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Abstract Background Magnetic fluid hyperthermia (MFH) represents a promising therapeutic strategy in cancer utilizing the heating capabilities of magnetic nanoparticles when exposed to an alternating magnetic field (AMF). Because the efficacy and safety of MFH treatments depends on numerous intrinsic and extrinsic factors, therefore, the proper MFH setups should focus on thermal energy dosed into the cancer cells. Methods In this study, we performed MFH experiments using human lung cancer A549 cells (in vitro) and NUDE Balb/c mice bearing human lung (A549) cancer (in vivo). In these two experimental models, the heat was induced by magnesium-doped iron(III) oxide nanoparticles coated with mPEG-silane (Mg0.1-γ-Fe2O3(mPEG-silane)0.5) when exposed to an AMF. Results We observed that the lung cancer cells treated with Mg0.1-γ-Fe2O3(mPEG-silane)0.5 (0.25 mg·mL−1) and magnetized for 30 min at 14.4 kA·m−1 yielded a satisfactory outcome in reducing the cell viability up to ca. 21% (in vitro). The activation energy calculated for this field strength was estimated for 349 kJ·mol−1. Both volumetric measurements and tumor mass assessments confirmed by magnetic resonance imaging (MRI) showed a superior thermal effect in mice bearing human lung cancer injected intratumorally with Mg0.1-γ-Fe2O3(mPEG-silane)0.5 nanoparticles (3 mg·mL−1) and subjected to an AMF (18.3 kA·m−1) for 30 min four times at weekly intervals. Research demonstrated that mice undergoing MFH exhibited a marked suppression of tumor growth (V = 169 ± 94 mm3; p

Extracellular vesicles (EVs) released from primary cell lines, originating from resected tissues during biopsies in patients with non-small cell lung cancer (NSCLC) revealing adenocarcinoma and squamous cell carcinoma subtypes, were examined for membrane proteomic fingerprints using a proximity barcoding assay. All the collected EVs expressed canonical tetraspanins (CD9, CD63, and CD81) highly coexpressed with molecules such as lysosome-associated membrane protein-1 (LAMP1–CD107a), sialomucin core protein 24 (CD164), Raph blood group (CD151), and integrins (ITGB1 and ITGA2). This representation of the protein molecules on the EV surface may provide valuable information on NSCLC subtypes and offer new diagnostic opportunities as next-generation biomarkers in personalized oncology.

BRAF inhibitors have improved the treatment of advanced or metastatic melanoma in patients that harbor a BRAFT1799A mutation. Because of new insights into the role of aberrant glycosylation in drug resistance, we designed and studied three novel vemurafenib derivatives possessing pentose-associated aliphatic ligands—methyl-, ethyl-, and isopropyl-ketopentose moieties—as potent BRAFV600E kinase inhibitors. The geometries of these derivatives were optimized using the density functional theory method. Molecular dynamic simulations were performed to find interactions between the ligands and BRAFV600E kinase. Virtual screening was performed to assess the fate of derivatives and their systemic toxicity, genotoxicity, and carcinogenicity. The computational mapping of the studied ligand–BRAFV600E complexes indicated that the central pyrrole and pyridine rings of derivatives were located within the hydrophobic ATP-binding site of the BRAFV600E protein kinase, while the pentose ring and alkyl chains were mainly included in hydrogen bonding interactions. The isopropyl-ketopentose derivative was found to bind the BRAFV600E oncoprotein with more favorable energy interaction than vemurafenib. ADME-TOX in silico studies showed that the derivatives possessed some desirable pharmacokinetic and toxicologic properties. The present results open a new avenue to study the carbohydrate derivatives of vemurafenib as potent BRAFV600E kinase inhibitors to treat melanoma.