Highlight: ABSTRACT Chemotherapy-induced peripheral neuropathy (CIPN) is the most common and severe neurological side effect of many commonly used chemotherapy agents. It affects more than 60% of cancer patients. Approximately 30%–40% of patients have persistent symptoms five months or longer after stopping treatment. Even years after completing chemotherapy, some patients still experience CIPN symptoms. CIPN increases the annual cost of healthcare, leads to detrimental dose reduction and even cessation of treatment, and severely affects cancer survivors’ quality of life. Chemotherapy induces neurotoxicity through a variety of mechanisms that lead to neuronal cell damage or cell death. This mechanism of neurotoxicity varies depending on the specific agent. CIPN is characterized predominantly by sensory axonal peripheral neuropathy. Motor and autonomic symptoms may appear, but less frequently. To diagnose CIPN, a thorough patient's history and neurological examination are required. The current approach to CIPN management focuses on managing the symptoms of neuropathic pain and reducing or stopping the chemotherapy agent when CIPN manifests. There is no proven or advised prophylaxis therapy for CIPN. The point of this review was to talk about how some commonly used chemotherapy agents (such as platinum-based compounds, taxanes, vinca alkaloids, bortezomib, and thalidomide) cause CIPN, how to diagnose it, and the newest treatments that are available.

Circadian regulation has emerged as an important modulator of ocular growth; however, its role in organizing retina–choroid transcriptomic responses during myopia development remains incompletely understood. In this study, we reanalyzed publicly available retinal and choroidal RNA-seq datasets from chick models of form-deprivation myopia using a multistage machine learning framework. A biologically motivated ZT8/12 circadian window was defined from prior published time-of-day transcriptomic evidence and evaluated using feature selection, cross-tissue and cross-stage validation, and external validation in an independent retinal dataset. Machine learning models classified the ZT8/12 window with high performance across onset and progression datasets, and control analyses indicated that this signal reflects a broad transcriptome-wide temporal state rather than a pattern unique to the 53-gene signature. The final gene signature is therefore interpreted as a stable representative subset of the ZT8/12-associated expression state. Cross-species functional enrichment and ortholog mapping suggested hypothesis-generating functional relationships between chicken genes and human orthologs. Overall, this work provides a computational framework for evaluating time-associated expression patterns in myopia and highlights circadian timing as a candidate component of retina–choroid biology requiring further functional validation.

Purpose To determine whether circadian timing defines critical molecular windows in myopia development and to assess the transferability of circadian gene programs across ocular tissues, disease stages, and species. Methods Publicly available retinal and choroidal RNA-seq datasets from chick models of form-deprivation myopia were analyzed using unsupervised transcriptomic profiling and multistage machine-learning classification. Circadian windows were defined based on Zeitgeber time, and samples were grouped accordingly for downstream analyses. Classification model robustness was evaluated through cross-tissue and cross-stage validation and further assessed using external validation in an independent dataset. Functional translation to humans was examined using ortholog-based Gene Ontology enrichment analysis to identify conserved biological processes and higher-order regulatory pathways. Results A circadian critical window at ZT8–ZT12 exhibited the strongest transcriptional divergence during both myopia onset and progression. Gene signatures derived from this window generalized across retina and choroid and remained predictive across disease stages, supporting coordinated molecular regulation between ocular tissues. External validation confirmed the reproducibility of these signatures despite differences in experimental design and gene coverage. Functional mapping revealed that conserved molecular components in chicks are reorganized into more complex neuroendocrine and regulatory networks in humans, indicating cross-species conservation with increased functional complexity. Conclusions Circadian timing strongly shapes myopia-related gene expression and underlies coordinated retina–choroid signaling. These findings highlight circadian biology as a key factor of refractive development and suggest that time-dependent mechanisms may influence myopia susceptibility, progression, and response to treatment.