Nanomaterial-based delivery systems have gained significant attention for their ability to provide high surface area, tunable porosity, and tailored surface chemistry, key features that enable efficient adsorption and controlled release of active agents. These advanced platforms offer versatile solutions for applications ranging from therapeutic delivery to environmental remediation, by improving loading capacity, release kinetics, and functional performance. Here we tailor a novel core-shell silica nanomaterial with a large complex internal structure in the core and shell, while silica surfaces are bridged by an organic crosslinker in the shell. Firstly, the organo-silica bridging agent (bivalent organic crosslinkers) DABCO-S was prepared through a simple nucleophilic substitution reaction between 3-chloropropyl-triethoxysilane and a strong base bivalent 1,4-diazabicyclo[2.2.2]octane (DABCO). Secondly, dendritic fibrous nanostructured silica (DFNS) was synthesized as the core nanostructure. Thirdly, DABCO-S bridges were integrated into the DFNS morphology surrounding the DFNS core under open-vessel reflux conditions. The resulting core-shell product, incorporating the DABCO-S bridges within the silica shell network around DFNS, is referred to as the DDC structure. This design was strategically chosen based on the hypothesis that such colloidal systems would serve as highly efficient adsorbents for sparsely soluble drug compounds. The pH-responsive DDC colloidal hybrid carriers were evaluated as biocompatible carriers for controlled doxorubicin (DOX) delivery. The results demonstrated that cancer cells exhibited lower viability when treated with DOX-loaded DDC colloidal hybrid carriers compared to free DOX or control groups, indicating an enhanced anticancer effect of the loaded carrier. The high drug loading capacity, encapsulation efficiency, and pH-responsive behavior of these colloidal hybrid carriers in varying cellular environments confirm their suitability as promising candidates for further studies. Future research could focus on incorporating targeting functionalities to enhance their potential as active drug delivery systems.

Applying molecular hybridization and ring variation as drug design approaches, a set of 2-hydrazinyl-5-(3-phenylallylidene)imidazole-4-ones 5 and 6a-k was designed and synthesized as multi-carbonic anhydrases inhibitors. The stereochemistry of the imine double bond in the newly synthesized compounds was evidenced by NOESY and ROESY analyses of a representative example. National Cancer Institute (NCl) evaluated all these synthesized compounds against 60 cancer cells, one dose preliminary antitumor estimation, where five compounds 6c, 6d, 6h, 6i, and 6k were the most active. It is noticeable that the presence of electron releasing groups with +M effect at the phenyl ring of arylidene hydrazinyl moiety significantly elevated the antitumor effect. The superior anticancer analogs 6h and 6i were chosen by the NCI for five-dose assessment. The mechanistic analysis of the most potent anticancer compounds was accomplished by assessing the inhibitory activity of these analogs toward hCAs I, II, IX, and XII. The outcomes displayed that compound 6i was the most promising CA inhibitor showing IC50 range of 0.04-0.16 μM. Additionally, compound 6i stimulated its antitumor and hCA inhibition effects by arresting the SK-MEL-5 cell cycle at G2/M phase as well as promoting the apoptotic cascade. Furthermore, in vivo bio-distribution of 131I-6i in tumor induced mice indicated a high level of localization in the tumor site without any significant accumulation in other body organs. The molecular docking study have been performed to assess their potentiality as considerable anticancer candidates.

Immune checkpoint inhibitors (ICIs) significantly improve survival in patients with mismatch repair-deficient (dMMR) or microsatellite instability-high (MSI) tumors. In 2022, ICIs were approved as first-line treatment with chemotherapy for advanced biliary tract cancers (BTCs). MSI/dMMR BTC represents a rare subtype, and its response to ICIs remains poorly understood. This multicenter real-world study aimed to describe clinical characteristics and outcomes of those patients.

OCTAVA (NCT05732805) was an international, multi-center, randomized, double-blind, phase III study evaluating the fixed-dose combination of nurulimab (anti-CTLA-4) and prolgolimab (anti-PD-1) (BCD-217, Nuru+Prolgo) followed by prolgolimab maintenance versus prolgolimab monotherapy as first-line treatment for unresectable or metastatic melanoma (un/mM). We present the primary analysis results.

Capecitabine, an oral anticancer agent, frequently causes hand-foot syndrome (HFS), affecting patients' quality of life and treatment adherence. However, such symptomatic toxicities are often difficult to detect in structured electronic health record (EHR) data. This study primarily aimed to validate a natural language processing (NLP) approach to identifying capecitabine-induced HFS from unstructured clinical text and demonstrate its application in evaluating medication-associated adverse event trends in real-world settings.

Oncology nurses working at a rural community infusion clinic observed an increase in infusion-related reactions while administering the first and second treatments of liposomal doxorubicin. Review of the package insert reveal.

Chemotherapy can contribute to chemotherapy-induced nausea and vomiting (CINV). The use of acupressure is a nonpharmacologic method to counteract general nausea and vomiting.

The addition of blinatumomab to chemotherapy is the new standard of care for most pediatric patients with B-lineage acute lymphoblastic leukemia (B-ALL), and its use has increased rapidly. Administering blinatumomab to pediatric patients is associated with a spectrum of unique challenges, resulting in variable practices across institutions.

Eg5 is a mitotic kinesin motor protein essential for the formation of bipolar spindles during cell division. Its inhibition disrupts mitosis, leading to cell cycle arrest and apoptosis in cancer cells. This makes Eg5 a promising target for chemotherapeutic interventions, especially in cases resistant to traditional treatments. In this study, a drug repurposing strategy was employed to design and synthesise quinoline-based Schiff base derivatives as potential Eg5 inhibitors. These compounds were subjected to in vitro biological evaluations, including cytotoxicity testing against the human breast cancer cell line MDA-MB-231 and the normal mouse fibroblast cell line L929 using the MTT assay. Enzymatic assays targeting Eg5 were also conducted. Among the synthesised molecules, compound (5) demonstrated significant Eg5 inhibition in enzymatic assays, with an IC50 of 2.544 ± 0.810 µM in the Malachite Green assay and 4.03 ± 2.027 µM in the steady-state ATPase assay, and moderate inhibition against triple-negative breast cancer cells (MDA-MB-231). Computational studies, including molecular docking, molecular dynamics simulations, and MM/GBSA free energy calculations, were performed to analyse binding interactions. ADMET properties were predicted using the QikProp module. The findings suggest that targeting mitosis through Eg5 inhibition may offer a strategic approach in chemotherapy, potentially enhancing treatment efficacy.

Mitotane is a drug widely indicated in patients with adrenocortical carcinoma. Several adverse events related to mitotane have been reported in 30 to 90% of patients. We present a case series of toxicities related to mitotane therapy and their management. Clinical and laboratory examinations to detect adverse events were carried out at baseline, monthly for the first six months and quarterly afterwards. Mitotane blood concentrations were measured by liquid chromatography. Six patients diagnosed with adrenocortical carcinoma and treated with mitotane were included, with hormone overproduction in four of them. Median time of follow up during mitotane therapy was 13 months [5-36]. All had adverse events related to mitotane detected during the first three months of treatment (median mitotane dose at first adverse event: 2 g/day). Four patients presented two or more adverse events. Endocrine side effects were the most frequently found (adrenal insufficiency, followed by hypothyroidism and hypercholesterolemia in order of frequency). Replacement therapy and/or statin treatment was prescribed as needed. Mitotane blood concentration in 3 of 4 patients was below the optimal range. Treatment with mitotane requires individualized care to mitigate the risks of adverse events, optimize therapeutic outcomes, and ensure patient safety.

High-price drugs (HPD) represent an economic problem for the health system. Dose banding has been shown to decrease costs. The objective was to determine the economic impact and safety of HPD dose standardization.

Boron neutron capture therapy (BNCT) is a re-emerging field to achieve precision treatment of malignant tumors with its unique biotargeting and heavy-ion effects, and combination therapy could effectively improve the therapeutic efficacy of BNCT. Herein, a tumor-targeted boron-containing nanozyme was prepared to achieve the combination of BNCT and catalytic therapy for the effective treatment of melanoma. Notably, the boron-containing nanoenzyme exhibited strong peroxidase-like catalytic activity, had skin melanoma cell selectivity, and could undergo a catalytic reaction within the tumor cells to induce apoptosis. During BNCT, the catalytic activity of the boron-containing nanoenzyme could be combined with BNCT to exert a more powerful therapeutic effect than a monotherapy. In the BNCT treatment of skin melanoma tumor-bearing mice, the boron-containing nanoenzyme had a strong tumor-targeting ability and could exert catalytic effects to effectively inhibit tumor growth. After combined treatment, the tumor volume of mice was significantly reduced, the survival time of tumor-bearing mice was prolonged, and the survival rate was remarkably improved. Meanwhile, the boron-containing nanoenzyme could enhance the efficacy of tumor treatment by inhibiting the epithelial-mesenchymal transition and extracellular matrix degradation in combination therapy. Thus, the boron-containing nanoenzyme is a promising boron-containing drug to achieve BNCT combined with catalytic therapy for tumor treatment and could facilitate biological applications of nanoenzyme-based materials in BNCT.

Poly (ADP-ribose) polymerase 1 (PARP-1) exhibits high expression levels in colorectal cancer (CRC) patients and participates in multiple DNA damage repair pathways, thereby emerging as an attractive target. Herein, we identified a series of PARP-1 inhibitors (termed as compounds 1-6) by pharmacophore modelling, virtual screening and biological evaluation. Enzyme inhibition assays demonstrated that compound-5 significantly inhibited PARP-1 activity (IC50 = 0.07 ± 0.01 nM) and exhibited high selectivity for PARP-1 among 63 different kinases. Molecular dynamic simulations indicated that compound-5 stably bound to the catalytic domain of PARP-1. Cellular assays demonstrated that compound-5 significantly inhibited the proliferation of a panel of human CRC cell lines (HCT116, SNU-1, Caco-2, HT-29). The data suggest that compound-5 may be a highly potent and selective PARP-1 inhibitor for CRC therapy.

Intensive Care Unit (ICU) admission is usually denied to patients with advanced hepatocellular carcinoma (HCC) due to the perceived poor prognosis associated with both cirrhosis and liver cancer. However, immunotherapy based on immune checkpoint inhibitors (ICI) has transformed the treatment landscape, and the role of critical care is becoming more relevant in managing adverse events. We aim to assess the outcome of patients with advanced HCC treated with ICI admitted to the ICU.

Systemic chemotherapy remains the primary treatment for metastatic triple-negative breast cancer, but its effectiveness is limited, and clinical outcomes are poor. FDA-approved molecular targeted therapies and immunotherapies address only a subset of breast cancer patients, overlooking tumor heterogeneity and complexity. Additionally, these therapies suffer from short local retention times and subtherapeutic concentrations at tumor sites. Here, we present peptide-based nanofibers (pNFP6) with significant lung targeting and retention properties for treating pulmonary metastases. The nanofibers display a 2D single-layer structure with a high aspect ratio (5 nm in width and 8 μm in length), promoting lung affinity. Shortly after systemic administration, 75% of the total pNFP6 reached the lungs, minimizing uptake by other organs and reducing off-target accumulations. Interactions between multiple nanofibers formed larger interfibril networks, enhancing local accumulation and retention. Light sheet fluorescence microscopy imaging revealed that pNFP6, when used as a drug (doxorubicin) carrier, macroscopically improved delivery to diseased lungs and offered sustained treatment. At a microscopic level, the drug-loaded pNFP6 (aldox-pNFP6) interacted with the cell surface and released the drug in close proximity. Compared to the clinically used free drug and liposomal formulation (Doxil), aldox-pNFP6 exhibited superior therapeutic outcomes with reduced toxicities. Overall, this approach provides full lung coverage, enabling continuous, localized release of a broad spectrum of antitumor activity.

Near-infrared photoimmunotherapy (NIR-PIT) is a targeted cancer treatment that uses antibody-IR700 conjugates and selectively destroys cancer cells expressing a target antigen when exposed to near-infrared (NIR) light. NIR-PIT not only destroys targeted cancer cells but also induces anticancer immune activation. Currently, epidermal growth factor receptor (EGFR) is the only clinically approved target for NIR-PIT. To expand the therapeutic potential of this therapy, we investigated EpCAM as a potential target for NIR-PIT.

Melanoma results in the formation of malignant tumors and is the deadliest form of skin cancer with high mortality rate. Immunotherapy for melanoma has made great breakthroughs in recent decades. However, low patient response rates and side effects due to the immunosuppressive tumor microenvironment (iTME) and tumor heterogeneity limit the clinical application of melanoma immunotherapy. The tumor microenvironment (TME) exhibits characteristics such as weak acidity, hypoxia, and aberrantly expressed proteases. By exploiting these features, researchers have developed stimuli-responsive drug delivery systems (DDSs) to enhance antitumor immune responses in melanoma patients. This review aims to clarify how stimuli-responsive DDSs enhance melanoma immunotherapy and guide their use as therapeutic agents. We summarize the categorization and design of these DDSs, analyze their immune-enhancing pathways, and discuss current challenges and future prospects in the field.

Quantum dots (QDs) have emerged as versatile nanomaterials with significant potential for cancer therapy due to their unique optical properties, biocompatibility and multifunctionality. Through surface modification, QDs can target tumor-specific biomarkers, serving both as direct therapeutic agents and precision drug delivery vehicles. Their ability to generate reactive oxygen species (ROS) under near-infrared light excitation enables the integration of photothermal and photodynamic therapies, enhancing antitumor efficacy. Additionally, QDs possess intrinsic antimicrobial properties that inhibit bacterial growth within the tumor microenvironment, reducing infection-related complications and improving therapeutic outcomes. Despite these advantages, challenges such as heavy metal toxicity and uncontrolled degradation remain, necessitating the development of non-toxic, heavy metal-free QDs and advanced surface engineering. This review discusses the molecular design, antitumor mechanisms, and clinical translation challenges of QD-based platforms, highlighting their emerging role in precision oncology and suggesting future directions in the development of smart, multifunctional systems that integrate multiple therapeutic modalities for enhanced cancer treatment.

Lung cancer is a severe malignant disease and causes plenty of deaths each year. The survival and prognosis are disappointing for patients with recurrence or metastasis. This is partially due to the lack of mechanisms underlying lung cancer. The ZEB1 gene was reported to promote progression in lung cancer. However, the mechanism of ZEB1 in lung cancer is a puzzle. ZEB1 and WNT7B were expressed more strongly in lung cancer cells. In clinical lung cancer tissues, ZEB1 was also overexpressed compared to the adjacent normal tissues. ZEB1 knockdown (ZEB1-KD) inhibited the activation of Wnt/β-catenin signaling. However, overexpression of WNT7B alleviated this inhibition. Furthermore, ZEB1 was shown to regulate the expression of WNT7B, and WNT7B was the bridge between ZEB1 and Wnt signaling. Cell proliferation and invasion ability were inhibited by ZEB1-KD, which was reversed by WNT7B overexpression. This regulation was supported by the expression patterns of PCNA, E-cadherin, and N-cadherin. In addition, much more cell apoptosis was induced in ZEB1-KD cells treated with Docetaxel compared to that without ZEB1-KD. This induction was reversed when WNT7B was overexpressed. Consistently, the IC50 value in the ZEB1-KD/Docetaxel group was much lower than that in the ZEB1-KD or Docetaxel alone group. In contrast, WNT7B overexpression increased the IC50 value of Docetaxel. In conclusion, ZEB1 positively regulates Wnt/β-catenin signaling in lung cancer and contributes to cancer progression. ZEB1 knockdown increases the efficacy of Docetaxel in lung cancer.

The critical role of neurotransmitters in the resistance to tumor immune checkpoint inhibitor (ICI) is becoming increasingly significant in therapeutic contexts. ICIs work by enhancing antitumor immunity through the blockade of the PD-1/PD-L1 and CTLA-4 pathways. However, only 20% of patients experience durable efficacy, and the challenge of drug resistance limits the clinical application of these therapies. Drug resistance is closely linked to various factors within the tumor microenvironment, including the distribution of tumor-infiltrating lymphocytes, the function of tumor-associated macrophages, low expression levels of PD-L1, variations in tumor mutational burden, dysregulation of antigen presentation, and both genetic and epigenetic changes in tumor cells. In recent years, the importance of the neural-immune axis has gained attention. Abnormal nerve fiber growth or irregular secretion of neurotransmitters can contribute to immune evasion. Neurotransmitters such as dopamine, norepinephrine, and serotonin influence the tumor microenvironment by regulating the expression of immune checkpoints and the function of immune cells, which can promote immune escape. As a result, therapeutic strategies that target neurotransmitters and their receptors hold promise for overcoming resistance to ICIs. These strategies may significantly enhance the efficacy of ICIs and pave the way for new approaches in cancer therapy. This article reviews the relevant mechanisms and proposes potential therapeutic strategies, offering new insights for the field.