Cosmc loss induces truncated O-glycosylation and accelerates Kras-driven pancreatic carcinogenesis

2026-07-31

Baris Mercanoglu

Nina Schraps

Anastasios D. Giannou

Jingxuan Zhou

Simon Kind

Maya Reinecke

Karl-Frederick Karstens

Benjamin Dreyer

Sönke Harder

Siwen Zhang

Eleftherios Papazoglou

Cenap Güngör

Nathaniel Melling

Hartmut Schlüter

Christoph Wagener

Maximilian Bockhorn

Thilo Hackert

Gerrit Wolters‐Eisfeld *

DOI：10.1016/j.neo.2026.101347

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Abstract

En 中文

• Tn antigen is frequently expressed in human PDAC and associates with tumor stage. • Cosmc loss accelerates early Kras-driven pancreatic neoplastic progression. • Cosmc-deficient tumors show increased fibrosis, proliferation, and altered mucin-associated glycosylation. • Cosmc loss induces a robust Tn-like glycoprotein phenotype in pancreatic tumors. • Glycoproteomic profiling links Cosmc loss to extracellular matrix and stromal remodeling.

Keywords:

Pancreatic cancer

PDAC

Cosmc

O-glycosylation

Tn antigen

Kras

Mouse model

Cosmc loss induces truncated O-glycosylation and accelerates Kras-driven pancreatic carcinogenesis

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