pancreatic ductal adenocarcinoma

[International Journal of Oncology] It was demonstrated that COUP‑TFII_V2 naturally occured in PDAC cells and in primary samples, where its expression was consistent with shorter overall survival and peripheral invasion.

[Nature Cancer] The authors review recent advances in targeted therapy and immunotherapy for treating subtypes of PDAC with diverse molecular alterations.

[EMBO Journal] Investigators showed that pancreatic ductal adenocarcinoma (PDA) cells could activate ketone body metabolism and that β-hydroxybutyrate was an alternative cell-intrinsic or systemic fuel that could promote PDA growth and progression.

[Cellular Oncology] Investigators describe recent advances in the understanding of pancreatic ductal metaplasia biology with a focus on its underlying cellular and molecular mechanisms, and in biomarker discovery with clinical implications for the management of pancreatic regeneration and tumorigenesis.

[Nucleic Acids Research] The authors showed that APE1 (apurinic/apyrimidinic endonuclease 1), a multifunctional DNA repair enzyme, is a G4-binding protein, and loss of APE1 abrogated the formation of stable G4 structures in cells.

[Frontiers in Oncology] UHMK1 expression was enhanced in PDAC, and high UHMK1 expression correlated with tumor stage, and lower overall survival.