ReviewAAPS PharmSciTech2024
From Bench to Bedside: ROS-Responsive Nanocarriers in Cancer Therapy.
Review in AAPS PharmSciTech, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Combinational studies of BOLD-100/KP1339 with established chemotherapeutics in gastrointestinal multicellular tumor spheroids.Cancer chemotherapy and pharmacology · 2026Article
- OCTN2-targeted and ROS-responsive hybrid polymeric micelles for oral delivery of docetaxel.Journal of nanobiotechnology · 2026Article
- Latest developments in photosensitizers: improving stability, specificity and responsiveness.Future medicinal chemistry · 2025Review
- Metformin and its Nanoformulations in Cancer Prevention and Therapy.Current pharmaceutical design · 2025Review
- Harnessing the interaction between redox signaling and senescence to restrain tumor drug resistance.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) play a dual role in cancer, acting as both signaling molecules that promote tumour growth and as agents that can inhibit tumour progression through cytotoxic effects. In cancer therapy, ROS-responsive drug delivery systems take advantage of the elevated ROS levels found in tumors compared to healthy tissues. These systems are engineered to release drugs precisely in response to increased ROS levels in tumour cells, allowing targeted and controlled treatment, minimizing side effects, and enhancing therapeutic outcomes. ROS generation in cancer cells is linked to metabolic changes, mitochondrial dysfunction, and oncogenic signaling, leading to increased oxidative stress. Tumour cells manage this by upregulating antioxidant defenses to prevent ROS from reaching harmful levels. This balance between ROS production and neutralization is critical for cancer cell survival, making ROS both a challenge and an opportunity for targeted therapies. ROS also connect inflammation and cancer. Chronic inflammation leads to elevated ROS, which can damage DNA and proteins, promoting mutations and cancer development. Additionally, ROS contribute to protein degradation, affecting essential cellular functions. Therapeutic strategies targeting ROS aim to either increase ROS beyond tolerable levels for cancer cells or inhibit their antioxidant defenses. Nanocarriers responsive to ROS show great potential in improving the precision of cancer treatments by releasing drugs specifically in high ROS environments, like tumors. This review discusses the mechanisms of ROS in cancer, its role in inflammation and protein degradation, and the advances in ROS-targeted nanocarrier therapies across different cancer types.
Indexed as
Identifiers
39668268What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.