Sökning: WFRF:(Lee Chaeyoung) > Spurdle Amanda B. > Association Between...
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000 | 11459naa a2202653 4500 | |
001 | oai:DiVA.org:umu-135977 | |
003 | SwePub | |
008 | 170629s2017 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1359772 URI |
024 | 7 | a https://doi.org/10.1001/jamaoncol.2016.59452 DOI |
040 | a (SwePub)umu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Haycock, Philip C.4 aut |
245 | 1 0 | a Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases A Mendelian Randomization Study |
264 | 1 | b American Medical Association,c 2017 |
338 | a print2 rdacarrier | |
520 | a IMPORTANCE: The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. OBJECTIVE: To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. DATA SOURCES: Genomewide association studies (GWAS) published up to January 15, 2015. STUDY SELECTION: GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. DATA EXTRACTION AND SYNTHESIS: Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. MAIN OUTCOMES AND MEASURES: Odds ratios (ORs) and 95% confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. RESULTS: Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [ 95% CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [ 95% CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [ 95% CI, 0.49-0.81]), celiac disease (OR, 0.42 [ 95% CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [ 95% CI, 0.05-0.15]). CONCLUSIONS AND RELEVANCE: It is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Cancer och onkologi0 (SwePub)302032 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cancer and Oncology0 (SwePub)302032 hsv//eng |
700 | 1 | a Burgess, Stephen4 aut |
700 | 1 | a Nounu, Aayah4 aut |
700 | 1 | a Zheng, Jie4 aut |
700 | 1 | a Okoli, George N.4 aut |
700 | 1 | a Bowden, Jack4 aut |
700 | 1 | a Wade, Kaitlin Hazel4 aut |
700 | 1 | a Timpson, Nicholas J.4 aut |
700 | 1 | a Evans, David M.4 aut |
700 | 1 | a Willeit, Peter4 aut |
700 | 1 | a Aviv, Abraham4 aut |
700 | 1 | a Gaunt, Tomr.4 aut |
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700 | 1 | a Ellis, Hayley Patricia4 aut |
700 | 1 | a Kurian, Kathreena M.4 aut |
700 | 1 | a Pooley, Karen A.4 aut |
700 | 1 | a Eeles, Rosalind A.4 aut |
700 | 1 | a Lee, Jeffrey E.4 aut |
700 | 1 | a Fang, Shenying4 aut |
700 | 1 | a Chen, Wei V.4 aut |
700 | 1 | a Law, Matthew H.4 aut |
700 | 1 | a Bowdler, Lisa M.4 aut |
700 | 1 | a Iles, Mark M.4 aut |
700 | 1 | a Yang, Qiong4 aut |
700 | 1 | a Worrall, Bradford B.4 aut |
700 | 1 | a Markus, Hugh Stephen4 aut |
700 | 1 | a Hung, Rayjean J.4 aut |
700 | 1 | a Amos, Chris I.4 aut |
700 | 1 | a Spurdle, Amanda B.4 aut |
700 | 1 | a Thompson, Deborah J.4 aut |
700 | 1 | a O'Mara, Tracy A.4 aut |
700 | 1 | a Wolpin, Brian4 aut |
700 | 1 | a Amundadottir, Laufey4 aut |
700 | 1 | a Stolzenberg-Solomon, Rachael4 aut |
700 | 1 | a Trichopoulou, Antonia4 aut |
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700 | 1 | a Canzian, Federico4 aut |
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700 | 1 | a Tumino, Rosario4 aut |
700 | 1 | a Svenson, Ulrikau Umeå universitet,Patologi4 aut0 (Swepub:umu)ulason03 |
700 | 1 | a van Rij, Andre4 aut |
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700 | 1 | a Jonas, Jost B.4 aut |
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710 | 2 | a Umeå universitetb Patologi4 org |
773 | 0 | t JAMA Oncologyd : American Medical Associationg 3:5, s. 636-651q 3:5<636-651x 2374-2437x 2374-2445 |
856 | 4 | u https://jamanetwork.com/journals/jamaoncology/articlepdf/2604820/jamaoncology_haycock_2017_oi_160090.pdf |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-135977 |
856 | 4 8 | u https://doi.org/10.1001/jamaoncol.2016.5945 |
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