Distinct epigenetic landscapes underlie the pathobiology of pancreatic cancer subtypes

Gwen Lomberk(Medical College of Wisconsin), Yuna Blum(La Ligue Contre le Cancer), Rémy Nicolle(La Ligue Contre le Cancer), Asha Nair(Mayo Clinic), Krutika S. Gaonkar(Mayo Clinic), Laëtitia Marisa(La Ligue Contre le Cancer), Angela Mathison(Medical College of Wisconsin), Zhifu Sun(Mayo Clinic), Huihuang Yan(Mayo Clinic), Nabila Elarouci(La Ligue Contre le Cancer), Lucile Armenoult(La Ligue Contre le Cancer), Mira Ayadi(La Ligue Contre le Cancer), Tamás Ördög(Mayo Clinic), Jeong‐Heon Lee(Mayo Clinic), Gavin R. Oliver(Mayo Clinic), Eric W. Klee(Mayo Clinic), Vincent Moutardier(Centre National de la Recherche Scientifique), Odile Gayet(Centre National de la Recherche Scientifique), Benjamin Bian(Centre National de la Recherche Scientifique), Pauline Duconseil(Centre National de la Recherche Scientifique), Marine Gilabert(Centre National de la Recherche Scientifique), Martin Bigonnet(Centre National de la Recherche Scientifique), Stéphane Garcia(Centre National de la Recherche Scientifique), Olivıer Turrini(Centre National de la Recherche Scientifique), Jean‐Robert Delpéro(Institut Pprime), Marc Giovannini(Institut Pprime), Philippe Grandval(Hôpital de la Timone), Mohamed Gasmi(Hôpital Nord), Véronique Secq(Hôpital Nord), Aurélien de Reyniès(La Ligue Contre le Cancer), Nelson Dusetti(Centre National de la Recherche Scientifique), Juan Iovanna(Centre National de la Recherche Scientifique), Raúl Urrutia(Mayo Clinic)
Nature Communications
May 11, 2018
Cited by 276Open Access
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Abstract

Recent studies have offered ample insight into genome-wide expression patterns to define pancreatic ductal adenocarcinoma (PDAC) subtypes, although there remains a lack of knowledge regarding the underlying epigenomics of PDAC. Here we perform multi-parametric integrative analyses of chromatin immunoprecipitation-sequencing (ChIP-seq) on multiple histone modifications, RNA-sequencing (RNA-seq), and DNA methylation to define epigenomic landscapes for PDAC subtypes, which can predict their relative aggressiveness and survival. Moreover, we describe the state of promoters, enhancers, super-enhancers, euchromatic, and heterochromatic regions for each subtype. Further analyses indicate that the distinct epigenomic landscapes are regulated by different membrane-to-nucleus pathways. Inactivation of a basal-specific super-enhancer associated pathway reveals the existence of plasticity between subtypes. Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.


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