Literature DB >> 33517887

A multilayered post-GWAS assessment on genetic susceptibility to pancreatic cancer.

Evangelina López de Maturana1,2, Juan Antonio Rodríguez3, Lola Alonso1,2, Oscar Lao3, Esther Molina-Montes1,2, Isabel Adoración Martín-Antoniano1,2, Paulina Gómez-Rubio1,2, Rita Lawlor4, Alfredo Carrato2,5, Manuel Hidalgo6,7, Mar Iglesias2,8, Xavier Molero9,10, Matthias Löhr11, Christopher Michalski12,13, José Perea14, Michael O'Rorke15,16, Victor Manuel Barberà17, Adonina Tardón18,19, Antoni Farré20, Luís Muñoz-Bellvís2,21, Tanja Crnogorac-Jurcevic22, Enrique Domínguez-Muñoz23, Thomas Gress24, William Greenhalf25, Linda Sharp26,27, Luís Arnes28,29,30, Lluís Cecchini2,8, Joaquim Balsells9,10, Eithne Costello25, Lucas Ilzarbe2,8, Jörg Kleeff12,13, Bo Kong12, Mirari Márquez1,2, Josefina Mora20, Damian O'Driscoll26, Aldo Scarpa4, Weimin Ye31, Jingru Yu31, Montserrat García-Closas32, Manolis Kogevinas19,33, Nathaniel Rothman32, Debra T Silverman32, Demetrius Albanes32, Alan A Arslan34,35,36, Laura Beane-Freeman32, Paige M Bracci37, Paul Brennan38, Bas Bueno-de-Mesquita39, Julie Buring40, Federico Canzian41, Margaret Du42, Steve Gallinger43, J Michael Gaziano44, Phyllis J Goodman45, Marc Gunter38, Loic LeMarchand46, Donghui Li47, Rachael E Neale48, Ulrika Peters49, Gloria M Petersen50, Harvey A Risch51, Maria José Sánchez52,53,54,55, Xiao-Ou Shu56, Mark D Thornquist49, Kala Visvanathan50, Wei Zheng56, Stephen J Chanock32, Douglas Easton57, Brian M Wolpin58, Rachael Z Stolzenberg-Solomon32, Alison P Klein59, Laufey T Amundadottir60, Marc A Marti-Renom61, Francisco X Real2,62,63, Núria Malats64,65.   

Abstract

BACKGROUND: Pancreatic cancer (PC) is a complex disease in which both non-genetic and genetic factors interplay. To date, 40 GWAS hits have been associated with PC risk in individuals of European descent, explaining 4.1% of the phenotypic variance.
METHODS: We complemented a new conventional PC GWAS (1D) with genome spatial autocorrelation analysis (2D) permitting to prioritize low frequency variants not detected by GWAS. These were further expanded via Hi-C map (3D) interactions to gain additional insight into the inherited basis of PC. In silico functional analysis of public genomic information allowed prioritization of potentially relevant candidate variants.
RESULTS: We identified several new variants located in genes for which there is experimental evidence of their implication in the biology and function of pancreatic acinar cells. Among them is a novel independent variant in NR5A2 (rs3790840) with a meta-analysis p value = 5.91E-06 in 1D approach and a Local Moran's Index (LMI) = 7.76 in 2D approach. We also identified a multi-hit region in CASC8-a lncRNA associated with pancreatic carcinogenesis-with a lowest p value = 6.91E-05. Importantly, two new PC loci were identified both by 2D and 3D approaches: SIAH3 (LMI = 18.24), CTRB2/BCAR1 (LMI = 6.03), in addition to a chromatin interacting region in XBP1-a major regulator of the ER stress and unfolded protein responses in acinar cells-identified by 3D; all of them with a strong in silico functional support.
CONCLUSIONS: This multi-step strategy, combined with an in-depth in silico functional analysis, offers a comprehensive approach to advance the study of PC genetic susceptibility and could be applied to other diseases.

Entities:  

Keywords:  3D genomic structure; Genetic susceptibility; Genome-wide association analysis; Local indices of genome spatial autocorrelation; Pancreatic cancer risk

Mesh:

Substances:

Year:  2021        PMID: 33517887      PMCID: PMC7849104          DOI: 10.1186/s13073-020-00816-4

Source DB:  PubMed          Journal:  Genome Med        ISSN: 1756-994X            Impact factor:   11.117


  79 in total

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