Resistance to oncolytic virotherapy is frequently associated with failure of tumor cells to get infected by the virus. Dimethyl fumarate (DMF), a common treatment for psoriasis and multiple sclerosis, also has anticancer properties. We show that DMF and various fumaric and maleic acid esters (FMAEs) enhance viral infection of cancer cell lines as well as human tumor biopsies with several oncolytic viruses (OVs), improving therapeutic outcomes in resistant syngeneic and xenograft tumor models. This results in durable responses, even in models otherwise refractory to OV and drug monotherapies. The ability of DMF to enhance viral spread results from its ability to inhibit type I interferon (IFN) production and response, which is associated with its blockade of nuclear translocation of the transcription factor nuclear factor κB (NF-κB). This study demonstrates that unconventional application of U.S. Food and Drug Administration-approved drugs and biological agents can result in improved anticancer therapeutic outcomes.
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http://dx.doi.org/10.1126/scitranslmed.aao1613 | DOI Listing |
Mult Scler Relat Disord
January 2025
Department of Nutrition and Drug Research, Faculty of Health Sciences, Institute of Public Health, Jagiellonian University Medical College, Skawińska Street 8, 31-066 Krakow, Poland. Electronic address:
Objective: This study aimed to review the efficacy and safety profile of disease-modifying therapies (DMTs) in patients with relapsing pediatric-onset multiple sclerosis (POMS).
Methods: A systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Published randomized controlled trials (RCTs), nonrandomized studies with a control group, large single-arm studies, and ongoing (unpublished) studies investigating the use of approved and unapproved DMTs in POMS were included.
Int J Nanomedicine
January 2025
Department of Medicine, Surgery and Pharmacy, University of Sassari, Sassari, Italy.
Purpose: Dimethyl fumarate (DMF), the first-line oral therapy for relapsing-remitting multiple sclerosis, is rapidly metabolized into monomethyl fumarate. The DMF oral administration provokes gastrointestinal discomfort causing treatment withdrawal. The present study aimed to develop an innovative formulation for DMF nasal administration.
View Article and Find Full Text PDFAntioxidants (Basel)
December 2024
Laboratory of Pharmacology, Kobe Pharmaceutical University, 4-19-1 Motoyamakita-machi, Higashinada-ku, Kobe 658-8558, Japan.
The NF-E2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway is a potential therapeutic target for central nervous system diseases. This review emphasizes the role of oxidative stress and neuroinflammation in neurodegenerative diseases, highlighting the therapeutic potential of Nrf2 activators such as dimethyl fumarate (DMF). DMF, initially administered for treating psoriasis, has demonstrated efficacy in multiple sclerosis and is metabolized to monomethyl fumarate, which may exert significant therapeutic effects.
View Article and Find Full Text PDFAntioxidants (Basel)
December 2024
Institute of Biomedical Sciences, Federal University of Rio de Janeiro (UFRJ), Avenida Carlos Chagas Filho 373, bloco F, 3° floor, room 301, Cidade Universitária, Rio de Janeiro CEP 21941-902, RJ, Brazil.
Obesity is characterized by an imbalance between energy intake and expenditure that triggers abnormal growth of adipose tissues. Dimethyl fumarate (DMF) and its primary active metabolite, monomethyl fumarate (MMF), are Nrf2 activators and have been recognized as strategic antioxidants. This study aimed to evaluate the potential of MMF and DMF to interfere with adipogenesis and obesity, and identify the molecular mechanisms involved.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Medicine, Division of Medical Oncology, University of Colorado Denver Anschutz Medical Campus, Aurora, Colorado USA.
Purpose: The development of endocrine resistance remains a significant challenge in the clinical management of estrogen receptor-positive () breast cancer. Metabolic reprogramming is a prominent component of endocrine resistance and a potential therapeutic intervention point. However, a limited understanding of which metabolic changes are conserved across the heterogeneous landscape of ER+ breast cancer or how metabolic changes factor into ER DNA binding patterns hinder our ability to target metabolic adaptation as a treatment strategy.
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