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Dynamic tracking of tumor microenvironment modulation using Kaede photoconvertible transgenic mice unveils new biological properties of viral immunotherapy.
Cancer Res Commun
January 2025
Candel Therapeutics, Needham, MA, United States.
CAN-2409 is a replication-defective adenovirus that delivers the herpes simplex virus (HSV)-thymidine kinase gene to infected cells. Intratumoral administration of CAN-2409 followed by prodrug results in the formation of a toxic metabolite able to induce immunogenic cell death, exposure of tumor-associated antigens, and activation of local and systemic immune responses. We used a dynamic labeling model with MC38 tumor cells implanted in photoconvertible Kaede mice.
View Article and Find Full Text PDFExploiting the Achilles' Heel of Viral RNA Processing to Develop Novel Antivirals.
Viruses
December 2024
Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A8, Canada.
Treatment options for viral infections are limited and viruses have proven adept at evolving resistance to many existing therapies, highlighting a significant vulnerability in our defenses. In response to this challenge, we explored the modulation of cellular RNA metabolic processes as an alternative paradigm to antiviral development. Previously, the small molecule 5342191 was identified as a potent inhibitor of HIV-1 replication by altering viral RNA accumulation at doses that minimally affect host gene expression.
View Article and Find Full Text PDFAdenovirus-Neutralizing and Infection-Promoting Activities Measured in Serum of Human Brain Cancer Patients Treated with Oncolytic Adenovirus Ad5-∆24.RGD.
Int J Mol Sci
January 2025
Amsterdam UMC location Vrije Universiteit Amsterdam, Medical Oncology, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.
Oncolytic adenoviruses derived from human serotype 5 (Ad5) are being developed to treat cancer. Treatment efficacy could be affected by pre-existing or induced neutralizing antibodies (NAbs), in particular in repeat administration strategies. Several oncolytic adenoviruses that are currently in clinical development have modified fiber proteins to increase their infectivity.
View Article and Find Full Text PDFMFN2-mediated decrease in mitochondria-associated endoplasmic reticulum membranes contributes to sunitinib-induced endothelial dysfunction and hypertension.
J Mol Cell Cardiol
January 2025
Department of Cardiology, Harbin Medical University Cancer Hospital, NHC Key Laboratory of Cell Transplantation, Department of Cardiology, Central Laboratory, The First Affiliated Hospital of Harbin Medical University, Institute of Metabolic Disease, Heilongjiang Academy of Medical Sciences, Heilongjiang Key Laboratory for Metabolic Disorder & Cancer Related Cardiovascular Diseases, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin, China. Electronic address:
Unlabelled: Treatment of cancer patients with tyrosine kinase inhibitors (TKIs) often results in hypertension, but the underlying mechanism remains unclear. This study aimed to examine the role of mitochondrial morphology and function, particularly mitochondria-associated endoplasmic reticulum membranes (MAMs), in sunitinib-induced hypertension.
Methods: Both in vitro and in vivo experiments performed to assesse reactive oxygen species (ROS), nitric oxide (NO), endothelium-dependent vasorelaxation, systemic blood pressure, and mitochondrial function in human umbilical vein endothelial cells (HUVECs) and C57BL/6 mouse aortic endothelial cells, under vehicle or sunitinib treatment condition.
Regulating astrocyte phenotype by Lcn2 inhibition toward ischemic stroke therapy.
Biomaterials
January 2025
Institute of Biomedical Engineering, College of Medicine, Southwest Jiaotong University, Chengdu, 610031, PR China.
Astrocytes can be reacted to "reactive astrocytes" after ischemia-reperfusion injury, in which A1 phenotype causes neuronal and oligodendrocyte death, whereas the A2 phenotype exerts neuroprotective effects, thus regulating reactive astrocyte to A2 type is a potential target for stroke therapy. Lcn2 level is highly associated with the phenotypic polarization of astrocytes. We found that silencing the Lcn2 gene by adeno-associated virus (AAV)-Lcn2 shRNA adenovirus resulted in a dramatic decrease in A1-type astrocytes and increase in A2 astrocytes in MCAO mice.
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