Alleviating psychological distress in women with breast cancer undergoing treatment is a major worldwide issue. The growing use of new technologies in healthcare to support patients requires a more in-depth appraisal of the optimal methods for delivering these interventions. The present study aims to explore the clinical potential of a 360° video of local landscapes to reduce psychological distress of breast cancer patients receiving intravenous chemotherapy. We presented the same content in two different viewing conditions (immersive vs. non-immersive) in order to isolate the specific effect of immersive technology.

Cyanine dyes usually serve as good fluorescence probes but not as efficient photosensitizers owing to the spin-forbidden intersystem crossing process and short excited-state lifetime. Nevertheless, the structure-derived energy release from the excited state could enable dyes to function efficiently. In this work, we developed cyanine dimers (2o-Cy, 2m-Cy, and 2p-Cy) based on exciton coupling effects by connecting two Cy5.5 molecules at the N-indole site with nonconjugated ortho/meta/para-bis(bromomethyl)benzene linkers. These dimers exhibited significantly enhanced molar extinction coefficients (32-45 × 104 M cm-1) as well as satisfactory triplet excited-state quantum yields (32-44%) and lifetimes (10.6-11.9 μs), leading to a substantially enhanced reactive oxygen species production along with efficient antitumor activity under both normoxic and hypoxic conditions. Furthermore, 2p-Cy NPs ablated primary tumors, inhibited distant tumor growth, and prevented metastatic regrowth via photoinduced innate immune activation. This dimer-based strategy represents a powerful approach to develop high-performance photosensitive dyes for antitumor photodynamic immunotherapy.

Ovarian cancer (OC) is associated with poor prognosis and immune evasion through PD-L1 expression. While anti-PD-L1 therapies have shown limited efficacy, combination strategies may enhance therapeutic outcomes. This study explores the potential of metformin to modulate the immune microenvironment and improve the efficacy of PD-L1 inhibitors in OC. An immunocompetent C57BL/6 mouse model of OC was used to evaluate the effects of metformin and PD-L1 inhibitors on tumor progression, immune cell infiltration, and cytokine expression. Mice received daily metformin treatment for 2 weeks, with PD-L1 inhibitors administered twice weekly. Tumor growth was monitored via volume measurements, immune cell infiltration was assessed by flow cytometry, and cytokine levels (Granzyme B, IFN-γ) were quantified using ELISA. Metformin significantly reduced tumor growth, increased CD8+ T cell infiltration, upregulated RBMS3, and elevated Granzyme B and IFN-γ expression. Additionally, metformin downregulated PD-L1 expression, and its combination with PD-L1 inhibitors further enhanced CD8+ T cell activity. Silencing RBMS3 reversed these effects, underscoring its critical role in immune modulation. These findings suggest that metformin, in combination with PD-L1 inhibitors, may enhance antitumor immune responses and improve treatment outcomes in OC. Targeting RBMS3 could represent a novel therapeutic approach for overcoming immune evasion in OC.

Near infrared (NIR) aggregation-induced emission (AIE)-based luminogens are emerging as powerful materials with significant potential in cancer diagnosis, imaging, and therapy applications. Of precise note are the rapidly progressing areas in the field encompassing deep-tissue imaging, resistance to photobleaching, and biomedicine. Unlike traditional aggregation-caused quenching (ACQ) fluorophores, AIE materials with NIR emissive features can revolutionize the broad transdisciplinary areas of biomedicine, therapy, and healing, making them highly effective for real-time monitoring and healthcare purposes. In this study, we have synthesized a (E)-2-(2-(4'-(2,2-diphenylvinyl)-[1,1'-biphenyl]-4-yl)vinyl)-1,3,3-trimethyl-3H-indol-1-ium, named as 3T, and explored its antiproliferative potential on MCF-7 and MDA-MB-231 breast cancer cells. The 3T molecule exhibited strong near-infrared (NIR) emission ranging from 600 to 800 nm in a 99% water fraction (fw). In silico target prediction and molecular docking identified potential target proteins and assessed their binding interactions and affinities. Further, in vitro studies demonstrated efficient cellular internalization and dose-dependent reduction in cell viability. The IC50 values of 32.26 and 35.75 μM were observed in MCF-7 and MDA-MB-231 cells, respectively. The treatment of 3T generated 2.1- and 1.9-fold increases in reactive oxygen species (ROS) for MCF-7 and MDA-MB-231 cells, respectively, and induced a change in mitochondrial membrane potential, leading to apoptosis, as confirmed by flow cytometry studies. The treatment was also effective for tumor spheroids. Thus, NIR AIEgen 3T offered several distinct advantages such as strong antiproliferative ability, stability, and imaging, positioning it as a potential candidate for cancer therapeutic applications.

Small-molecule targeting of ribonucleic acid (RNA) is a new and promising therapeutic approach, but it requires the discovery of small compounds that can specifically target particular RNA structures. In this context, a comprehensive description of the photophysical interaction features of phenothiazinium dyes such as thionine (TH)/methylene blue (MB) with transfer ribonucleic acid (tRNA) is examined by spectrophotometric titration and molecular docking analysis. After binding with tRNA, TH/MB dyes displayed emission, and absorption characteristics were significantly changed. The observed tRNA-induced spectral alterations are attributed to energy transfer from guanine base pairs, likely resulting from an intercalative interaction mode proposed for tRNA. The negative free energy change value (ΔG = ~ - 27.5 kJ mol-1) of the TH/MB dye-tRNA systems suggests that the present binding interaction is highly favorable and spontaneous. The conformational alterations of the tRNA with both dyes were verified using circular dichroism analyses. Molecular docking test results indicated that TH/MB dye molecules bonded to the tRNA cavity in a specific pattern. The novelty of this study resides in a unique role for TH/MB dyes in tRNA dysfunction, expanding our understanding of how TH/MB dyes and their tRNA complexes were used in in vitro cytotoxic investigations of human lung cancer cells.

The cytotoxic complex [(Htom6-Me){NiII(OAc)}2](OAc) (H2tom6-Me = 2,7-bis(di(6-methylpyridine-2-yl-methyl)aminomethyl)-1,8-naphthalenediol) is supposed to bind in the aquated form [(Htom6-Me){NiII(OH2)2}2]3+ to two neighboring phosphate diesters of the DNA backbone. To further support this intended molecular mode of action, difunctional ligands in the form of the dicarboxylates succinate and glutarate are used here to mimic two neighboring phosphates of the DNA backbone. The complex [(Htom6-Me){NiII(OAc)}2](OAc) is treated with 3 equiv. HCl to protonate the acetates providing presumably [(Htom6-Me){NiII(OH2)2}2]3+, which is reacted with the dicarboxylates yielding the complexes [(Htom6-Me){NiII(μ-succ)NiII}]+ and [(Htom6-Me){NiII(μ-glut)NiII}]+ confirmed by single-crystal X-ray diffraction. The sterical constraints of the dicarboxylates enforces shorter Ni⋯Ni distances demonstrating the flexibility of the coordination compartments despite the rigid 1,8-naphthalenediol backbone. These steric constraints by the pull effect of the organic spacers affect the NiII-ligand bonds and are reflected in FTIR and UV-Vis-NIR spectroscopic but not magnetic signatures. The comparison to a related CuII complex indicates a severe impact of the 6-methyl groups of the pyridine donors on the relative orientation of the anticipated phosphate binding sites in these complexes. The consequences for a rational strengthening of the binding to DNA and hence increase of the cytotoxicity by possible ligand modifications are discussed.

In our work, we focused on the development of nanostructured lipid carriers (NLCs) loaded with dexibuprofen (DXI) and their application for cancer therapy by proposing the binding of phospholipids with this non-steroidal anti-inflammatory drug (NSAID) to obtain new delivery systems.

Cisplatin (cis-diamminedichloroplatinum II, CDDP), a widely used chemotherapeutic agent, is clinically limited by nephrotoxicity. Rhein, an anthraquinone from Radix Rhein Et Rhizome, shows nephroprotective potential. This study investigated Rhein's protective effects and mechanisms in CDDP-induced acute kidney injury (AKI).

This study aimed to investigate the pharmacological mechanisms of Shugan Jianpi Formula (SGJPF) in treating TNBC using network pharmacology and molecular biology approaches.

Combination of multiple therapies is a common approach to treating patients with unresectable hepatocellular carcinoma (uHCC). The impact of immune checkpoint inhibitors (ICIs) on prognosis in uHCC patients treated with transarterial chemoembolization (TACE) and lenvatinib remains unclear.

Immune checkpoint inhibitors (ICIs) significantly improve survival in lung cancer patients. However, checkpoint inhibitor pneumonitis (CIP) remains a critical safety concern. This meta-analysis systematically evaluates demographic, clinical, and laboratory risk factors associated with CIP development to guide risk-stratified management.

The use of immune checkpoint inhibitors (ICIs) has revolutionized cancer treatment, particularly in lung cancer. However, their use in patients with pre-existing autoimmune diseases (PADs) presents unique challenges. PADs, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and psoriasis, complicate the clinical management of lung cancer due to concerns about worsening autoimmune symptoms during ICI therapy. This review summarized the safety and efficacy of ICIs in lung cancer patients with PAD, focusing on the available clinical evidence, the optimal timing of ICI initiation, and the potential predictive biomarkers for immune-related adverse events (irAEs). Future prospective studies are needed to establish definitive guidelines for the use of ICIs in this population, with a focus on identifying patients at risk, managing ICI resumption after irAE and developing new medications with durable control of both cancer and PAD.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Many researchers have previously reported that natural compounds from plants or Chinese Traditional Herbs have a potential to treat NSCLC. But it has not been reported that phytol can treat NSCLC. In this research, we first exposed this effect on A549 cells and researched the mechanism.

Multimodal tumor therapy based on "all-in-one" nanoplatforms enhances therapeutic efficacy, simplifies the construction process, and improves material utilization. Elemental selenium was successfully supported on upconversion nanoparticles (UCNPs) to constitute the near-infrared (NIR) light-responsive UCNP@Se heterostructures for the first time. Under 980 nm irradiation, the UCNP@Se heterostructures could not only produce holes and superoxide radicals •O2- but also catalyze the generation of hydroxyl radicals •OH by highly elevated levels of H2O2 in tumor cells to kill the tumor cells. In addition to the superior photocatalytic performance, elemental selenium itself also exhibited inherent inhibition activity against tumor cells. On the basis of the binding of anthracycline anticancer drugs such as doxorubicin (DOX) to the supported elemental selenium through Cu2+ bridging coordination, the UCNP@Se-Cu-DOX drug delivery system was constructed. The introduction of Cu2+ not only improved the efficient loading of DOX but also achieved the "AND" logic-controlled release of DOX under the combined stimuli of low pH and overexpressed glutathione (GSH) in tumor cells. Moreover, the loaded Cu2+ reacted with the overexpressed GSH to generate the active species CuII-GSSG upon NIR light irradiation, which further promoted tumor cell apoptosis. The NIR light-responsive UCNP@Se-Cu-DOX drug delivery system achieved the combination tumor therapy of selenium therapy, photocatalytic therapy, and logic-gated chemotherapy and has great potential applications in tumor therapy.

This study evaluated the effectiveness of a mobile application in tracking symptoms and improving symptom management and quality of life (QoL) among breast cancer patients undergoing chemotherapy in Thailand.

Temozolomide (TMZ), which is an alkylating agent, is the standard chemotherapeutic drug used for glioma treatment. However, the development of resistance to TMZ limits its efficacy. Thus, identifying novel therapeutic targets is necessary.

Tremendous efforts have been devoted to developing chemodynamic cancer therapy (CDT) platforms targeting intracellular antioxidant defense systems to realize an enhanced efficacy. However, such a strategy can be severely limited by the activation of compensatory antioxidant defense mechanisms in cancer cells. Herein, we present the rational design of a nanozyme-based CDT platform that can perturb compensatory antioxidant mechanisms in cancer cells for improved therapeutic efficacy. In the formulation, the metal-organic framework-based disruptor with peroxidase-mimicking activity can not only catalyze the conversion of the intracellular hydrogen peroxide into highly cytotoxic hydroxyl radicals for cancer cell killing but also disrupt the intracellular glutathione peroxidase 4-dihydroorotate dehydrogenase compensatory antioxidant system to provide significantly reinforced CDT efficacy. The present study sheds light on improving the outcomes of therapeutics that rely on the induction of oxidative stress by integrating the ability to disrupt intracellular compensatory antioxidant defense mechanisms into nanomedicine design.

Protein arginine methyltransferase 5 (PRMT5) is an epigenetic-related enzyme that has been shown to be a promising target for the treatment of human cancers. In prostate cancer, gene knockout has been shown to inhibit cancer cells by regulating the androgen receptor (AR), but this method has no effect on advanced prostate cancer without AR expression, and existing anticancer drugs are effective only in the current stage and promote the progression of cancer to advanced prostate cancer. We hope to design and synthesize a new compound that can inhibit prostate cancer at different stages. A series of candidate PRMT5 inhibitor molecules were designed on the basis of virtual molecular docking screening, and the binding mode was predicted via molecular docking simulation. Prostate cancer cell proliferation was detected by CCK-8, EdU, and flow assays, which verified the changes in the cancer cell cycle. Migration and invasion assays verified the effects of the compounds on the metastatic function of prostate cancer cells. Finally, Western blotting was used to detect the mechanism of action of the compounds in the treatment of prostate cancer. In prostate cancer, gene knockout has been shown to inhibit cancer cells by regulating the AR, but it has no effect on advanced prostate cancer without AR expression, and existing anticancer drugs are effective only in the current stage and promote the progression of cancer to advanced prostate cancer. SJL2-1 may be a promising compound for novel therapies for early androgen-sensitive prostate cancer and advanced castration-resistant prostate cancer (CRPC).

Temozolomide (TMZ) remains the cornerstone chemotherapy for glioma, yet intrinsic and acquired resistance mechanisms significantly limit its clinical effectiveness. This review summarizes the multifaceted molecular pathways contributing to TMZ resistance, including enhanced DNA repair mechanisms such as O6-methylguanine-DNA methyltransferase (MGMT), mismatch repair (MMR), and base excision repair (BER). Additional resistance factors include genetic mutations that affect the drug response, dysregulated non-coding RNAs (miRNAs, lncRNAs, and circRNAs), glioma stem cells (GSCs), cytoprotective autophagy, an immunosuppressive tumor microenvironment (TME), altered signaling pathways, and active drug efflux transporters. Recent advancements to overcome these resistance mechanisms, including enhancing TMZ bioavailability through nanoparticle-based delivery systems and the inhibition of efflux transporters, have been explored. Novel therapeutic approaches that target DNA repair pathways and manipulate autophagy are highlighted. Immunotherapeutic interventions reversing immune suppression and metabolic strategies targeting tumor metabolism offer additional avenues. Emerging therapies such as CRISPR-based gene editing, phytochemical combinations, repurposed drugs, and novel TMZ analogs designed to bypass MGMT-mediated resistance are also discussed. This review highlights current developments and identifies emerging areas, with the goals of enhancing clinical outcomes and prolonging survival for glioma patients.

This review aimed to evaluate the effects of exercise-based interventions on cancer therapy-related cardiovascular toxicity (CTR-CVT) in individuals with cancer.