ReviewDiscover oncology2025
Mechanisms of cancer-induced neurophysiological dysfunction and therapeutic strategies.
Review in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Pre-treatment cognitive impairment in patients with NSCLC: Prevalence and psychosocial factors.IBRO neuroscience reports · 2026Article
- Diagnostic performance of SD-ΔRR during physical stressors for identifying diabetic sensorimotor polyneuropathy.Journal of diabetes investigation · 2026Article
- Driving innovation in cancer symptom science through translational research: bridging science and practice.Current opinion in supportive and palliative care · 2026Review
- Depression and breast cancer: research progress and prospects from an interdisciplinary perspective.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurophysiological alterations represent a growing concern in oncology, affecting both the central and peripheral nervous systems through diverse mechanisms. These include direct tumor infiltration, paraneoplastic immune responses, systemic inflammation, metabolic dysregulation, and treatment-induced neurotoxicity. Neurological complications range from cognitive impairment and peripheral neuropathy to motor deficits and autonomic dysfunction. Paraneoplastic syndromes mediated by immune cross-reactivity and inflammatory cytokines such as IL-6 and TNF-α contribute to neural disruption. Cancer therapies, particularly chemotherapy, radiotherapy, and immunotherapy, increase these alterations, resulting in persistent or progressive neurological deficits. Diagnostic tools such as functional MRI, electroencephalography (EEG), cerebrospinal fluid biomarkers, and circulating tumor DNA (ctDNA) are used for earlier detection and reduced stratification risk. Management strategies incorporate neuroprotective agents (e.g., amifostine), cognitive rehabilitation, and non-invasive neuromodulation techniques. These techniques include transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS). Personalized neuro-oncological care is guided by biomarker-driven profiling and digital health monitoring. Pediatric patients and long-term survivors require special attention due to vulnerability to neurodevelopmental disruption. A multidisciplinary and anticipatory approach is essential for preserving neurological function and enhancing quality of life across the cancer continuum. Advances in diagnostics and therapeutics are reshaping the integration of neurophysiology within comprehensive cancer care.
Indexed as
Identifiers
What Socratic 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 Socratic graph.