Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with poor prognosis due to early metastasis, low diagnostic rates at early stages, and resistance to current therapeutic regimens. Despite numerous studies and clinical trials, the mortality rate for PDAC has shown limited improvement. Therefore, there is a pressing need to attain. a more comprehensive molecular characterization to identify biomarkers enabling early detection and evaluation of treatment response. MicroRNA (miRNAs) are critical regulators of gene expression on the post-transcriptional level, and seem particularly interesting as biomarkers due to their relative stability, and the ability to detect them in fixed tissue specimens and biofluids. Deregulation of miRNAs is common and affects several hallmarks of cancer and contribute to the oncogenesis and metastasis of PDAC. Unique combinations of upregulated oncogenic miRNAs (oncomiRs) and downregulated tumor suppressor miRNAs (TsmiRs), promote metastasis, characterize the tumor and interfere with chemosensitivity of PDAC cells. Here, we review several oncomiRs and TsmiRs involved in chemoresistance to gemcitabine and FOLFIRINOX in PDAC and highlighted successful/effective miRNA-based therapy approaches in vivo. Integrating miRNAs in PDAC treatment represents a promising therapeutic avenue that can be used as guidance for personalized medicine for PDAC patients.
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http://dx.doi.org/10.1007/s10555-023-10127-w | 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 PDFFront Genet
January 2025
Department of Oncology, The Third Affiliated Hospital of Nanjing Medical University, Changzhou, China.
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterized by a dismal prognosis. Treatment outcomes exhibit substantial variability across patients, underscoring the urgent need for robust predictive models to effectively estimate survival probabilities and therapeutic responses in PDAC.
Methods: Metabolic and immune-related genes exhibiting differential expression were identified using the TCGA-PDAC and GTEx datasets.
Pan Afr Med J
October 2024
Department of Hepato-Gastroenterology, University Hospital of Mohammed VI, Marrakech, Morocco.
Pancreas divisum occurs during development when the ventral and dorsal buds of the pancreas do not fuse. It is the most common congenital anomaly of the pancreas. Patients with this condition are usually asymptomatic, but almost 25% of these patients experience recurrent pancreatitis, which may progress to chronic pancreatitis.
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.
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