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Nanoplatforms for Cancer Theranostics / Nanoparticles: Synthesis and Applications · Journal article
Discover Materials · September 10, 2026
Raises a question worth testing. It does not answer one.
This minireview examines mechanistic pathways of nanoparticle toxicity in cancer therapy, including oxidative stress, immune activation, and genotoxicity, alongside mitigation strategies such as surface functionalization and biocompatible coatings. It synthesizes existing knowledge on nanotoxicity mechanisms rather than presenting new experimental evidence, and proposes future directions including AI-assisted prediction and standardized safety frameworks to support clinical translation.
Journal article.
Oxidative stress from lysosomal membrane permeabilization, mitochondrial dysfunction, and cytoplasmic redox enzyme dysregulation identified as key drivers of ROS generation and cellular toxicity Carbon nanotubes exhibit high drug-loading capacity but documented genotoxic and oxidative liabilities Cerium oxide nanoparticles demonstrate context-dependent behavior: antioxidant or cytotoxic properties determined by physicochemical properties and intracellular context
No quantitative comparison of toxicity profiles across nanoparticle types or evidence for the effectiveness of mitigation strategies Oxidative stress from lysosomal membrane permeabilization, mitochondrial dysfunction, and cytoplasmic redox enzyme dysregulation identified as key drivers of ROS generation and cellular toxicity
Clinicians and researchers should recognise that nanoparticle safety in cancer therapy requires mechanism-informed toxicity screening and rational design strategies. This review underscores the need for standardised safety assessment frameworks and physicochemical characterisation before clinical translation.
This is a mechanistic minireview that examines nanotoxicity pathways and mitigation strategies in cancer therapy without presenting new experimental data or clinical evidence, making it exploratory rather than confirmatory or practice-changing.
Clinicians and researchers should recognise that nanoparticle safety in cancer therapy requires mechanism-informed toxicity screening and rational design strategies. This review underscores the need for standardised safety assessment frameworks and physicochemical characterisation before clinical translation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
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Nanomedicine has emerged as a transformative strategy in cancer therapy, enabling precision drug delivery, improved therapeutic efficacy, and personalized treatment paradigms. Despite these advances, clinical translation remains constrained by unresolved nanotoxicity concerns. This minireview critically examines the mechanistic basis of nanoparticle-induced toxicity in oncology, with a particular focus on oxidative stress arising from lysosomal membrane permeabilization, mitochondrial dysfunction, and cytoplasmic redox enzyme dysregulation, which collectively disrupt cellular redox homeostasis and drive excessive reactive oxygen species (ROS) generation. Key ROS-amplifying pathways, including NADPH oxidase activation, redox-sensitive signalling cascades, and Fenton-like reactions associated with metal-based nanoparticles, are highlighted as central mediators of cellular injury. Immune activation and signaling pathway perturbations are discussed in the context of chronic inflammation and altered tumor–immune interactions. The review further addresses nano-genotoxicity as a critical safety endpoint, encompassing DNA strand breaks, chromosomal instability, epigenetic reprogramming, and persistent gene expression alterations. The dualistic nature of nanomedicine is illustrated using representative nanomaterials, including carbon nanotubes (CNTs), which exhibit high drug-loading capacity alongside documented genotoxic and oxidative liabilities, and cerium oxide nanoparticles, whose antioxidant or cytotoxic behavior is dictated by physicochemical properties and intracellular context. Strategies to mitigate nanotoxicity are discussed, including surface functionalization, biocompatible coatings, biodegradable nanocarriers, and mechanism-informed toxicity screening approaches aligned with regulatory expectations. Finally, emerging directions are outlined, emphasizing artificial intelligence–assisted nanotoxicity prediction, computational modeling of nano–bio interactions, standardized safety assessment frameworks, and interdisciplinary collaboration as critical enablers of safe clinical translation. These insights support the rational design of safer nanomedicines and reinforce the need for mechanistic toxicology to guide their development for cancer care.
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