Traction-assisted endoscopic submucosal dissection (TA-ESD) using dental floss substantially reduces procedural times without increasing adverse event rates. However, few studies have described the clinical outcomes following TA-ESD for prepyloric and pyloric neoplasms. Therefore, this study aimed to investigate the clinical outcomes of patients treated with TA-ESD for prepyloric and pyloric neoplasms.

We retrospectively analyzed the data of 208 patients who underwent ESD for prepyloric and pyloric neoplasms between 2016 and 2021 at Pusan National University Hospital. The patients were categorized into the conventional ESD (C-ESD) (n=173) and TA-ESD (n=35) groups. One-to-two propensity score matching (PSM) was performed between both groups.

In the unmatched cohort, compared with the C-ESD group, the TA-ESD group had a significantly greater rate of resection defects exceeding half of the circumference of the pylorus (45.7% vs 27.2%, p=0.048), a lower complete resection rate (85.7% vs 97.1%, p=0.014), a higher positive vertical margin rate (5.7% vs 0.0%, p=0.028), and a longer procedural time (34.2±26.1 minutes vs 25.3±22.0 minutes, p=0.036). After PSM, the TA-ESD group required a significantly shorter procedural time than did the C-ESD group (30.1±18.1 minutes vs 40.4±23.7 minutes, p=0.031). No statistically significant differences were observed in other variables between the two groups.

Compared to C-ESD, TA-ESD significantly shortened the procedural time for treating prepyloric and pyloric neoplasms. However, no significant differences were observed in the complete resection rate or in adverse events between the two groups.

Hepatocellular carcinoma (HCC) is a major cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Apoptin, encoded by the VP3 gene of the chicken anemia virus, selectively induces apoptosis in cancer cells while sparing normal cells. We previously engineered a recombinant oncolytic adenovirus (Ad-VP3) capable of high-level Apoptin expression in tumor cells. In this study, we evaluated the antitumor activity of Ad-VP3 in the human HCC cell line Hep3B. CCK-8, crystal violet, Hoechst 33342 staining, flow cytometry, and tumor sphere formation assays revealed that Ad-VP3 inhibited cell viability, proliferation, and stemness. Annexin V staining, JC-1/TMRM probes, and Western blot analysis demonstrated induction of apoptosis and reduction of mitochondrial membrane potential. Wound-healing, Transwell, and BioCoat invasion assays, along with Western blotting, confirmed suppression of migration and invasion. Ad-VP3 significantly inhibited the viability, proliferation, migration, and invasion of Hep3B cells in a time- and dose-dependent manner. It induced mitochondrial membrane potential loss and apoptosis, downregulated stemness-related proteins (ALDH1A1, KLF4, and Sox2), and suppressed epithelial-mesenchymal transition markers (Snail, Twist1, Slug, Vimentin, and MMP-9), indicating strong antitumor activity. The recombinant oncolytic adenovirus Ad-VP3 exerts potent antitumor effects on hepatocellular carcinoma cells by inducing mitochondrial dysfunctionmediated apoptosis and impairing stemness and metastatic potential, suggesting its promise as a novel therapeutic strategy for HCC.

This study examined the long-term transcriptomic reprogramming in peripheral blood mononuclear cells (PBMCs) of severe COVID-19 patients and its effects for cancer development. RNA sequencing was conducted on PBMCs obtained from healthy controls, COVID-19 patients without pneumonia, and COVID-19 patients exhibiting severe pneumonia one year post-infection. Differential gene expression analysis identified a sustained pro-oncogenic molecular signature, especially among severe COVID-19 patients. Functional enrichment analysis revealed a substantial enrichment of cancer-associated pathways, encompassing apoptosis, viral carcinogenesis, and transcriptional dysregulation. Notably, the autophagy-related gene SQSTM1/P62 was recognized as a distinctive hub gene within the severe COVID-19 patients, interacting with pivotal genes associated with inflammation, apoptosis, and cancer advancement. Survival analysis demonstrated that elevated expression of COVID-19-associated hub genes correlated with unfavorable prognosis in various cancer types, including adrenocortical carcinoma, bladder urothelial carcinoma, and brain lower-grade glioma. These findings indicate that severe COVID-19 infection may establish a systemic milieu favorable to cancer development or recurrence, highlighting the necessity of prolonged oncological monitoring in these patients. Finding specific molecular targets and pathways can help us understand how COVID-19 might be linked to a higher risk of cancer.

Glutamine addiction in human melanoma is a premier example of the cancer hallmark of metabolic reprogramming. In the present study, we investigate the presence of metabotropic glutamate receptor 1 (mGluR1/GRM1) and glutaminase (GLS1/GLS) in canine oral malignant melanoma (OMM) and those of low malignant potential, termed histologically well-differentiated melanocytic neoplasm of the lips and oral mucosa (HWDMN). We used immunohistochemistry (IHC) and qPCR to evaluate mGluR1 and GLS1 protein expression and RNA expression, respectively. Nearly 20% of OMM cases had an mGluR1 IHC score ≥ 1, while none of the HWDMN cases had any expression. Due to low IHC expression, only 10 cases were selected for determination of GRM1 RNA expression, and none were positive. GLS RNA expression did not differ between OMM and HWDMN. A GLS1 IHC score ≥ 1 was significantly higher in OMM cases and highly specific (95%) for correctly identifying tumors with a Ki67 index ≥ 19.5. These results may have been negatively impacted by use of a brown chromogen for IHC labeling among background pigment, particularly in HWDMN. Ultimately, these findings suggest that canine OMM does not heavily rely on mGluR1 for tumorigenesis or progression. Differential GLS1 protein expression warrants further investigation with protein quantification.

Mesenchymal stromal/stem cells (MSCs) appear in many studies, and their utilization is a developing area of study. Scientists are investigating the abilities of MSCs and the possibilities of using them in anticancer therapies, as well as combining such therapies with those currently used clinically. This article provides an overview of MSC-based therapeutic strategies, assessing their potential in the context of cancer treatment. These are engineering or biotechnological approaches that utilize the natural properties of MSCs in a targeted and therapeutically effective manner. The review focuses on innovative methods such as genetic modifications to express desired therapeutic molecules, highlighting their potential applications in clinical practice. Innovative strategies include modifications to express anticancer proteins, miRNA (microRNA), siRNA (small interfering RNA), lncRNA (long non-coding RNA), and circRNA (circular RNA) that induce specific effects, as well as the delivery of therapeutic genes and oncolytic viruses. However, further studies are required to address the existing impediments, which are also discussed in this review. A major challenge in the clinical application of MSCs is their bidirectional role, an issue that remains a central focus of current research and is examined in this article.

Non-muscle invasive bladder cancer (NMIBC) has limited therapeutic options and high recurrence rates. Photoimmunotherapy (PIT) enables targeted tumor ablation using antibody-photosensitizer conjugates and light activation. We evaluated EGFR, Nectin-4, and TROP-2 as PIT targets using cysteine-modified antibodies conjugated to the photosensitizer WB692-CB2.

Antibodies derived from Cetuximab (Cmb, anti-EGFR), Enfortumab (Enf, anti-Nectin-4), and Sacituzumab (Sac, anti-TROP-2) were engineered with T120C and D265C mutations in the heavy chains for site-specific dye conjugation. Binding of the conjugates to BC cells was tested by flow cytometry and light-induced cytotoxicity of the conjugates, alone or in combination, was assessed by viability assays following irradiation.

Cysteine-modified antibodies were produced as intact IgG molecules and were efficiently conjugated with WB692-CB2 without loss of antigen specificity. Sac^T120C/D265C-WB692-CB2 showed the highest target binding and achieved near-complete cell killing at a red-light dose of 32 J/cm². Cmb^T120C/D265C-WB692-CB2 required a fourfold higher light dose for comparable efficacy, while Enf^T120C/D265C-WB692-CB2 demonstrated lower potency. No cytotoxicity was observed in antigen-negative cells. Combined treatment enhanced cytotoxicity, indicating additive phototherapeutic effects.

Our findings suggest that PIT targeting EGFR, Nectin-4, or TROP-2 merits further preclinical development as a targeted therapeutic approach for NMIBC, including potential combinatorial or personalized strategies.

Chondroitin sulfate (CS)-based nanoparticles have emerged as versatile and multifunctional platforms for cancer therapy, integrating effective drug delivery with diagnostic capabilities. Their ability to exploit the enhanced permeability and retention (EPR) effect enables selective accumulation within tumor tissues, while surface modification with CS enhances targeting efficiency through strong conformational and electrostatic affinity for CD44 receptors, which are overexpressed in many cancer cells. In addition, CS interacts with E-selectin, providing dual-targeting capabilities superior to those of other polysaccharides such as hyaluronic acid. A wide variety of CS-derived nanostructures-including micelles, nanogels, hybrid liposomes, and CS-drug conjugates-have shown great potential not only in drug delivery but also in advanced therapeutic modalities such as photodynamic, sonodynamic, and immunotherapy. This review discusses recent advances (2020-2025) in CS-based nanoplatforms for cancer therapy, with particular emphasis on the role of CS within nanostructures. It highlights how the functionalization of nanoparticles with CS represents a powerful strategy to improve colloidal stability, pharmacokinetics, and receptor-mediated uptake, thereby enabling controlled, site-specific drug release and reducing off-target toxicity. Ultimately, these advances open new opportunities for cancer treatment, with the potential for bench-to-clinic translation through the integration of AI-guided design, organelle-specific targeting, multi-pathway modulation, and immune system engagement.

Background: Photodynamic therapy (PDT) with indocyanine green (ICG) offers a promising, minimally invasive approach for selective tumor ablation in breast cancer. This study investigates the stability, cellular uptake, and photodynamic efficacy of ICG in CRL-2314 breast cancer cells compared with HTB-125 normal mammary epithelial cells, with a focus on population density-dependent cytotoxicity. Cells were incubated with 50 µM ICG for 1-3 h and irradiated with a 780 nm laser. Viability was assessed using the Muse^® Count & Viability Kit at 1-3 h. ICG uptake kinetics were quantified by flow cytometry. Singlet oxygen (¹O₂) generation was confirmed via 1270 nm phosphorescence and Stern-Volmer quenching. ICG uptake saturated at 2 h (89 ± 4% positive cells), with lysosomal colocalization. In CRL-2314 cells, viability decreased density- and time-dependently, reaching 40 ± 5% at 1 × 10⁶ cells after 3 h (p < 0.0001), with IC₅₀ = 23.8 µM (95% CI: 20-27 µM) at 72 h. HTB-125 cells maintained > 80% viability even at 300 µM, yielding no IC₅₀. Two-way ANOVA confirmed cell line specificity (F = 428.7, p < 0.0001). ICG-PDT exhibits high selectivity and density-dependent efficacy against CRL-2314 cells with minimal toxicity to HTB-125, driven by enhanced uptake, sustained ¹O₂ production, and differential metabolic responses. These findings support ICG-PDT as a precision modality for breast cancer therapy.

Chemoresistance is the leading cause of mortality in cancer patients. The poor clinical prognosis and limited therapeutic options for acute myeloid leukemia (AML) patients demand the development of new therapeutic strategies capable of overcoming chemoresistance and avoiding toxic side effects in normal cells. Sodium caseinate (SC), a derivative of casein protein found in milk, has demonstrated a dual role: it inhibits the proliferation of several murine AML cell lines while promoting the proliferation of normal hematopoietic cells. Furthermore, we previously showed that SC can modulate the expression of genes associated with chemoresistance in mouse cells. However, its biological effects on cytarabine-resistant human leukemia cells remain unclear. Here, we developed the HL60-CR50 subline, resistant to cytarabine, and investigated the effects of SC. We demonstrated that SC significantly reduced cell proliferation, decreased SIRT1 levels, increased acetylated p53, activated cleaved caspase-3, and enhanced apoptosis in cytarabine-resistant cells. These findings suggest that SC might have potential as a therapeutic adjuvant for AML, providing efficacy in chemoresistant cases compared with cytarabine treatment alone.

Multidrug resistance (MDR) presents a significant challenge in the treatment of glioblastoma. We evaluated six novel adamantane-sclareol hybrids that integrate a natural labdane diterpene scaffold with an adamantane moiety to address this issue. Compounds 2, 5, and 6 demonstrated the ability to bypass P-glycoprotein (P-gp)-mediated resistance in resistant U87-TxR cells and induced collateral sensitivity, with compound 2 exhibiting the highest selectivity for glioblastoma compared to normal glial cells. Mechanistic studies revealed that compounds 2 and 5 selectively triggered early apoptosis in MDR cells, significantly elevated levels of H₂O₂ and peroxynitrite, and disrupted mitochondrial membrane potential. Additionally, these compounds altered the expression of key genes involved in glutathione (GSH) and thioredoxin (Trx) antioxidant defense systems and increased ASK1 protein levels, indicating the activation of ROS-driven apoptotic signaling. Both compounds inhibited P-gp function, leading to enhanced intracellular accumulation of rhodamine 123 (Rho 123) and synergistically sensitized U87-TxR cells to paclitaxel (PTX). A preliminary Rag1 xenograft study demonstrated that compound 5 effectively suppressed tumor growth without causing significant weight loss. Collectively, these findings position adamantane-sclareol hybrids, particularly compounds 2 and 5, as promising strategies that exploit an MDR-associated reactive oxygen species (ROS) vulnerability, combining selective cytotoxicity, redox disruption, and P-gp modulation to eliminate resistant glioblastoma cells and enhance the efficacy of chemotherapeutics.