Immune checkpoint inhibitors (ICIs) can essentially treat cancer but only in a small subset of patients. Treatment strategies capable of effectively and robustly sensitizing refractory patients to ICIs represent a highly coveted yet unmet clinical need. In this study, we identified DJ-1 as a negative T cell regulator. DJ-1 knockout boosts antitumor immunity and significantly potentiates PD-1 and TIM-3 blockades in murine cancer models. Single-cell sequencing of tumor-infiltrating CD45+ cells revealed that DJ-1 deficiency indirectly activates T cells by reprogramming macrophages. Mechanistically, loss of DJ-1 increases reactive oxygen species (ROS) in macrophages, activating NF-κB/STAT3 signaling to promote differentiation into Cxcl9+ immune-stimulatory phenotypes while reducing immune-suppressive Spp1+ macrophages. Notably, this reprogramming may be stable across tumor microenvironments because the transplanted DJ-1-deficient macrophages maintain T cell-activating capacity. Pharmacological inhibition of DJ-1 by disulfiram markedly potentiated antitumor efficacy of PD-1 blockade. This designates DJ-1 as a promising target for overcoming immune checkpoint resistance and optimize combination therapies.

Oral mucositis is a frequent adverse effect of chemotherapy that significantly affects patients' quality of life and treatment continuity. Despite its clinical relevance, effective preventive strategies remain limited. This study aims to compare the efficacy and safety of betamethasone mouthwash with those of sodium gualenate hydrate mouthwash for preventing chemotherapy-induced oral mucositis.

Chemotherapy-induced hypersensitivity reactions (CIHSRs) are common in outpatient infusion settings, requiring infusion nurses to recognize and respond quickly for optimal outcomes. This article supports novice nurses by outl.

Chemotherapy-induced peripheral neuropathy (CIPN) is a common side effect of cancer therapy. Patients who experience CIPN can develop symptoms in their hands and feet, which may affect function and quality of life. Cryotherap.

Patients with gynecologic cancer may receive multiple lines of carboplatin therapies. Risk of a hypersensitivity reaction (HSR) increases after more than six doses and when resuming treatment after a platinum-based treatment break. This can lead to the discontinuation of therapy or to a complicated and time-consuming desensitization protocol for future cycles. Premedications or extended infusion times have shown varied results in reducing HSRs.

In this study, hydrazine ligands were synthesized from thiophene-2-carboxylic acid/benzo[b]thiophene-2-carboxylic acid hydrazides and 1,3-diphenyl-1H-pyrazole-4-carbaldehyde, along with their Co(II), Ni(II), Cu(II), and Zn(II) complexes. The synthesized compounds were thoroughly characterized and originally evaluated for their anticancer and antimicrobial potentials. Building on these findings, the compounds were evaluated against A549 and DU145 cancer cells, the IMR-90 cell line, and clinically relevant microbial strains. Among them, the Cu(II) and Zn(II) complexes (9, 10) emerged as most active, with the Cu(II) complex (9) showing pronounced anticancer efficacy against both cancer cell lines while maintaining lower sensitivity toward IMR-90 cells. Remarkably, the Cu(II) (9) and Zn(II) (6, 10) complexes exhibited outstanding antimicrobial activity, with MIC values (0.0052-0.0104 µmol/mL) comparable to those of established reference drugs, underscoring their strong therapeutic potential. Molecular docking supported the observed bioactivities, with compound (9) showing strong binding to the 4ZXT protein (-9.98 kcal/mol). Similarly, compound (10) revealed favorable binding with target protein, yielding docking scores of -9.43 kcal/mol. These interactions confirm the compounds' strong biological affinity and therapeutic potential. ADMET results indicate favorable pharmacokinetics, supporting their drug-likeness. Their broad bioactivity provides a solid basis for future clinical studies and novel drug development.

Telomerase is active in the majority of high-risk neuroblastomas, a pediatric tumor associated with poor patient outcomes. In other cancer types, resistance to immune checkpoint blockade was overcome by induction of telomere dysfunction using the telomerase substrate precursor 6-thio-2'-deoxyguanosine (6-thio-dG). Here, we explored whether induction of telomere dysfunction improves the anti-tumor efficacy of immune checkpoint inhibition in neuroblastoma. 6-thio-dG treatment induced the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway and programmed cell death ligand-1 (PD-L1) expression in murine neuroblastoma cells in vitro. In a MYCN;ALKF1174L-driven transgenic neuroblastoma mouse model, 6-thio-dG treatment delayed tumor growth and prolonged survival. Treatment with anti-PD-L1 also led to growth delay and improved survival, which occurred; however, only after an initial lag phase. Combination with anti-PD-L1 improved the anti-tumor effects of 6-thio-dG and overcame the initial lag phase of anti-PD-L1 treatment. Mechanistically, 6-thio-dG combined with anti-PD-L1 treatment induced cGAS and PD-L1 expression and promoted immune cell infiltration in the tumors. Our findings suggest that 6-thio-dG treatment activates the cGAS-STING pathway in neuroblastoma and that induction of telomere dysfunction in combination with immune checkpoint blockade boosts intratumoral immune cell infiltration and improves survival in a high-risk neuroblastoma mouse model.

Hyperthermia has been used as an adjuvant therapy alongside radiotherapy and chemotherapy for cancer treatment in some countries. However, since the 2000s, growing evidence has indicated that hyperthermia exerts regulatory effects not only on cancer cells but also on stromal immune cells and the research interest in this topic has grown notably in the current "era of immunotherapy". Of particular interest to oncoimmunologists and hyperthermia researchers, recent studies have shown that hyperthermia modulates the expression of a wide range of immune checkpoint and co-stimulatory molecules. In addition to the PD-1/PD-L1 and CTLA-4/CD80/CD86 checkpoints previously reported and intensively discussed in existing reviews, recent studies indicate that hyperthermia exerts a broader regulatory effect on many other checkpoint and co-stimulatory molecules, include TIGIT/CD155, Tim-3/Gal-9, OX40/OX40L, and 4-1BB/4-1BBL on T cells, CD47/SIRPα on macrophages, and CD40/CD40L on dendritic cells. The present review aims to provide a complementary update, focusing specifically on recent advances in understanding how hyperthermia regulates the expression of these newer targets, as well as preclinical evidence for combining hyperthermia with novel therapeutic agents targeting these molecules. The insights gained from these preclinical studies could serve as a valuable foundation for future experimental investigations and clinical translation.

Urological Cancers pose a serious threat to human health and represent a major challenge to healthcare systems worldwide. Among these, bladder cancer (BC), prostate cancer (PCa), and renal cancer (RC) are the most prevalent. Primary clinical management involves local or radical resection. However, for patients with advanced or inoperable disease, as well as those at high risk of post-surgical recurrence, chemotherapy remains an essential alternative or adjuvant treatment. Nevertheless, the lack of tumor targetability leads to low bioavailability and significant side effects of drugs, limiting the clinical application of chemotherapeutic agents. In recent years, plant lectins have gained significant attention in cancer therapy research owing to their unique tumor-recognition capabilities. Unlike traditional chemotherapeutic agents, they inherently bind specifically to abnormal glycans on urological tumor cells, endowing them with unparalleled targeted therapy advantages and great potential to address traditional chemotherapy's core limitations and improve clinical outcomes. This paper presents a systematic, comprehensive and structured review with integrated critical analysis of the progress in this field. It first describes the clinical treatment methods for common urinary system tumors, including an analysis of the importance and limitations of chemotherapy. It then elaborates on the biological activities and antitumor mechanisms of plant lectins, highlighting on recent advances in the use of native lectins and lectin-modified drug delivery systems (DDS) for treating these malignancies. Finally, based on full collation and overall understanding of the existing literature, the application limitations of plant lectins are summarized, and their prospects are discussed.

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by thrombosis in arteries, veins or small blood vessels, and/or obstetric APS (OAPS), as well as persistent positive antiphospholipid antibodies. In recent years, some authors have proposed that the pathogenesis of APS is closely related to activation of vascular endothelial cells, immune cells, and complement activation. However, further exploration is still needed. Previous studies have shown that the mammalian target of rapamycin (mTOR) is associated with pro-inflammatory and pro-coagulant processes. This indicates that the activation of the mTOR signaling pathway may function as an intermediate mediator, causing immune disorders, thereby leading to thrombosis and OAPS. Therefore, we should correctly understand the potential pathogenic role of the mTOR signaling pathway in APS, which will be more conducive to clinicians' understanding of the pathogenesis of this disease and the search for new therapeutic targets. We hope this can open up a new window for the management of APS.

Terminalia macroptera (Combretaceae) is an important medicinal plant in the traditional pharmacopeia in most tropical areas, where its different parts are used in treating illnesses including cancer.

Pharmacovigilance has revealed an alarming correlation between certain medications and a higher risk of cancer. In this narrative review, included research from 2020 to 2025, along with a few seminal older studies, so that it provides a clear picture of which drugs actually set off cancer and mechanisms involved at the molecular level. An extensive literature review of the subject was designed on PubMed, Embase, Scopus, and Web of Science using systematic search. Search words and phrases included: "Carcinogenic drugs," "drug-induced cancer," "medication-induced carcinogenesis," "immunosuppressant cancer risk," "hormone therapy and cancer," "chemotherapy-induced secondary malignancies," and names of relevant drugs.

Skin rash is the most common adverse effect in patients with cancer receiving epidermal growth factor receptor inhibitors (EGFRIs), which can impair quality of life and lead to treatment discontinuation. Numerous primary studies have explored factors that may predict the development of skin rash. However, the wide range of variables and substantial heterogeneity among these studies limit the availability of high-quality, synthesised evidence. A comprehensive scoping review is therefore warranted to systematically map and synthesise the risk factors for EGFRI-induced skin rash in patients with cancer.

Despite advancements in multimodal therapies, oral squamous cell carcinoma (OSCC) continues to exhibit poor clinical outcomes, particularly in advanced and recurrent cases. Recent studies have identified the calcium-binding protein S100A2 as a critical mediator of OSCC progression and resistance to therapy. Our prior work demonstrated that cytoplasmic overexpression of S100A2 in oral cancer patients is associated with tumor recurrence and reduced survival. Given its reported role in promoting epithelial-to-mesenchymal transition (EMT), cellular proliferation, and invasiveness, we investigated the in vitro functional impact of S100A2 inhibition in OSCC.

Breast cancer (BC) is a complex illness that affects millions of women globally. As its incidence rises, new treatment strategies are needed. Veratrum viride, a traditional medicinal herb, is known for its therapeutic potential, yet its molecular mechanism of action against BC remains unclear. The purpose of this preliminary investigation is to assess V. viride's anti-breast cancer potential by identifying its active compounds and using bioinformatics techniques to clarify their multi-target mechanisms.

Both CDK2 (cyclin-dependent kinase 2) and EGFR (epidermal growth factor receptor) play significant roles in the development and progression of colorectal cancer. In vitro studies of several hydroxyxanthone derivatives for the treatment of WiDr cancer cell lines have revealed potential anticancer activity against colorectal cancer. The present study aims to identify hydroxyxanthone derivatives as potential drug candidates for colorectal cancer treatment through an in silico approach.

Cervical cancer is the second leading cause of mortality in women globally, with its incidence increasing due to multidrug resistance (MDR) and adverse side effects associated with chemotherapeutic agents. Hence, this study was carried out to investigate the selective cytotoxicity and apoptotic induction potential of Buddleja polystachya leaf diethyl ether (BPL-DE) extract on cervical cancer HeLa cell lines.

The aim of the study was to determine how the chemotherapeutic alkylating agent dacarbazine, together with the application of the miR-204-5p mimic in vivo, affects the presence of disseminated melanoma cells in distant organs - the lungs and liver.

Monastrol, a DHPM-based Eg5 inhibitor with well-known antiproliferative activity but limited therapeutic potential due to poor solubility and low bioavailability, was selected as the lead compound for the design of styryl-modified 3,4-dihydropyrimidin-2(1H)-ones with an improved pharmaceutical profile. Twelve derivatives (10-21) were synthesized via the Biginelli reaction and evaluated for cytotoxicity in HeLa and MCF-7 cells. Styryl derivatives 16 and 17 emerged as the most active. In HeLa cells, derivatives 17 (IC50 = 1.3 µM) and 16 (IC50 = 3.7 µM) were approximately 85-fold and 30-fold more potent than monastrol (IC50 = 111 µM), respectively. In MCF-7 cells, derivatives 16 and 17 displayed 18- to 20-fold higher potency than monastrol, respectively. Biological results also indicate that styryl derivatives 16 and 17 induce apoptosis in both HeLa and MCF-7 cells. In HeLa cells, activation of caspase-8, -9, and -3 suggests the involvement of both intrinsic and extrinsic pathways. In contrast, in MCF-7 cells, the increased expression of p53 and p21, together with PARP cleavage, suggests a p53-dependent apoptotic response. Derivatives 16 and 17 emerged as promising Eg5 inhibitors from docking studies, but their poor aqueous solubility (0.2-0.7 µM), despite high biological stability, highlights the need for formulation strategies to improve drug-like properties.

Antineoplastic treatment commonly leads to nausea and vomiting (NV), which considerably affects the quality of life and adherence to therapy of patients. This study aimed to analyze the incidence of NV induced by antineoplastic agents using the Japanese Adverse Drug Event Report (JADER) database and to explore novel antiemetic therapies for oral antineoplastic agents.