Reactive oxygen species (ROS)-mediated cancer therapy using light or ultrasound (US) has been widely approached as a non-invasive and inspiring alternative treatment. Sonodynamic therapy (SDT), a non-invasive therapeutic modality of cancer, is an outcome of low-intensity US effect on cancer cells using a sonosensitizer, which results in heat and ROS production followed by cell death. The aim of this study was synthesis, characterization and cancer SDT application of a nickel ferrite/carbon nanocomposite (NiFeO/C), as a sonosensitizer. SDT was carried out by applying a 1.0-MHz US radiation at 1.0 W cm of power density and 100% pulse ratio for 60 s. A significant C540 (B16/F10) cell killing was observed in vitro due to ROS production of 100 μg mL of NiFeO/C upon SDT. In addition, SDT of melanoma cancer in a mouse model using intratumorally injected NiFeO/C of 100 μg mL produced remarkable efficacious recovery in the tumor and significant necrosis (up to 60%) in histological assessments, while injection of NiFeO/C or US irradiation alone induced no healing effect. Therefore, SDT using NiFeO/C attained success in destroying melanoma cancer and can be developed and introduced as an alternative treatment strategy for melanoma cancer. In furtherance of SDT, magnetic resonance (MR) imaging (1.5 T) in an agarose phantom indicated the effectiveness of NiFeO/C as a negative contrast agent in transverse relaxation time-weighted imaging with a corresponding relaxation rate (r) of 78.9 mmol L s. The results confirmed the applicability of the nanocomposite as a theranostics agent for simultaneous SDT and MR imaging.
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http://dx.doi.org/10.1016/j.pdpdt.2019.05.023 | DOI Listing |
Cell Syst
January 2025
Rutgers Cancer Institute, Rutgers, the State University of New Jersey, New Brunswick, NJ, USA. Electronic address:
Treatment resistance poses a significant challenge in the care of cancer patients. Hirsch et al. applied computational and genomic approaches, examining gene expression dynamics from a mouse model of melanoma at single-cell resolution to reveal that semi-heritable non-genetic alterations in tumor cell populations confer adaptive resistance to treatment.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Center for Health Information Partnerships, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Background: Cancer-associated cachexia can inhibit immune checkpoint inhibitor (ICI) therapy efficacy. Cachexia's effect on ICI therapy has not been studied in large cohorts of cancer patients aside from lung cancer. We studied associations between real-world routinely collected clinical cachexia markers and disability-free, hospitalization-free and overall survival of cancer patients.
View Article and Find Full Text PDFJ Clin Invest
January 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.
Stimulator of interferon genes (STING) agonists have been developed and tested in clinical trials for their antitumor activity. However, the specific cell population(s) responsible for such STING activation-induced antitumor immunity have not been completely understood. In this study, we demonstrated that endothelial STING expression was critical for STING agonist-induced antitumor activity.
View Article and Find Full Text PDFNeurol Res Int
January 2025
Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosi, Mexico.
Alpha-synuclein (ASyn), a marker of Parkinson's disease (PD) and other neurodegenerative processes, plays pivotal roles in neuronal nuclei and synapses. ASyn and its phosphorylated form at Serine 129 (p-ASyn) are involved in DNA protection and repair, processes altered in aging, neurodegeneration, and cancer. To analyze the localization of p-ASyn in skin biopsies of PD patients and melanoma.
View Article and Find Full Text PDFJ Immunother Precis Oncol
February 2025
Department of Melanoma Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Introduction: Uveal melanoma remains a disease with aggressive behavior and poor prognosis despite advances in clinical management. Because monotherapy with immune checkpoint inhibitors has led to limited improvement in response rates, combination with other agents that act on the biological basis of oncogenesis has been proposed as a possible therapeutic strategy.
Methods: We designed a phase 1b trial to test the safety and tolerability of selinexor in combination with immune checkpoint inhibitors in patients with advanced uveal melanoma.
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