Author

Irene Esposito

Düsseldorf University HospitalORCID 0000-0002-0554-2402Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 2 Genomics· 1 Pathology· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 3 Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Approach:deep learning· 1

Frequent Co-Authors

Francisco X. RealiD· 2 shared Natalia del PozoiD· 2 shared Sami Alexander SafiiD· 2 shared Wolfram Trudo KnoefeliD· 2 shared Abhimanyu DasGupta· 1 shared Alain CouvineauiD· 1 shared Alberto DelaidelliiD· 1 shared Ana CuadradoiD· 1 shared

Activity by Year

2020-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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2 shared papersCancer Biology

Francisco X. RealORCID

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4 papers

Recent·Most cited

GALE-dependent glycoproteome remodelling is a determinant of oncogenic RAS transformation

Frauke Stölting, Rita Vesce, César Rodríguez-Santana, Marina Ciscar, Alberto Delaidelli, Qiaochu Lin, Christian Ballmeyer, Sophie Chan, Ramona Lesch, Ruitong Li, Abhimanyu DasGupta, Bin Yu, Daniel Picard, Vithusan Suppiyar, Francesco Casini, , Jonathan K. M. Lim

This study identifies GALE as a key regulator of glycoproteome remodelling in RAS-driven cancer, showing its role in sialylation and tumorigenicity.

bioRxiv · Jun 23, 2026 · PreprintCancer Biology

GATA4 loss promotes mutant Kras-driven pancreatic ductal adenocarcinoma in the absence of canonical precursor lesions

Francesc Madriles, Mónica P. de Andrés, Mikhail Chesnokov, Jaime Martínez de Villarreal, Direna Alonso‐Curbelo, Natalia del Pozo, Mar Iglesias, Enrique Carrillo de Santa Pau, Juan Iovanna, Francisco Soriano, Ana Cuadrado, Mirari Marques, Javier Muñoz, Irene Esposito, Paola Martinelli, , Francisco X. Real

This study shows that GATA4 loss in Kras-mutant mice leads to PDAC without canonical precursor lesions, identifying a new lesion type and revealing GATA4's role in inflammatory programs.

bioRxiv · May 26, 2026 · PreprintCancer Biology

Loss of HNF1b drives pancreatic Intraductal Papillary Mucinous Neoplasms (IPMN) initiation

Diane Lorenzo, Lina Aguilera Munoz, Louis MARSTRAND-DAUCE, Anaïs Chassac, Pascal Nicole, Lingkang Meng, Laurence Heidet, Bertrand Knebelmann, Camille Pignolet, Sabrina Doblas, Alain Couvineau, Iréne Esposito, Vinciane Rebours, Rémy Nicolle, Jerome F. Cros, , Cécile Haumaître

This study shows that loss of HNF1B contributes to IPMN initiation and identifies its role as a tumor suppressor in pancreatic ductal cells.

bioRxiv · Jun 12, 2025 · PreprintPathology

HNF1A recruits UTX to activate a differentiation program that suppresses pancreatic cancer

Mark Kalisz, Edgar Bernardo, Anthony Beucher, Miguel Angel Maestro, Natalia del Pozo, I.R. Hernández Millán, Lena Häberle, Martin Schlensog, Sami Alexander Safi, Wolfram Trudo Knoefel, Vanessa Grau, Matías G. De Vas, Karl B. Shpargel, Eva Cristina Vaquero, Terry Magnuson, , Jorge P. Ferrer

This study shows HNF1A recruits UTX to activate a differentiation program that suppresses pancreatic cancer by remodeling enhancers and inhibiting oncogenic pathways.

The EMBO Journal · Mar 10, 2020Peer-reviewedGenomics