Marine-derived collagen peptides have been acknowledged for their therapeutic potential, especially in cancer therapy and inflammation management. The aim of this study was to investigate the molecular mechanisms that contribute to the anticancer, anti-inflammatory and antioxidant properties of yellowfin tuna collagen peptides (YFTCP) utilizing a network pharmacology approach. The YFTCP was extracted from the bones of yellowfin tuna (Thunnus albacares) and subsequently hydrolyzed with trypsin. Seventeen peptides were discovered using liquid chromatography in conjunction with high-resolution mass spectrometry (LC-HRMS). A network pharmacology method was utilized to investigate the interactions between the discovered peptides and their biological targets. Additionally, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to identify pertinent biological pathways involved in the anticancer, antioxidant, and anti-inflammatory effects of these peptides. GO analysis revealed key associations between YFTCP and critical cancer- and inflammation-related genes encoding proteins such as CCND1, SRC, AKT1, IL-1β, TNF, and PPARG, which exhibited significant interactions. These proteins are essential for the regulation of the cell cycle, the development of tumors, and the response to inflammatory stimuli. The KEGG analysis also revealed that YFTCP was involved in a number of critical pathways, such as endocrine resistance, cancer pathways, Kaposi sarcoma-associated herpesvirus infection, proteoglycans in cancer, and human cytomegalovirus infection. These findings highlight the potential use of YFTCP as a multifaceted therapeutic agent, indicating their role in regulating important biological pathways associated with cancer development and inflammation. This study provides new valuable insights into the pharmacological properties of YFTCP, paving the way for future studies and drug development focused on these bioactive peptides.

Current anti-breast cancer drugs have limited efficacy and often cause severe side effects, highlighting the need for bioactive agents that could overcome these limitations. Curcumin, a phenolic compound from Curcuma domestica, has antineoplastic activity but has low solubility in physiological media, while moringa oil is a key component of the oil- phase nanocarrier and also possesses anticancer properties. The aim of this study was to develop a moringa oil-based nanocarrier system containing curcumin and to analyze its anticancer effects on MDA-MB-231 cell lines, focusing on the underlying mechanisms involving B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax) proteins. Additionally, the study investigated the side effects of the nanocarrier system following acute administration in animals. The anticancer effects were evaluated in vitro using MDA-MB-231 cell lines, while the acute toxicity assessment was conducted in healthy female Wistar rats. The nanocarrier system was formulated using moringa oil, Cremophor RH40, and PEG 400. Its cytotoxicity against MDA-MB-231 cells was assessed using the 3-(4,5- dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. DNA fragmentation, apoptosis, and the expression of Bax and Bcl-2 proteins were analyzed via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays, flow cytometry, and western blotting. Acute toxicity was further evaluated in female Wistar rats. The results demonstrated that the moringa oil-based nanocarrier system containing curcumin inhibited cell proliferation and induced apoptosis in MDA-MB-231 cells. Curcumin suppressed tumorigenesis by modulating Bcl-2 and Bax protein expression. Our data indicated that the combination of curcumin and moringa oil in a nanocarrier system had greater anticancer potential than either component alone. Moreover, administration of the nanocarrier system did not result in any clinically significant changes in body weight, behavior, or organ weight indicative of toxicological effects. No treatment-related histopathological abnormalities were observed at terminal necropsy. In conclusion, this novel combination of curcumin and moringa in nanocarrier system has better anticancer potential; nevertheless, further studies are needed to confirm this in cancer animal models.

Glioma, a highly malignant central nervous system tumor, exhibits aggressive invasiveness, extensive infiltration, and poor prognosis. Conventional treatments such as surgery, radiotherapy, and chemotherapy are hindered by limitations including the inability to overcome the blood-brain barrier (BBB), drug resistance, and high recurrence rates. Ferroptosis induced by nanoparticle-based systems offers an innovative strategy for glioma therapy by efficiently traversing the BBB, precisely delivering ferroptosis inducers, enhancing tumor accumulation, and enabling stimuli-responsive drug release. These features collectively improve the induction efficiency of ferroptosis in glioma cells. Various nanoplatforms, including inorganic nanoparticles, biomimetic carriers, and polymer-based systems, have demonstrated potential in crossing the BBB, inducing ferroptosis, and suppressing glioma progression. These systems enhance reactive oxygen species generation, deplete glutathione, and disrupt tumor microenvironment defense mechanisms, achieving synergistic therapeutic effects. The integration of ferroptosis with nanotechnology is emerging as a promising, non-invasive strategy for the treatment of gliomas, offering substantial therapeutic potential.

Venetoclax is a selective small-molecule BCL-2 inhibitor that has been approved for treating hematologic malignancies. Co-administration with CYP3A inhibitors, such as voriconazole, poses a high risk of drug-drug interactions (DDIs) that can increase venetoclax exposure. This study aimed to develop a population pharmacokinetics (PopPK) model to characterize the PK properties of venetoclax when co-administered with voriconazole.

The search for effective methods of treatment and prevention of oncological diseases, despite the successes achieved in recent decades, remains one of the most urgent issues in modern medicine. It is known that chemotherapy and radiation therapy are based on the induction of cell death by increasing the intracellular concentration of reactive oxygen species (ROS). To increase the effectiveness of chemo- and radiotherapy, inducing and increasing oxidative stress in tumor cells has been proposed. A new class of promising adjuvants in combination with anticancer therapy, which has already been shown to be effective in preclinical and clinical studies, includes natural and synthetic polyphenols. Polyphenolic compounds not only exhibit antitumor activity but also significantly reduce the resistance of tumor cells to chemo- and radiotherapy. However, almost all chemotherapeutic drugs and regimens of radiation treatment have a damaging toxic effect on normal tissues, which significantly affects the quality of life of patients, and treatment options for managing these side effects are limited. In this regard, some of the most promising agents for the management of toxic side effects are natural polyphenols. This study discusses the possible molecular mechanisms and prospects for the clinical use of natural and synthetic polyphenolic compounds in chemo- and radiotherapy. In addition, the protective role/effect of polyphenols on the effects of chemoand radiotherapy in tumor patients is discussed.

Ethacrynic acid is a dynamic agent holding alpha-beta unsaturated carbonyl unit in its structure which imparts superiority and extraordinary advantage of displaying multiple biological activities such as anticancer, antiviral, anti-malarial effect, diuretic effect and inhibits the Glutathione-s-transferase p1-1 enzyme which produces hindrance in the pathway of apoptosis. Ethacrynic acid is an inhibitor of Glutathione-s-transferases. EtA by itself act as an anticancer agent at higher concentration and also increases effectiveness of other compounds used in cancer treatment by preventing their detoxification, all these facts attracted our attention to develop and evaluate novel structural analogues of ethacrynic acid for their inhibitory effect on GSTs and anti-cancer activity in breast cancer.

Breast cancer is the most common type of cancer among women. Steroidal or non-steroidal aromatase inhibitors (NSAIs) are used clinically, and in most cancer diseases, resistance is the most important problem.

Cancer has been the cause of the highest number of deaths in the human population despite the development and advancement in treatment therapies. The toxicity, drug resistance, and side effects of the current medicaments and therapies have left the void for more research and development. One of the possibilities to fill this void is by incorporating Triazole moieties within existing anticancer pharmacophores to develop new hybrid drugs with less toxicity and more potency. The placement of nitrogen in the triazole ring has endowed its characterization of being integrated with anticancer pharmacophores via bioisosteric replacement, click chemistry and organocatalyzed approaches. This review paper emphasizes the discussions from articles published from the early 2000s to the current 2020s about the triazole-based derivatives used in anticancer therapy, elaborating more on their chemical structures, target receptors or enzymes, mechanism of action, structure-activity relationships, different triazole-derived hybrid drugs under clinical and nonclinical trials, and recent advancements toward developing more potent and less toxic anticancer agents.

Triple-negative breast cancer (TNBC) is a highly aggressive subtype characterized by the absence of estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2. RAD51 is associated with homologous recombination repair (HRR), a crucial DNA repair mechanism. This paper reports the development and efficacy of a novel targeted RAD51 degrader compound, TRD2, for treating TNBC. TRD2 is synthesized by linking a RAD51 binder to the ligand of the E3 ligase cereblon (CRBN). The results showed that TRD2 effectively reduces the RAD51 protein levels in TNBC cells and exhibits potent anticancer effects in vitro and in vivo. Mechanistic studies showed that TRD2 induces RAD51 ubiquitination and subsequent proteasomal degradation by binding to CRBN. Furthermore, TRD2 demonstrated significant tumor growth inhibition in a mouse xenograft model of TNBC. These findings highlight the potential of TRD2 as a promising therapeutic approach in TNBC, leveraging Proteolysis-targeting chimera (PROTAC) technology to degrade the overexpressed RAD51 protein selectively. The study emphasizes the importance of targeting DNA damage repair core proteins and suggests that TRD2 could overcome challenges posed by resistance to conventional therapies. Nevertheless, additional experiments will be needed to validate these observations and explore the potential impacts on other proteins and cancer types. Overall, this research introduces a novel strategy for TNBC treatment, addressing the limitations of current therapeutic options.

Surgical resection of the tumor remains the preferred treatment for most solid tumors at an early stage, however, residual tumor cells after surgical resection poses a considerable obstacle in cancer treatment. Here, we developed a gel carrier using a cellulose-based gel-forming polymer (CT) combined with gelatin sponge (GS) to fill the resection cavity and delay postoperative residual tumor growth. The fabricated gel exhibited a porous nature along with gradual swelling and erosion over time. Curcumin (Cur) and apatinib (Apa) were loaded into CT gel (CT-CA), and a sustained release behavior was observed at pH 7.4 and 6.4 at 37 °C. The preclinical studies indicated that the mouse weight and tissue exhibited no apparent change after administration of the GS-CT compared with the control. The in vivo fluorescence images showed that GS-CT has the capability to regulate the release of Cur and Apa, facilitating the accumulation of these two agents at the surgical tumor site. Moreover, GS-CT loaded Cur and Apa (GS-CT-CA) delayed postoperative residual tumor growth in intraperitoneal and subcutaneous postoperative mouse models. These findings demonstrated that our gel carrier system significantly prevents postoperative residual tumor growth because of enhanced drug accumulation and sustained drug release at the tumor site.

Treatment of gestational trophoblastic disease (GTD) with chemotherapy is a success story for medical oncology; a combination of chemosensitive disease with a sensitive tumour marker makes GTD an eminently curable disease. However, 0·5-5·0% of women with this cancer continue to die as a result of multidrug resistance. PD-L1 is strongly expressed in these tumours, making them a target for immune therapy with immune checkpoint inhibitors such as pembrolizumab.

While new intrathoracic adenopathy in a patient with cancer can represent progression of disease, the differential diagnosis is broad. Sarcoid-like reactions (SLR) remain an underreported source of lymphadenopathy in patients treated with immune checkpoint inhibitors (ICI), with limited reports in patients with cancers other than melanoma.

Based on results of randomized clinical trials, polyADP-ribose polymerase inhibitors (PARPi) have become the standard of care in patients with platinum-sensitive recurrent ovarian cancer (OvC) in patients responding to platinum chemotherapy. However, little is known about their impact on survival in a real-world setting.

Malignant pleural effusion (MPE) is a severe complication in lung cancer, characterized by an immunosuppressive tumor microenvironment (TME) and limited therapeutic options. This study investigates the role of IL-6 in regulating immune suppression and tumor progression in MPE and evaluates the efficacy of dual IL-6 and PD-L1 blockade.

Immune checkpoint blockade (ICB) therapy has shown promising clinical efficacy in cancer treatment, but only a subset of patients experience significant therapeutic responses. Tumor cells respond to internal and external stresses, such as hypoxia and nutrient deprivation, by activating the unfolded protein response (UPR) in the tumor microenvironment. This response helps maintain homeostasis, promoting malignant progression, chemotherapy resistance, and immune escape. In this study, single-cell RNA sequencing (scRNA-seq) data from non-small cell lung cancer (NSCLC) patients treated with ICB revealed upregulation of thioredoxin (TXN) expression in the epithelial tissues of LUAD (lung adenocarcinoma) and LUSC (lung squamous cell carcinoma) patients with minimal pathological remission. High TXN expression was also associated with "cold tumors," characterized by a lack of T cells and low levels of chemokine receptors and immunomodulators. Experimental results showed that TXN was highly expressed in NSCLC tissues, and its knockdown significantly inhibited the proliferation and migration of A549 and SK-MES-1 cells. Furthermore, TXN knockdown enhanced T-cell-mediated cytotoxicity against these tumor cells, suggesting that TXN contributes to immune escape in NSCLC by promoting tumor cell proliferation and migration while inhibiting immune killing. Notably, TXN knockdown also upregulated CD40 expression, indicating that TXN may regulate immune escape in lung cancer through CD40 modulation.

This study aimed to assess the effectiveness of combining selenium nanoparticles (SeNPs) with mitomycin C (MMC) in treating the T24 high-grade bladder cancer cell line to decrease MMC dosage and alleviate its side effects. The T24 (EJ138) cell line was exposed to various concentrations of SeNPs and MMC to identify the IC50 values via the MTT assay. The IC50 of MMC was then lowered by 25%, 50%, and 75%, and different SeNPs concentrations were added, to find the new IC50 values of these combinations. Apoptosis rates were measured using Annexin-V/PI staining, while the DNA cell cycle was analyzed using the PI staining method. The scratch-wound assay, colony-forming assay, and Hoechst staining were employed to examine the cell migration, proliferative capacity, and nuclear morphology, respectively. Real-time PCR assessed the expression levels of SNAIL, E-cadherin, and genes related to angiogenesis and proliferation (VEGF-C and HIF-1α), alongside the apoptosis markers (Bcl-2 and BAX). The co-administration of SeNPs and MMC (178.8 µM SeNPs + 14.9 µM MMC) significantly increased the rate of early apoptosis in the T24 cell line compared to MMC alone (29.8 µM, p < 0.0001). Additionally, SeNPs and MMC induced cell cycle arrest at the SubG1/G1 and G2/M phases, respectively. This effect was observed in the combination group at both phases. Similar to MMC alone, the combination group inhibited cell proliferation, colony formation, and migration in T24 cells (p > 0.05). Our findings indicate that the treatment with the combination increased the expression of apoptosis-related genes and decreased angiogenesis and proliferation-related gene expression similar to MMC alone (p > 0.05). The combined administration of MMC and SeNPs enhances the antitumor efficacy on the T24 cell line. It is proposed that the concurrent use of SeNPs and MMC could effectively reduce the required dosage of MMC, thus minimizing its negative side effects.

Surufatinib is a novel, China-developed small-molecule tyrosine kinase inhibitor that demonstrates high selectivity for VEGFR, FGFR1, and CSF1R. Surufatinib has been approved for the treatment of neuroendcrine tumors, including pancreatic neuroendocrine tumors (PNEN) and non-pancreatic neuroendocrine tumors (N-pNEN). The purpose of this retrospective study is to assess Surufatinib's safety and effectiveness in patients with various advanced solid malignancies. The general clinical statistics and follow-up data of patients treated with Surufatinib for advanced solid tumors at Zhejiang Provincial People's Hospital between January 2021 and April 2024 were gathered. Enhanced CT was used to assess the effectiveness during that time, and cases side effects were gathered. Survival rates of different diseases were analyzed using the Kaplan-Meier method. A total of 28 eligible patients were enrolled in this study. At the end of follow-up, treatment with Surufatinib resulted in the following outcomes: Complete response (CR) in 0 cases (0.0%), Partial response (PR) in 5 cases (17.9%), Stable disease (SD) in 7 cases (25.0%), and Progressive disease (PD) in 16 cases (57.1%). Objective response rate (ORR) and Disease control rate (DCR) were 17.9% and 42.9%, respectively. In the PNEN group, ORR was 33.3%, DCR was 66.7%, median progression-free survival (mPFS) was 11 months, while median overall survival (mOS) was 17 months. In the N-pNEN group, ORR was 14.3%, DCR was 42.3%, mPFS was 6 months and mOS was 7 months. ORR was 8.3%, DCR was 25%, mPFS was 2 months, and mOS was 2 months. The most common adverse reactions included hypoproteinemia, proteinuria, bone marrow suppression and gastrointestinal toxicity, and which of them were grade 1 to grade 2. In advanced solid tumors beyond PNEN, Surufatinib demonstrates clinically meaningful survival benefits for patients refractory to standard therapies, with a generally manageable safety profile.

Therapeutic drug monitoring (TDM) is used to optimize drug therapy by ensuring efficacy or preventing toxicity. For a limited number of cytotoxic antineoplastic drugs, for aminoglycoside antibiotics, and for vancomycin the use of TDM is common practice. In this article, we summarize recent advances and indications for the TDM of antineoplastic agents in children, focusing on protein kinase inhibitors and the cytotoxic drug fludarabine. We also summarize recent recommendations for antimicrobial TDM of beta-lactam antibiotics and vancomycin.

Pharmacogenomics remains underutilized in pediatric oncology, despite the existence of evidence-based guidelines. Implementation of pharmacogenomics-informed prescribing could improve medication safety and efficacy in pediatric oncology patients, who are at high risk of adverse drug reactions. This study examines the prevalence of high-risk pharmacogenomic phenotypes and the prescription of relevant medications in a diverse Australian pediatric oncology cohort, highlighting the potential impact of pharmacogenomic testing in this unique population. Whole genome sequencing data from 180 patients were analyzed to assess 14 genes with evidence-based pharmacogenomic guidelines relevant to pediatric oncology. Over 90% of patients had at least one high-risk phenotype, with 20% presenting four or more. Ondansetron, mercaptopurine, omeprazole, pantoprazole, and voriconazole were commonly prescribed medications that have pharmacogenomic prescribing recommendations, with the latter three showing the highest actionability rates. High-risk phenotypes were most frequently observed for CYP2C19 and CYP2D6, with 30% of patients having a high-risk phenotype for both genes. This study underscores the potential utility of pharmacogenomics in pediatric oncology patients across a range of pharmacogenes and commonly prescribed medications. The findings support advocacy for implementing broad, pre-emptive pharmacogenomic testing in oncology patients to improve treatment safety and efficacy.

This study examines the impact of continuous infusion chemotherapy via femoral artery catheterization on Golgi protein 73 (GP73) and alpha fetoprotein heterogeneity (AFP-L3) in liver cancer patients. A retrospective analysis was conducted on 108 liver cancer patients treated from January 2020 to December 2022, divided into two groups: transarterial chemoembolization (TACE) and continuous infusion regional arterial chemotherapy via femoral artery catheterization (CIFAC), with 54 patients in each group. Serum tumor markers, liver function, adverse reactions, quality of life, and 1-year survival rate were analyzed and compared between the two groups of patients. Prior to treatment, no significant differences were observed in tumor markers, liver function, and quality of life between groups (P > 0.05). After 60 and 90 days, the CIFAC group exhibited significantly lower levels of GP73, AFP, and AFP-L3 compared to TACE (P < 0.05). Additionally, CIFAC patients had lower levels of alanine aminotransferase (ALT), aspartate transaminase (AST), indocyanine green (ICG15) (P < 0.05), reduced adverse reactions (nausea, vomiting, etc.), and higher Karnofsky scores (P < 0.05). The one-year survival rate of the CIFAC group was significantly higher than that of the TACE group (P < 0.05). Continuous infusion chemotherapy through femoral artery catheterization can help reduce serum tumor marker levels, improve liver function, and reduce adverse reactions in liver cancer patients.