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.

Ribociclib is a CDK4/6 inhibitor used to treat HR+/HER2- breast cancer. Despite regulatory documents suggesting that ribociclib may inhibit both CYP3A and OATP1B-type transport in vitro, it is unclear whether CDK4/6 inhibitors interact with these mechanisms in vivo. Based on two cases of severe rhabdomyolysis in patients taking a CDK4/6 inhibitor and simvastatin, a CYP3A and OATP1B substrate, we tested the hypothesis that CDK4/6 inhibitors may precipitate drug-drug interactions through these mechanisms.

Malignant pleural effusion (MPE) portends poor prognosis in advanced cancer. Strategies that integrate potent tumor killing with immunosuppressive microenvironment reprogramming are crucial for the treatment of MPE. Studies show that irradiated tumor cell-derived microparticles (RT-MPs) possess natural tumor-targeting cytotoxicity and innate immune activation properties. To further boost the tumoricidal effects of RT-MPs, we developed innovative chemoradiotherapy-integrated tumor cell-derived microparticles (CR-MPs) by loading RT-MPs with chemotherapeutic agents, including methotrexate (MTX), monomethyl auristatin E (MMAE), or doxorubicin (DOX). CR-MPs exhibited superior tumoricidal activity over both RT-MPs and free drugs against a range of tumors. Specifically, MTX-loaded CR-MPs (CR-MPs@MTX) triggered mitochondrial oxidative stress and immunogenic ferroptosis in tumor cells, while directly reprogramming macrophages toward the M1 phenotype and stimulating dendritic cells via cGAS-STING/NF-κB pathway activation. In murine MPE models, CR-MPs effectively suppressed tumor progression, extended survival, and demonstrated favorable biosafety. When combined with immunotherapy, this approach achieved a cure rate of up to 70%, induced durable immunological memory, and retained efficacy against chemotherapy-resistant tumors. This study establishes CR-MPs as a novel platform with robust therapeutic efficacy against MPE, highlighting their translational potential as a precision concurrent chemoradiotherapy strategy for MPE management in clinical settings.

Although cisplatin (CDDP) is widely employed in combination immunotherapy, no CDDP-based regimen has shown a survival benefit when treating the ovarian cancers. This is mainly because the impact of CDDP on immunotherapy is not fully understood. A critical gap concerns how CDDP reshape the tumour microenvironment, especially through extracellular vesicles (EVs)-mediated communication. In this work, using human and murine ovarian cancer cells as a model, we demonstrate that CDDP boosts the secretion of EVs from cancer cells, while exerting no such effect on non-cancerous cells. These CDDP-induced tumour-derived EVs, in turn, drive the differentiation of CD4+ T cells towards immunosuppressive regulatory T cells (Treg cells), which are known to limit the efficacy of immunotherapy. Based on next-generation sequencing, a significant enrichment of miR-181a-5p was identified in CDDP-induced tumour-derived EVs, and further functional studies confirmed that this microRNA promoted Treg cell differentiation via suppressing sirtuin 1 (SIRT1), a key regulator of the transcription factor forkhead box protein P3 (FOXP3). Importantly, inhibition of miR-181a-5p abrogated the Treg-promoting effect of CDDP-induced tumour-derived EVs, a finding further validated in vivo, where blockade of miR-181a-5p not only impaired Treg differentiation but also restored T-cell-mediated antitumour immunity and restrained tumour growth. Together, these findings uncover a previously unrecognised mechanism by which CDDP exacerbates immunosuppression via miR-181a-5p-enriched EVs and suggest that targeting this pathway could improve the therapeutic efficacy of combination immunotherapy in ovarian cancer.

To elucidate how ALX Homeobox 4 (ALX4) modulates cisplatin sensitivity via DNA damage regulation in breast cancer (BC), this study explored the established role of mRNA-mediated DNA repair in driving chemoresistance.

This study designs and synthesizes a series of vitexin derivatives to evaluate their inhibitory activity against human colon cancer HCT-116 cells and to explore the underlying mechanisms. Antiproliferative effects are assessed using the CCK-8 assay. Molecular docking with Schrödinger software and molecular dynamics simulations analyze interactions between candidate compounds and CDK1. Cell cycle distribution is determined by flow cytometry, while western blotting, immunofluorescence, and CDK inhibition assays evaluate CDK1/cyclin B expression. Most derivatives show stronger inhibitory activity than the parent compound. Vitexin exhibits an IC₅₀ of 210.23 ± 40.89 μM, whereas Butylated vitexin (M3) displays markedly enhanced potency (IC₅₀ = 8.73 ± 1.40 μM) and induces G₂/M phase arrest. Molecular docking reveals strong binding affinity between M3 and CDK1 (Docking score -10.127), and molecular dynamics simulations confirm the stability of the M3-CDK1 complex with inhibitory effects comparable to flavopiridol (FP). Furthermore, M3 downregulates CDK1/cyclin B expression in HCT-116 cells (IC₅₀ = 9.83 ± 2.65 μM). M3 may suppress HCT-116 cell proliferation by targeting CDK1/cyclin B and inducing G₂/M phase arrest.

This network meta-analysis evaluated the efficacy of 5-hydroxytryptamine-3 (5-HT3) receptor antagonists, with or without Dexamethasone (D), for preventing chemotherapy-induced nausea and vomiting (CINV) in patients undergoing highly emetogenic chemotherapy (HEC) who were limited to these regimens.

Cancer stem cells (CSCs) contribute to an immunosuppressive microenvironment through complex mechanisms and tumor-immune interactions. However, the key determinants of CSC characteristics in driving tumor progression, immune suppression, and response to ICIs remain unclear and require systematic investigation. This study developed a quantitative systems pharmacology (QSP) model covering various CSC properties, thereby capturing the temporal dynamics and CSC-immune interactions in triple-negative breast cancer (TNBC). Using the unified longitudinal dataset of tumor growth, CSC frequency, and immune cell dynamics that we obtained from BALB/c mice bearing wild-type or Cd274-knockout 4T1 cells under various inoculation conditions, which provides multi-dimensional insights into CSC-related biology, the QSP model was calibrated and validated. Simulations and sensitivity analysis indicated that TNBC tumors with strong stemness exhibited significantly accelerated tumor growth and reduced infiltration of cytotoxic immune cells such as cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. These were associated with CSCs' enhanced self-renewal capacity, stemness maintenance, secretion of transforming growth factor beta (TGF-β) and vascular endothelial growth factor (VEGF), and PD-1/PD-L1-mediated immunosuppression. ICIs showed minimal efficacy in tumors with enhanced stemness, which was also linked to the aforementioned characteristics. Both the administration sequence and initiation timing of ICIs differentially influenced the therapeutic outcomes. These findings elucidate the roles of CSCs in TNBC progression, tumor immunity, and ICI efficacy while identifying the key underlying CSC characteristics, suggesting the potential value of assessing CSC biomarkers or abundance before ICI treatment and support the development of ICIs and anti-CSC combination therapies.

This study aimed to investigate institutional factors associated with the clinical implementation of gonadotropin-releasing hormone (GnRH) analogs for ovarian protection in women receiving chemotherapy among fertility preservation facilities in Japan.

Multiple myeloma (MM) is an incurable hematological malignancy with excessive bone marrow infiltration and pro-inflammatory microenvironment. In clinical practice, melphalan, an alkylating agent, and dexamethasone, a glucocorticoid widely used in MM regimens, provide clinical benefits. However, their efficacy is still limited by systemic toxicity, poor tumor selectivity, and the difficulty maintaining a predefined drug ratio at the tumor site. To address these challenges, we designed a supramolecular peptide-drug conjugate prodrug nanosystem (HMD NPs) composed of β-cyclodextrin-modified hyaluronic acid (HA-β-CD) scaffold and dual-drug conjugates, Ada-M-GFLG-D. In this design, MA and DEX are conjugated via a cathepsin B-cleavable GFLG linker and functionalized with adamantane for host-guest assembly, which allows co-delivery of the two drugs at a fixed 1:1 stoichiometric ratio. The resulting HMD NPs exhibited excellent stability, efficient cellular uptake. Ada-M-GFLG-D remains encapsulated within nanoparticles under physiological conditions. However, upon exposure to MM-mimicking intracellular conditions, HMD NPs undergo an enzyme-activation process, rapidly releasing both drugs. Cellular experiments demonstrate potent anti-tumor effects and significant downregulation of inflammatory pathways. In animal models, HMD NPs markedly suppress tumor progression, reducing bone marrow infiltration, relieving osteolytic damage, and showing favorable biocompatibility. These findings provide a promising strategy for improving therapeutic efficacy against MM.

An exopolysaccharide (EPS) isolated from Enterococcus faecium was functionalized with folic acid (FA) via carbodiimide-mediated coupling using 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride and N-Hydroxysuccinimide. This reaction facilitated the formation of an amide linkage between the primary amine group of FA and the carboxyl group of the EPS. The synthesized FA-functionalized EPS (FA-EPS) was further incorporated into a photothermally active coordination polymer matrix along with an anticancer drug to achieve a controlled drug release system targeting SH-SY5Y neuroblastoma cells. Physical interactions between polar groups of FA-EPS and drugs, including hydrogen bonding, electrostatic forces, and π-π stacking, enable efficient drug encapsulation within the FA-EPS matrix, resulting in controlled and sustained drug release that enhances therapeutic efficacy and minimizes toxicity. Moreover, the integration with the coordination polymer imparted photothermal properties, resulting in a synergistic enhancement of apoptosis through combined chemo-photothermal therapy. Flow cytometric analysis was subsequently performed to evaluate apoptosis in SH-SY5Y cells treated with the prepared composites, confirming the targeted and multifunctional therapeutic efficacy of these composites.