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1. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases A Mendelian Randomization Study

Author

Haycock, PC, Burgess, S, Nounu, A, Zheng, J, Okoli, GN, Bowden, J, Wade, KH, Timpson, NJ, Evans, DM, Willeit, P, Aviv, A, Gaunt, T, Hemani, G, Mangino, M, Ellis, HP, Kurian, KM, Pooley, KA, Eeles, RA, Lee, JE, Fang, SY, Chen, WV, Law, MH, Bowdler, LM, Iles, MM, Yang, Q, Worrall, BB, Markus, HS, Hung, RJ, Amos, CI, Spurdle, AB, Thompson, DJ, O'Mara, TA, Wolpin, B, Amundadottir, L, Stolzenberg-Solomon, R, Trichopoulou, A, Onland-Moret, C, Lund, E, Duell, EJ, Canzian, F, Severi, G, Overvad, K, Gunter, MJ, Tumino, R, Svenson, U, van Rij, A, Baas, AF, Bown, MJ, Samani, NJ, van t'Hof, FNG, Tromp, G, Jones, GT, Kuivaniemi, H, Elmore, JR, Johansson, M, Mckay, J, Scelo, G, Carreras-Torres, R, Gaborieau, V, Brennan, P, Bracci, PM, Neale, RE, Olson, SH, Gallinger, S, Li, DH, Petersen, GM, Risch, HA, Klein, AP, Han, JL, Abnet, CC, Freedman, N D, Taylor, PR, Maris, JM, Aben, KK, Kiemeney, LA, Vermeulen, SH, Wiencke, JK, Walsh, KM, Wrensch, M, Rice, T, Turnbull, C, Litchfield, K, Paternoster, L, Standl, M, Abecasis, GR, SanGiovanni, JP, Li, Y, Mijatovic, V, Sapkota, Y, Low, SK, Zondervan, KT, Montgomery, GW, Nyholt, DR, van Heel, D A, Hunt, K, Arking, DE, Ashar, FN, Sotoodehnia, N, Woo, D, Rosand, J, Comeau, ME, Brown, W M, Silverman, EK, Hokanson, JE, Cho, MH, Hui, J, Ferreira, MA, Thompson, PJ, Morrison, AC, Felix, Janine, Smith, NL, Christiano, AM, Petukhova, L, Betz, RC, Fan, X, Zhang, XJ, Zhu, CH, Langefeld, CD, Thompson, SD, Wang, FJ, Lin, X, Schwartz, DA, Fingerlin, T, Rotter, JI, Cotch, MF, Jensen, RA, Munz, M, Dommisch, H, Schaefer, AS, Han, F, Ollila, HM, Hillary, RP, Albagha, O, Ralston, SH, Zeng, CJ, Zheng, W, Shu, XO, Reis, A, Uebe, S, Huffmeier, U, Kawamura, Y, Otowa, T, Sasaki, T, Hibberd, ML, Davila, S, Xie, G, Siminovitch, K, Bei, JX, Zeng, YX, Forsti, A, Chen, B (Bowang), Landi, S, Franke, A, Fischer, A, Ellinghaus, D, Flores, C, Noth, I, Ma, SF, Foo, JN, Liu, JJ, Kim, JW, Cox, DG, Delattre, O, Mirabeau, O, Skibola, CF, Tang, CS, Garcia-Barcelo, M, Chang, KP, Su, WH, Chang, YS, Martin, NG, Gordon, S, Wade, TD, Lee, C, Kubo, M, Cha, PC, Nakamura, Y, Levy, D, Kimura, M, Hwang, SJ, Hunt, S, Spector, T, Soranzo, N, Manichaikul, A, Barr, G, Kahali, B, Speliotes, E, Yerges-Armstrong, L, Cheng, CY (Ching-Yu), Jonas, JB, Wong, TY, Fogh, I, Lin, K, Powell, JF, Rice, K, Relton, CL, Martin, RM, Smith, GD, Haycock, PC, Burgess, S, Nounu, A, Zheng, J, Okoli, GN, Bowden, J, Wade, KH, Timpson, NJ, Evans, DM, Willeit, P, Aviv, A, Gaunt, T, Hemani, G, Mangino, M, Ellis, HP, Kurian, KM, Pooley, KA, Eeles, RA, Lee, JE, Fang, SY, Chen, WV, Law, MH, Bowdler, LM, Iles, MM, Yang, Q, Worrall, BB, Markus, HS, Hung, RJ, Amos, CI, Spurdle, AB, Thompson, DJ, O'Mara, TA, Wolpin, B, Amundadottir, L, Stolzenberg-Solomon, R, Trichopoulou, A, Onland-Moret, C, Lund, E, Duell, EJ, Canzian, F, Severi, G, Overvad, K, Gunter, MJ, Tumino, R, Svenson, U, van Rij, A, Baas, AF, Bown, MJ, Samani, NJ, van t'Hof, FNG, Tromp, G, Jones, GT, Kuivaniemi, H, Elmore, JR, Johansson, M, Mckay, J, Scelo, G, Carreras-Torres, R, Gaborieau, V, Brennan, P, Bracci, PM, Neale, RE, Olson, SH, Gallinger, S, Li, DH, Petersen, GM, Risch, HA, Klein, AP, Han, JL, Abnet, CC, Freedman, N D, Taylor, PR, Maris, JM, Aben, KK, Kiemeney, LA, Vermeulen, SH, Wiencke, JK, Walsh, KM, Wrensch, M, Rice, T, Turnbull, C, Litchfield, K, Paternoster, L, Standl, M, Abecasis, GR, SanGiovanni, JP, Li, Y, Mijatovic, V, Sapkota, Y, Low, SK, Zondervan, KT, Montgomery, GW, Nyholt, DR, van Heel, D A, Hunt, K, Arking, DE, Ashar, FN, Sotoodehnia, N, Woo, D, Rosand, J, Comeau, ME, Brown, W M, Silverman, EK, Hokanson, JE, Cho, MH, Hui, J, Ferreira, MA, Thompson, PJ, Morrison, AC, Felix, Janine, Smith, NL, Christiano, AM, Petukhova, L, Betz, RC, Fan, X, Zhang, XJ, Zhu, CH, Langefeld, CD, Thompson, SD, Wang, FJ, Lin, X, Schwartz, DA, Fingerlin, T, Rotter, JI, Cotch, MF, Jensen, RA, Munz, M, Dommisch, H, Schaefer, AS, Han, F, Ollila, HM, Hillary, RP, Albagha, O, Ralston, SH, Zeng, CJ, Zheng, W, Shu, XO, Reis, A, Uebe, S, Huffmeier, U, Kawamura, Y, Otowa, T, Sasaki, T, Hibberd, ML, Davila, S, Xie, G, Siminovitch, K, Bei, JX, Zeng, YX, Forsti, A, Chen, B (Bowang), Landi, S, Franke, A, Fischer, A, Ellinghaus, D, Flores, C, Noth, I, Ma, SF, Foo, JN, Liu, JJ, Kim, JW, Cox, DG, Delattre, O, Mirabeau, O, Skibola, CF, Tang, CS, Garcia-Barcelo, M, Chang, KP, Su, WH, Chang, YS, Martin, NG, Gordon, S, Wade, TD, Lee, C, Kubo, M, Cha, PC, Nakamura, Y, Levy, D, Kimura, M, Hwang, SJ, Hunt, S, Spector, T, Soranzo, N, Manichaikul, A, Barr, G, Kahali, B, Speliotes, E, Yerges-Armstrong, L, Cheng, CY (Ching-Yu), Jonas, JB, Wong, TY, Fogh, I, Lin, K, Powell, JF, Rice, K, Relton, CL, Martin, RM, and Smith, GD

Published
2017

3. Narcolepsy risk loci outline role of T cell autoimmunity and infectious triggers in narcolepsy.

Author

Ollila HM, Sharon E, Lin L, Sinnott-Armstrong N, Ambati A, Yogeshwar SM, Hillary RP, Jolanki O, Faraco J, Einen M, Luo G, Zhang J, Han F, Yan H, Dong XS, Li J, Zhang J, Hong SC, Kim TW, Dauvilliers Y, Barateau L, Lammers GJ, Fronczek R, Mayer G, Santamaria J, Arnulf I, Knudsen-Heier S, Bredahl MKL, Thorsby PM, Plazzi G, Pizza F, Moresco M, Crowe C, Van den Eeden SK, Lecendreux M, Bourgin P, Kanbayashi T, Martínez-Orozco FJ, Peraita-Adrados R, Benetó A, Montplaisir J, Desautels A, Huang YS, Jennum P, Nevsimalova S, Kemlink D, Iranzo A, Overeem S, Wierzbicka A, Geisler P, Sonka K, Honda M, Högl B, Stefani A, Coelho FM, Mantovani V, Feketeova E, Wadelius M, Eriksson N, Smedje H, Hallberg P, Hesla PE, Rye D, Pelin Z, Ferini-Strambi L, Bassetti CL, Mathis J, Khatami R, Aran A, Nampoothiri S, Olsson T, Kockum I, Partinen M, Perola M, Kornum BR, Rueger S, Winkelmann J, Miyagawa T, Toyoda H, Khor SS, Shimada M, Tokunaga K, Rivas M, Pritchard JK, Risch N, Kutalik Z, O'Hara R, Hallmayer J, Ye CJ, and Mignot EJ

Subjects
Humans, Autoimmunity genetics, Influenza, Human epidemiology, Influenza, Human genetics, Influenza A Virus, H1N1 Subtype genetics, Autoimmune Diseases epidemiology, Autoimmune Diseases genetics, Influenza Vaccines adverse effects, Narcolepsy chemically induced, Narcolepsy genetics
Abstract

Narcolepsy type 1 (NT1) is caused by a loss of hypocretin/orexin transmission. Risk factors include pandemic 2009 H1N1 influenza A infection and immunization with Pandemrix®. Here, we dissect disease mechanisms and interactions with environmental triggers in a multi-ethnic sample of 6,073 cases and 84,856 controls. We fine-mapped GWAS signals within HLA (DQ0602, DQB1*03:01 and DPB1*04:02) and discovered seven novel associations (CD207, NAB1, IKZF4-ERBB3, CTSC, DENND1B, SIRPG, PRF1). Significant signals at TRA and DQB1*06:02 loci were found in 245 vaccination-related cases, who also shared polygenic risk. T cell receptor associations in NT1 modulated TRAJ*24, TRAJ*28 and TRBV*4-2 chain-usage. Partitioned heritability and immune cell enrichment analyses found genetic signals to be driven by dendritic and helper T cells. Lastly comorbidity analysis using data from FinnGen, suggests shared effects between NT1 and other autoimmune diseases. NT1 genetic variants shape autoimmunity and response to environmental triggers, including influenza A infection and immunization with Pandemrix®., (© 2023. The Author(s).)

Published
2023
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4. Beyond a Binary Classification of Sex: An Examination of Brain Sex Differentiation, Psychopathology, and Genotype.

Author

Phillips OR, Onopa AK, Hsu V, Ollila HM, Hillary RP, Hallmayer J, Gotlib IH, Taylor J, Mackey L, and Singh MK

Subjects
Adolescent, Brain diagnostic imaging, Child, Cohort Studies, Databases, Factual, Diffusion Magnetic Resonance Imaging, Female, Genome-Wide Association Study, Genotype, Humans, Male, Phenotype, Philadelphia, Psychopathology, Young Adult, Brain physiopathology, Chromosomes, Human genetics, Sex Characteristics, Sex Differentiation genetics
Abstract

Objective: Sex differences in the brain are traditionally treated as binary. We present new evidence that a continuous measure of sex differentiation of the brain can explain sex differences in psychopathology. The degree of sex-differentiated brain features (ie, features that are more common in one sex) may predispose individuals toward sex-biased psychopathology and may also be influenced by the genome. We hypothesized that individuals with a female-biased differentiation score would have greater female-biased psychopathology (internalizing symptoms, such as anxiety and depression), whereas individuals with a male-biased differentiation score would have greater male-biased psychopathology (externalizing symptoms, such as disruptive behaviors)., Method: Using the Philadelphia Neurodevelopmental Cohort database acquired from database of Genotypes and Phenotypes, we calculated the sex differentiation measure, a continuous data-driven calculation of each individual's degree of sex-differentiating features extracted from multimodal brain imaging data (magnetic resonance imaging [MRI] /diffusion MRI) from the imaged participants (n = 866, 407 female and 459 male)., Results: In male individuals, higher differentiation scores were correlated with higher levels of externalizing symptoms (r = 0.119, p = .016). The differentiation measure reached genome-wide association study significance (p < 5∗10 -8 ) in male individuals with single nucleotide polymorphisms Chromsome5:rs111161632:RASGEF1C and Chromosome19:rs75918199:GEMIN7, and in female individuals with Chromosome2:rs78372132:PARD3B and Chromosome15:rs73442006:HCN4., Conclusion: The sex differentiation measure provides an initial topography of quantifying male and female brain features. This demonstration that the sex of the human brain can be conceptualized on a continuum has implications for both the presentation of psychopathology and the relation of the brain with genetic variants that may be associated with brain differentiation., (Copyright © 2018 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.)

Published
2019
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5. The NASA Twins Study: A multidimensional analysis of a year-long human spaceflight.

Author

Garrett-Bakelman FE, Darshi M, Green SJ, Gur RC, Lin L, Macias BR, McKenna MJ, Meydan C, Mishra T, Nasrini J, Piening BD, Rizzardi LF, Sharma K, Siamwala JH, Taylor L, Vitaterna MH, Afkarian M, Afshinnekoo E, Ahadi S, Ambati A, Arya M, Bezdan D, Callahan CM, Chen S, Choi AMK, Chlipala GE, Contrepois K, Covington M, Crucian BE, De Vivo I, Dinges DF, Ebert DJ, Feinberg JI, Gandara JA, George KA, Goutsias J, Grills GS, Hargens AR, Heer M, Hillary RP, Hoofnagle AN, Hook VYH, Jenkinson G, Jiang P, Keshavarzian A, Laurie SS, Lee-McMullen B, Lumpkins SB, MacKay M, Maienschein-Cline MG, Melnick AM, Moore TM, Nakahira K, Patel HH, Pietrzyk R, Rao V, Saito R, Salins DN, Schilling JM, Sears DD, Sheridan CK, Stenger MB, Tryggvadottir R, Urban AE, Vaisar T, Van Espen B, Zhang J, Ziegler MG, Zwart SR, Charles JB, Kundrot CE, Scott GBI, Bailey SM, Basner M, Feinberg AP, Lee SMC, Mason CE, Mignot E, Rana BK, Smith SM, Snyder MP, and Turek FW

Subjects
Adaptive Immunity, Body Weight, Carotid Arteries diagnostic imaging, Carotid Intima-Media Thickness, DNA Damage, DNA Methylation, Gastrointestinal Microbiome, Genomic Instability, Humans, Male, Telomere Homeostasis, Time Factors, United States, United States National Aeronautics and Space Administration, Adaptation, Physiological, Astronauts, Space Flight
Abstract

To understand the health impact of long-duration spaceflight, one identical twin astronaut was monitored before, during, and after a 1-year mission onboard the International Space Station; his twin served as a genetically matched ground control. Longitudinal assessments identified spaceflight-specific changes, including decreased body mass, telomere elongation, genome instability, carotid artery distension and increased intima-media thickness, altered ocular structure, transcriptional and metabolic changes, DNA methylation changes in immune and oxidative stress-related pathways, gastrointestinal microbiota alterations, and some cognitive decline postflight. Although average telomere length, global gene expression, and microbiome changes returned to near preflight levels within 6 months after return to Earth, increased numbers of short telomeres were observed and expression of some genes was still disrupted. These multiomic, molecular, physiological, and behavioral datasets provide a valuable roadmap of the putative health risks for future human spaceflight., (Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Published
2019
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6. Complex HLA association in paraneoplastic cerebellar ataxia with anti-Yo antibodies.

Author

Hillary RP, Ollila HM, Lin L, Desestret V, Rogemond V, Picard G, Small M, Arnulf I, Dauvilliers Y, Honnorat J, and Mignot E

Subjects
Breast Neoplasms complications, Breast Neoplasms genetics, Female, Haplotypes, Humans, Ovarian Neoplasms complications, Ovarian Neoplasms genetics, Genetic Predisposition to Disease genetics, HLA Antigens genetics, Paraneoplastic Cerebellar Degeneration genetics
Abstract

Anti-Yo paraneoplastic cerebellar degeneration (PCD) is a devastating autoimmune complication of gynecological cancers. We hypothesized that as for other autoimmune diseases, specific HLA haplotypes are associated. We conducted high resolution HLA typing of Class I/Class II in 40 cases versus ethnically matched controls. Three cases with anti-Yo antibodies and peripheral neuropathy were also included. We detected protective effects of DPA1*01:03~DPB1*04:01 (OR=0, p=0.0008), DRB1*04:01~DQA1*03:03(OR=0, p=0.0016) and DPA1*01:03~DPB1*04:01 (OR=0.35, p=0.0047) overall. Increased DRB1*13:01~DQA1*01:03~DQB1*06:03 was also found in PCD ovarian cases (OR=5.4, p=0.0016). These results suggest differential genetic susceptibility to anti-Yo per cancer and with a primary HLA Class II involvement., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Published
2018
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7. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study.

Author

Haycock PC, Burgess S, Nounu A, Zheng J, Okoli GN, Bowden J, Wade KH, Timpson NJ, Evans DM, Willeit P, Aviv A, Gaunt TR, Hemani G, Mangino M, Ellis HP, Kurian KM, Pooley KA, Eeles RA, Lee JE, Fang S, Chen WV, Law MH, Bowdler LM, Iles MM, Yang Q, Worrall BB, Markus HS, Hung RJ, Amos CI, Spurdle AB, Thompson DJ, O'Mara TA, Wolpin B, Amundadottir L, Stolzenberg-Solomon R, Trichopoulou A, Onland-Moret NC, Lund E, Duell EJ, Canzian F, Severi G, Overvad K, Gunter MJ, Tumino R, Svenson U, van Rij A, Baas AF, Bown MJ, Samani NJ, van t'Hof FNG, Tromp G, Jones GT, Kuivaniemi H, Elmore JR, Johansson M, Mckay J, Scelo G, Carreras-Torres R, Gaborieau V, Brennan P, Bracci PM, Neale RE, Olson SH, Gallinger S, Li D, Petersen GM, Risch HA, Klein AP, Han J, Abnet CC, Freedman ND, Taylor PR, Maris JM, Aben KK, Kiemeney LA, Vermeulen SH, Wiencke JK, Walsh KM, Wrensch M, Rice T, Turnbull C, Litchfield K, Paternoster L, Standl M, Abecasis GR, SanGiovanni JP, Li Y, Mijatovic V, Sapkota Y, Low SK, Zondervan KT, Montgomery GW, Nyholt DR, van Heel DA, Hunt K, Arking DE, Ashar FN, Sotoodehnia N, Woo D, Rosand J, Comeau ME, Brown WM, Silverman EK, Hokanson JE, Cho MH, Hui J, Ferreira MA, Thompson PJ, Morrison AC, Felix JF, Smith NL, Christiano AM, Petukhova L, Betz RC, Fan X, Zhang X, Zhu C, Langefeld CD, Thompson SD, Wang F, Lin X, Schwartz DA, Fingerlin T, Rotter JI, Cotch MF, Jensen RA, Munz M, Dommisch H, Schaefer AS, Han F, Ollila HM, Hillary RP, Albagha O, Ralston SH, Zeng C, Zheng W, Shu XO, Reis A, Uebe S, Hüffmeier U, Kawamura Y, Otowa T, Sasaki T, Hibberd ML, Davila S, Xie G, Siminovitch K, Bei JX, Zeng YX, Försti A, Chen B, Landi S, Franke A, Fischer A, Ellinghaus D, Flores C, Noth I, Ma SF, Foo JN, Liu J, Kim JW, Cox DG, Delattre O, Mirabeau O, Skibola CF, Tang CS, Garcia-Barcelo M, Chang KP, Su WH, Chang YS, Martin NG, Gordon S, Wade TD, Lee C, Kubo M, Cha PC, Nakamura Y, Levy D, Kimura M, Hwang SJ, Hunt S, Spector T, Soranzo N, Manichaikul AW, Barr RG, Kahali B, Speliotes E, Yerges-Armstrong LM, Cheng CY, Jonas JB, Wong TY, Fogh I, Lin K, Powell JF, Rice K, Relton CL, Martin RM, and Davey Smith G

Subjects
Adult, Aged, Aged, 80 and over, Cardiovascular Diseases genetics, Female, Genome-Wide Association Study, Germ-Line Mutation, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Risk Assessment methods, Telomere genetics, Genetic Predisposition to Disease genetics, Mendelian Randomization Analysis methods, Neoplasms genetics, Telomere Homeostasis genetics
Abstract

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.

Published
2017
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