Oxidative stress could lead to a variety of body dysfunctions, including neurodegeneration and cancer, which are closely associated with intracellular signal transducers such as reactive oxygen species (ROS). It has been suggested that ROS is the upstream regulator of autophagy, and that it provides a negative feedback regulation to remove oxidative damage. Defects in the ROS-autophagic redox homeostasis could lead to the increased production of ROS and the accumulation of damaged organelles that in turn promote metabolic reprogramming and induce tumorigenesis. One significant characteristic of pancreatic cancer is the reprogramming of cellular energy metabolism, which facilitates the rapid growth, invasiveness, and the survival of cancer cells. Thus, the rectification of metabolic dysfunction is essential in therapeutic cancer targeting. Isoliquiritigenin (ISL) is a chalcone obtained from the plant , which is a powdered root licorice that has been consumed for centuries in different regions of the world. ISL is known to be a natural antioxidant that possesses diversified functions, including redox regulation in cells. This review contains discussions on the herbal source, biological properties, and anticancer potential of ISL. This is the first time that the anticancer activities of ISL in pancreatic cancer has been elucidated, with a coverage of the involvement of antioxidation, metabolic redox regulation, and autophagy in pancreatic cancer development. Furthermore, some remarks on related compounds of the isoflavonoid biosynthetic pathway of ISL will also be discussed.
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http://dx.doi.org/10.3390/antiox11071349 | DOI Listing |
Phys Imaging Radiat Oncol
January 2025
Department of Radiation Oncology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, North 15 West 7, Kita-ku, Sapporo, Hokkaido 060-8638, Japan.
Background And Purpose: Radiation-induced lymphopenia (RIL) may be associated with a worse prognosis in pancreatic cancer. This study aimed to develop a normal tissue complication probability (NTCP) model to predict severe RIL in patients with pancreatic cancer undergoing concurrent chemoradiotherapy (CCRT).
Materials And Methods: We reviewed pancreatic cancer patients treated at our facility for model training and internal validation.
Ann Transl Med
December 2024
Institute for Tumor Immunology, Center for Tumor Biology and Immunology, Philipps-University Marburg, Marburg, Germany.
One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells.
View Article and Find Full Text PDFAnn Transl Med
December 2024
Department of Clinical Oncology, The Christie NHS Foundation Trust, Manchester, UK.
World J Gastrointest Oncol
January 2025
Faculty of Medicine, Carol Davila University of Medicine and Pharmacy, Bucharest 050474, Romania.
Background: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive lethal malignancy with limited options for treatment and a 5-year survival rate of 11% in the United States. As for other types of tumors, such as colorectal cancer, aberrant lipid synthesis and reprogrammed lipid metabolism have been suggested to be associated with PDAC development and progression.
Aim: To identify the possible involvement of lipid metabolism in PDAC by analyzing in tumoral and non-tumoral tissues the expression level of the most relevant genes involved in the long-chain fatty acid (FA) import into cell.
World J Gastrointest Oncol
January 2025
Department of Automatic Control Engineering, Feng Chia University, Taichung 407, Taiwan.
In this editorial, we will discuss the article by Tang published in the recent issue of the . They explored an innovative approach to enhancing gemcitabine (GEM) delivery and efficacy using human bone marrow mesenchymal stem cells (HU-BMSCs)-derived exosomes. The manufacture of GEM-loaded HU-BMSCs-derived exosomes (Exo-GEM) has been optimized.
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