Details

Autor(en) / Beteiligte

• Fingerlin, Tasha E
• Murphy, Elissa
• Zhang, Weiming
• Peljto, Anna L
• Brown, Kevin K
• Steele, Mark P
• Loyd, James E
• Cosgrove, Gregory P
• Lynch, David
• Groshong, Steve
• Collard, Harold R
• Wolters, Paul J
• Bradford, Williamson Z
• Kossen, Karl
• Seiwert, Scott D
• du Bois, Roland M
• Garcia, Christine Kim
• Devine, Megan S
• Gudmundsson, Gunnar
• Isaksson, Helgi J
• Kaminski, Naftali
• Zhang, Yingze
• Gibson, Kevin F
• Lancaster, Lisa H
• Cogan, Joy D
• Mason, Wendi R
• Maher, Toby M
• Molyneaux, Philip L
• Wells, Athol U
• Moffatt, Miriam F
• Selman, Moises
• Pardo, Annie
• Kim, Dong Soon
• Crapo, James D
• Make, Barry J
• Regan, Elizabeth A
• Walek, Dinesha S
• Daniel, Jerry J
• Kamatani, Yoichiro
• Zelenika, Diana
• Smith, Keith
• McKean, David
• Pedersen, Brent S
• Talbert, Janet
• Kidd, Raven N
• Markin, Cheryl R
• Beckman, Kenneth B
• Lathrop, Mark
• Schwarz, Marvin I
• Schwartz, David A

Titel

Genome-wide association study identifies multiple susceptibility loci for pulmonary fibrosis

Ist Teil von

• Nature genetics, 2013-06, Vol.45 (6), p.613-620

Ort / Verlag

New York: Nature Publishing Group US

Erscheinungsjahr

2013

Quelle

MEDLINE

Beschreibungen/Notizen

• Tasha Fingerlin, David Schwartz and colleagues report a genome-wide association study of fibrotic idiopathic interstitial pneumonia. Their results confirm known risk variants at MUC5B and TERT and identify several new regions associated with disease susceptibility. We performed a genome-wide association study of non-Hispanic, white individuals with fibrotic idiopathic interstitial pneumonias (IIPs; n = 1,616) and controls ( n = 4,683), with follow-up replication analyses in 876 cases and 1,890 controls. We confirmed association with TERT at 5p15, MUC5B at 11p15 and the 3q26 region near TERC , and we identified seven newly associated loci ( P meta = 2.4 × 10 −8 to 1.1 × 10 −19 ), including FAM13A (4q22), DSP (6p24), OBFC1 (10q24), ATP11A (13q34), DPP9 (19p13) and chromosomal regions 7q22 and 15q14-15. Our results suggest that genes involved in host defense, cell-cell adhesion and DNA repair contribute to risk of fibrotic IIPs.