Oral cancer, the most prevalent type of cancer in the head and neck region, has an overall five-year survival rate of less than 50%. Key risk factors for its development include tobacco use, alcohol consumption, betel nut chewing, and infections with human papillomavirus (e.g., HPV-16 and HPV-18). While various diagnostic technologies have been developed, some of which have progressed to regulatory-approved in vitro diagnostic systems, there has been no significant improvement in survival rates for patients with oral squamous cell carcinoma despite advancements in surgery, radiotherapy, and chemotherapy. This has prompted the exploration of gene therapy as a novel approach to treating oral cancer. Research indicates that genomic abnormalities and misregulations contribute to both spontaneous and hereditary malignancies. Gene therapy involves the introduction of genetic material into target cells, aiming to minimize harm to surrounding tissues. Various gene therapy techniques, including gene addition therapy, oncolytic virotherapy, suicide gene therapy, excision gene therapy, immunotherapy, and nucleic acid-based therapies, have been investigated both in vitro and in vivo. This review explores these innovative gene therapy strategies, highlighting their potential to address the limitations of conventional treatments and improve outcomes for oral cancer patients.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10528-025-11078-3 | DOI Listing |
The development of targeted therapy for patients with multiple myeloma (MM) is hampered by the low frequency of actionable genetic abnormalities. Gain or amplification of chromosome 1q (1q+) is the most frequent arm-level copy number gain in patients with MM and is associated with higher risk of progression and death despite recent therapeutic advances. Thus, developing targeted therapy for MM patients with 1q+ stands to benefit a large portion of patients in need of more effective management.
View Article and Find Full Text PDFOncotarget
March 2025
Worldwide Innovative Network (WIN) Association - WIN Consortium, Chevilly-Larue, France.
The human genome project ushered in a genomic medicine era that was largely unimaginable three decades ago. Discoveries of druggable cancer drivers enabled biomarker-driven gene- and immune-targeted therapy and transformed cancer treatment. Minimizing treatment not expected to benefit, and toxicity-including financial and time-are important goals of modern oncology.
View Article and Find Full Text PDFSkin Therapy Lett
March 2025
Center for Clinical Studies, Webster, TX, USA.
Psoriatic arthritis (PsA) is a chronic, inflammatory disease with heterogeneous clinical features. The pathogenesis of PsA involves a complex interplay of genetic, immunologic, and environmental factors, leading to the activation of the immune system and subsequent inflammation. Over the past decade, the understanding of the immune mechanisms underlying PsA has advanced significantly, particularly regarding the role of the interleukin-23/T helper 17 pathway in the disease process.
View Article and Find Full Text PDFEuropace
March 2025
Clinical Cardiac Academic Group, Genetic and Cardiovascular Sciences Institute, City-St George's University of London, London, UK.
Atrial fibrillation (AF) is one of the most common cardiac diseases and a complicating comorbidity for multiple associated diseases. Many clinical decisions regarding AF are currently based on the binary recognition of AF being present or absent with the categorical appraisal of AF as continued or intermittent. Assessment of AF in clinical trials is largely limited to the time to (first) detection of an AF episode.
View Article and Find Full Text PDFSci Transl Med
March 2025
Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!