Immune checkpoint inhibitors (ICIs) are an important treatment option in bladder cancer, but clinical trials have demonstrated that they are associated with immune-related adverse events (irAEs), such as rash, hypothyroidism, hyperthyroidism, and others. This study aimed to evaluate real-world evidence of these irAEs using the FDA Adverse Event Reporting System (FAERS).

Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal solid malignancies, characterized by aggressive biology and a paucity of effective treatments. Activating mutations in KRAS occur in more than 90% of cases and are fundamental to tumor initiation, progression, therapeutic resistance, and immune exclusion, establishing KRAS as the dominant oncogenic driver in PDAC. Long considered undruggable, KRAS has recently become a viable therapeutic target with the development of allele-specific inhibitors as well as pan-RAS(ON) agents capable of broadly suppressing mutant RAS signaling. Preclinical models and early-phase clinical trials demonstrate meaningful antitumor activity, with emerging evidence of tumor microenvironment remodeling and delayed resistance. Combination strategies integrating KRAS-directed therapies with chemotherapy, vertical pathway inhibition, immunotherapy, and emerging approaches such as KRAS degradation and RNA-targeted approaches are being explored to improve the depth and durability of response. Together, these advances signal a paradigm shift toward molecularly guided treatment strategies in PDAC and offer a promising path forward in a disease with substantial unmet clinical need.

Cantharidin (CTD) is a natural anticancer compound whose clinical application is limited by poor water solubility, low bioavailability, and significant toxicity. To develop a more effective and safer therapeutic strategy, we proposed a synergistic combination therapy by integrating CTD with staurosporine (STS), a protein kinase inhibitor that shares complementary mechanisms of action targeting the mTOR/HIF-1α/VEGF pathway. We further developed an aptamer-guided liposomal nanosystem for the co-delivery of CTD and STS (Apt/CTD-STS/NL), aiming to enhance tumor targeting, improve bioavailability, and reduce the systemic toxicity of both drugs.

In Japan, amrubicin hydrochloride (AMR) is occasionally administered to patients with recurrent small cell lung cancer (SCLC). AMR therapy can induce febrile neutropenia (FN), a complication that may be fatal or compromise therapeutic efficacy due to treatment interruption or dose reduction. Identifying risk factors for FN is therefore critical to ensuring safe and effective AMR administration. Current evidence on this issue remains limited to small case series, underscoring the need for more robust studies. We conducted a multicenter retrospective analysis to examine predictors of FN during AMR treatment for recurrent SCLC. Patients who received AMR between April 1, 2013, and March 31, 2023, were included. The cohort comprised 256 patients, divided into 192 without FN and 64 with FN. Multivariate analysis demonstrated that performance status (PS) >2 (odds ratio: 5.8, 95% confidence interval: 1.70-19.80, p=0.005) and hematocrit (HCT) (odds ratio: 0.93, 95% confidence interval: 0.877-0.994, p=0.033) were significantly associated with FN development. These findings suggest that PS and HCT may serve as key indicators for predicting FN during AMR therapy in patients with recurrent SCLC.

Myrsine linearis (Lour.) is a medicinal plant in Vietnam that was used to treat various diseases. However, the phytochemical and biological activities of this plant have not been extensively investigated. Therefore, this study extracted the essential oil from Myrsine linearis leaves (MLEO), followed by the identification of phytochemical components and the evaluation of anti-inflammatory and anticancer activities in vitro and in silico. The results showed that major constituents in MLEO were β-caryophyllene (11.3 %), α-humulene (10.3 %), caryophyllene oxide (4.6 %), and spathulenol (4.3 %). MLEO inhibited the protein denaturation (IC50 =34.01±5.64 µg/mL) and inhibited nitric oxide release in LPS-induced macrophage with the value of 33.19±1.78 %. The main compounds in MLEO bound to cyclooxygenase-2 and nitric oxide synthase, with binding energy values ranging from -6.1 to -7.5 kcal/mol, similar to those of positive controls. Additionally, MLEO demonstrated cytotoxicity against different cancer cells, with IC50 values ranging from 20.26±1.1 µg/mL to 21.11±1.41 µg/mL. Therefore, MLEO is a promising candidate for supporting the treatment of diseases relating to inflammation and cancer.

Peritoneal metastasis (PM) from gastric cancer (GC) is associated with poor prognosis and limited treatment options. We investigated a novel peritoneal-targeted therapy using CF33-human sodium iodide symporter (hNIS), a chimeric orthopoxvirus, combined with anti-PD-L1 immune checkpoint blockade in an immunocompetent mouse model of GCPM.

Oral systemic anti-cancer therapies improve convenience, but also shift responsibility for treatment management to the patient. Education, communication, and models of care must adapt to support safe, equitable, and sustainable oral anti-cancer treatment.

Despite the remarkable success of immune checkpoint inhibitor (ICI) therapy in solid tumors, immune-related adverse events (irAEs) have posed great challenges in the whole-course management of ICI immunotherapy. Reliable biomarkers helping to predict irAEs are still limited and lacking.

Tumor dynamic models are vital for evaluating oncology treatments and guiding clinical drug development decisions. However, few studies rigorously assess their predictive capabilities, especially when forecasting tumor trajectories from clinical trials with short or inconsistent follow-up across treatment arms. Poor predictive performance or biases related to follow-up time could potentially limit the general utility of tumor growth inhibition (TGI) models. This study quantitatively evaluates prediction bias across several established tumor dynamic models, comparing five classical pharmacometric TGI models with the deep learning-based Tumor Dynamic Neural-ODE (TDNODE) framework. Using time-truncated clinical trial data from 3106 patients with non-small cell lung cancer (NSCLC) across four completed atezolizumab phase III studies, we consistently observed moderate-to-high positive bias in the predictions from pharmacometric models, particularly with more limited follow-up. By examining the structures of these models and comparing them to observed data, we highlight how the assumed kinetic patterns potentially lead to biased parameter estimation and systemic overestimation of tumor size when applied to immature datasets. In contrast, the TDNODE framework, using deep learning, demonstrated promising early results, exhibiting improved predictive performance in the same evaluations. These findings underscore the critical need to address prediction bias in tumor dynamic modeling with immature data and to consider alternative approaches to established paradigms for certain drug development applications. This study also generally demonstrates the potential of novel methods, such as deep learning, to potentially enhance the reliability of tumor dynamics modeling, especially in challenging early-phase clinical decision-making scenarios.

Chemotherapy-induced nausea and vomiting (CINV) is a common and severe adverse effect of breast cancer (BC) treatment that compromises treatment adherence and quality of life. This meta-analysis aims to assess the prevalence and risk factors of CINV in BC patients, thereby providing clinical insights for its prevention and improvement. Patient/material and methods: Relevant literature was identified through an extensive search of electronic databases from their inception up to July 10, 2025: PubMed, Web of Science, Embase, Cochrane, CNKI, Wanfang, and VIP databases on prevalence rates, odds ratios (OR), and corresponding 95% confidence intervals (CI) were extracted for analysis.

Anticancer peptides (ACPs) are increasingly recognized as promising therapeutic candidates due to their ability to selectively target cancer cells. However, the systematic discovery of novel ACPs, particularly from high-throughput sequencing datasets, remains hindered by technical and methodological limitations. Current prediction frameworks require pre-extracted peptide sequences, involve manual preprocessing, and yield variable results, which restricts their applicability for large-scale, data-driven discovery.

Resistance to 5-fluorouracil (5-FU) remains a major challenge in the treatment of colorectal cancer (CRC). Here, we identify ETS variant transcription factor 7 (ETV7) as significantly upregulated in CRC tissues and cell lines, with elevated expression associated with poor clinical prognosis. Functional assays demonstrate that ETV7 enhances CRC cell proliferation, invasion, and resistance to 5-FU. Mechanistically, ETV7 transcriptionally upregulates CXCL1, leading to increased neutrophil recruitment and enhanced formation of neutrophil extracellular traps (NETs). The resulting NETs-enriched tumor microenvironment promotes tumor aggressiveness and chemoresistance. Pharmacological inhibition of CXCL1 or degradation of NETs effectively attenuates ETV7-driven malignant phenotypes in vitro and in vivo. Collectively, these findings establish an ETV7-CXCL1-NETs axis that contributes to 5-FU resistance in CRC and suggest that targeting this pathway may improve chemotherapy response.

Although targeted therapy has made significant advances in cancer treatment throughout these years, drug resistance still remains a major obstacle. Plenty of evidence has proved that abnormal expression of receptor tyrosine kinase AXL is associated with targeted therapy resistance and poor clinical outcomes. AXL drives drug resistance through diverse mechanisms, including altering tumor cell phenotypes, orchestrating DNA damage response process, promoting the activation of bypass signals, or interacting with other receptor tyrosine kinases. Preclinical and clinical studies have demonstrated that combined inhibition of AXL and the other target can enhance the efficacy of various targeted therapies and improve outcomes for patients with drug resistance. This review summarizes recent advances in the specific roles of AXL in targeted therapy resistance and AXL-targeted treatment strategies. It further explores the potential clinical value of combinatorial approaches involving AXL inhibition and discusses future directions for its application in developing novel targeted therapies and advancing precision oncology treatment. 
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Tumor mutational burden (TMB) and PD-L1 are established biomarkers for guiding immune checkpoint inhibitor (ICI) therapy in advanced non-small cell lung cancer (NSCLC). As ICI use expands into early-stage disease, we explored the feasibility of using TMB, which can be determined via a comprehensive genomic profiling assay along with EGFR and ALK genomic alterations, as a biomarker for outcomes in both neoadjuvant and adjuvant settings. TMB-high status (≥10 mut/Mb) showed a numerically higher, but not statistically significant, rate of pathological complete response among patients receiving neoadjuvant ICI and significantly associated with more favorable time to recurrence in patients receiving adjuvant ICI, particularly among patients with PD-L1 expression <50%. TMB should be considered in future early-stage NSCLC ICI clinical trials to further validate these results.

Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous subtype of breast cancer, with limited treatment options due to the absence of estrogen receptors, progesterone receptors, and human epidermal growth factor receptor 2 (HER2) expression. This characteristic renders TNBC resistant to hormone-based and HER2-targeted therapies, leaving cytotoxic chemotherapy as the predominant strategy and highlighting the urgency for novel interventions. In this study, we investigated the mechanism of action of GL24, a potent 4-(phenylsulfonyl)morpholine-based small molecule with selective tumor suppression effects on metastatic TNBC cells, while being ineffective against TNBC cells derived from the primary tumor site, using gene co-expression analysis. By considering the distinct phenotypic responses induced by GL24, we tailored our co-expression analysis approach, selecting gene pairs that exhibited differential co-expression in effective cells while excluding gene pairs that also showed differential patterns in non-effective cells. Constructing a co-expression network from these differential pairs, followed by enrichment analysis and functional annotation, revealed specific gene interactions and molecular pathways associated with GL24-mediated TNBC inhibition. These insights supported the previously established findings that showed convergence on apoptosis based on differentially expressed genes, while also providing complementary information by highlighting pathways involved in metabolic alterations, proliferation, and migration or invasion. This expanded understanding advances the knowledge of the mechanisms of GL24 in combating TNBC.

While anti-programmed death-1 (anti-PD-1) therapy has revolutionized lung cancer treatment, its efficacy remains limited by an immunosuppressive tumor microenvironment (TME). We therefore investigated whether combining anti-PD-1 inhibitor with catgut embedding at the Zusanli acupoint (CIAA) could enhance anti-tumor immunity by reprogramming the TME in a lung cancer mouse model. Combining in vivo tumor monitoring, multi-parametric immune profiling (flow cytometry, IHC, ELISA), and multi-omics analyses (transcriptomics and metabolomics), we found that the combination therapy was associated with enhanced tumor growth inhibition. This effect correlated with a comprehensive TME transformation: conversion to an immunologically active state with increased effector immune cell infiltration (CD8⁺ T, CD4⁺ T, B cells, macrophages) and decreased regulatory T cells, coupled with suppression of pro-tumorigenic factors (VEGF, IL-6). Integrated omics analysis suggests that the combined treatment may modulate tumor-stroma interaction pathways (e.g., PI3K-Akt, focal adhesion) and rewire immunometabolic networks (e.g., tryptophan metabolism). Our study provides hypothesis-generating correlative data positioning CIAA as a potential adjunct capable of remodeling the TME to potentiate anti-PD-1 therapy in lung cancer.

Melanoma, an aggressive cancer with a poor prognosis, is difficult for early diagnosis, and there are limited drug treatments. Biologically active molecules, especially polyphenols and flavonoids, have a great therapeutic potential; however, their applications are limited by low aqueous solubility and bioavailability.

Nitrosylcobalamin (NO-Cbl) is a vitamin B12 analog designed to exploit the "Trojan horse" vulnerability created by the heightened need of cancer cells for cobalamin and one-carbon metabolism. Building on our recent biophysical studies confirming the affinity of NO-Cbl for intrinsic factor, this work aimed to investigate the mechanistic basis for the selective anticancer activity of NO-Cbl through the cobalamin transport axis and lysosomal processing.

Monoclonal antibodies (mAbs) targeting immune checkpoint pathways such as programmed cell death protein 1 (PD-1)/PD-L1 are central to modern immunotherapy, yet scalable methods to assess their functional blockade remain limited. We present a bead-based flow cytometry assay for quantifying the inhibition of PD-1/PD-L1 interaction by antibodies. Recombinant human PD-1 protein was conjugated to polystyrene beads, and its interaction with recombinant human PD-L1 protein labeled with a fluorochrome was measured. The inhibitory activity of an anti-PD-L1 mAb was quantified based on their ability to disrupt this interaction. The assay was validated for intra- and inter-assay precision, in addition, functionality was confirmed using a T cell coculture assay. The assay demonstrated dose-dependent inhibition by the αPD-L1 mAb, with a calculated mean IC50 of 3.122 µg/mL. The method proved to be reproducible for the determination of antibody blocking activity, with relative standard deviation (RSD) < 20% between three independent runs. At the concentration approximating the IC50 detected on the bead assay, the antibody significantly restored CD69 expression on the T cell surface (p = 0.0001) in a coculture in vitro system. In addition, the methodology could successfully distinguish the blocking capacity of two anti-PD-L1 antibodies with different affinities. This high-throughput compatible platform offers a reliable tool for screening PD-1/PD-L1 blocking antibodies, supporting immunotherapy discovery and development.

This study aimed to evaluate the predictive value of the hemoglobin, albumin, lymphocyte, and platelet (HALP) score for pulmonary infections in patients with non-small cell lung cancer (NSCLC) undergoing chemotherapy.