance of phylum Synergistota, class Synergistia, and order Synergistales were significantly associated with a reduced risk of severe neutropenia; conversely, enrichment of phylum Firmicutes C, class Negativicutes, phylum Firmicutes I, and class Bacilli A, order Paenibacillales were significantly associated with an increased risk of severe neutropenia (p range: 0.012-2.32 × 10
    Conclusions: Our study suggests that gut microbiota may be a potential preventive target to reduce chemotherapy-induced toxicity.
    Language English
    Publishing date 2024-02-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1429-1
    ISSN 1097-0142 ; 0008-543X ; 1934-662X
    ISSN (online) 1097-0142
    ISSN 0008-543X ; 1934-662X
    DOI 10.1002/cncr.35229
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  10. Article ; Online: Evaluating polygenic risk scores in assessing risk of nine solid and hematologic cancers in European descendants.

    Choi, Jungyoon / Jia, Guochong / Wen, Wanqing / Long, Jirong / Zheng, Wei

    International journal of cancer

    2020  Volume 147, Issue 12, Page(s) 3416–3423

    Abstract: Genome-wide association studies (GWAS) have identified many genetic risk variants for cancers. The utility of these variants in assessing risk of esophageal, gastric and endometrial cancers, as well as melanoma, glioma, diffuse large B-cell lymphoma, ... ...

    Abstract Genome-wide association studies (GWAS) have identified many genetic risk variants for cancers. The utility of these variants in assessing risk of esophageal, gastric and endometrial cancers, as well as melanoma, glioma, diffuse large B-cell lymphoma, follicular lymphoma, chronic lymphoid leukemia and multiple myeloma, has not been adequately investigated. We constructed a site-specific polygenic risk score (PRS) for each of these nine cancers using their GWAS-identified risk variants. Using data from 400 807 participants of European descent in the UK Biobank, a population-based cohort study, we estimated the hazard ratios of each cancer associated with its PRS using Cox proportional hazard models. During a median follow-up of 5.8 years, 3905 incident cases of these nine cancers were identified in the cohort. The area under the receiver operating characteristic curve ranged from 0.53 to 0.69 for these cancers. Except for esophageal cancer, significant dose-response associations were observed between PRS and cancer risk. Compared to individuals in the middle quintile (40%-60%) at an average risk, those among the highest 5% of the PRS had a twofold elevated risk of melanoma, glioma, follicular lymphoma or multiple myeloma, and a fourfold elevated risk of chronic lymphoid leukemia. Using PRS, 63.0% of the participants could be classified as having an over twofold elevated risk for at least one cancer. The PRS derived using risk variants identified to date by GWAS showed the potential in identifying individuals at a significantly elevated risk of cancer for prevention.
    MeSH term(s) Cohort Studies ; Endometrial Neoplasms/epidemiology ; Endometrial Neoplasms/genetics ; Esophageal Neoplasms/epidemiology ; Esophageal Neoplasms/genetics ; European Continental Ancestry Group/genetics ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Glioma/epidemiology ; Glioma/genetics ; Hematologic Neoplasms/epidemiology ; Hematologic Neoplasms/genetics ; Humans ; Male ; Melanoma/epidemiology ; Melanoma/genetics ; Multifactorial Inheritance ; Polymorphism, Single Nucleotide ; Stomach Neoplasms/epidemiology ; Stomach Neoplasms/genetics ; United Kingdom/ethnology
    Language English
    Publishing date 2020-07-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.33176
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