Regenerative medicine investigates the conversion of pancreatic ductal cells into functional islet cells, offering innovative treatments for conditions such as diabetes. Ductal cells, primarily supporting the pancreas' exocrine functions, can differentiate into various cell types, including islet cells, under specific conditions, opening new avenues in research and therapy. The outlined protocol elaborates on the conversion process, covering ductal cell differentiation induction, and insulin-producing capacity assessment. The primary objective is to address the shortage of insulin-secreting cells for transplantation, thereby advancing diabetes treatment methodologies.
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http://dx.doi.org/10.1007/7651_2024_558 | DOI Listing |
Front Immunol
January 2025
Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.
Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal forms of cancer, and despite low incidence rates, it remains the sixth leading cause of cancer related deaths worldwide. Immunotherapy, which aims to enhance the immune system's ability to recognize and eliminate cancer cells, has emerged as a promising approach in the battle against PDAC. PARP7, a mono-ADP-ribosyltransferase, is a negative regulator of the type I interferon (IFN-I) pathway and has been reported to reduce anti-tumour immunity.
View Article and Find Full Text PDFMol Ther Oncol
March 2025
Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Pancreatic cancer is among the most challenging tumors to treat, and due to its immune tolerance characteristics, existing immunotherapy methods are not effective in alleviating the disease. Oncolytic virus therapy, a potential new strategy for treating pancreatic cancer, also faces the limitation of being ineffective when used alone. Elucidating the key host endogenous circular RNAs (circRNAs) involved in M1 virus-mediated killing of pancreatic ductal adenocarcinoma (PDAC) cells may help overcome this limitation.
View Article and Find Full Text PDFCancer Manag Res
January 2025
Department of Thoracic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Background: Signaling pathways centered on the G-protein ADP-ribosylation factor 6 (Arf6) and its downstream effector ArfGAP with the SH3 Domain, Ankyrin Repeat and PH Domain 1 (AMAP1) drive cancer invasion, metastasis, and therapy resistance. The Arf6-AMAP1 pathway has been reported to promote receptor recycling leading to programmed cell death-ligand 1 (PD-L1) overexpression in pancreatic ductal carcinoma. Moreover, AMAP1 regulates of nuclear factor-kappa B (NF-κB), which is an important molecule in inflammation and immune activation, including tumor immune interaction through PD-L1 regulation.
View Article and Find Full Text PDFIUBMB Life
January 2025
Department of Hepatopancreatobiliary Surgery, Ningbo Medical Center Lihuili Hospital (The Affiliated Lihuili Hospital, Ningbo University), Ningbo, Zhejiang, People's Republic of China.
The prevalent intra- and intertumoral heterogeneity results in undesirable prognosis and therapy failure of pancreatic cancer, potentially resulting from cellular senescence. Herein, integrated analysis of bulk and single-cell RNA-seq profiling was conducted to characterize senescence-based heterogeneity in pancreatic cancer. Publicly available bulk and single-cell RNA sequencing from pancreatic cancer patients were gathered from TCGA-PAAD, PACA-AU, PACA-CA, and GSE154778 datasets.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Department of Hepato-Biliary-Pancreatic Surgery, General Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, PR China.
Purpose: Glucose starvation induces the accumulation of disulfides and F-actin collapse in cells with high expression of SLC7A11, a phenomenon termed disulfidptosis. This study aimed to confirm the existence of disulfidptosis in pancreatic ductal adenocarcinoma (PDAC) and elucidate the role of Cancer Susceptibility 8 (CASC8) in this process.
Methods: The existence of disulfidptosis in PDAC was assessed using flow cytometry and F-actin staining.
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