Sleep State in Lung Cancer: A Retrospective Analysis

Lung cancer remains the leading cause of cancer-related mortality globally, with tumor progression closely linked to the immune microenvironment. Sleep disorders (e.g., insomnia, obstructive sleep apnea \[OSA\]) affect 40-50% of lung cancer patients and may promote tumorigenesis via chronic inflammation, immune suppression, and metabolic dysregulation. Preclinical and epidemiological studies suggest that chronic sleep deprivation reduces NK cell activity, elevates pro-inflammatory cytokines (IL-6, TNF-α), and upregulates angiogenic factors (VEGF), though clinical evidence remains scarce. This study aims to: Evaluate associations between sleep disorders and immunosuppressive phenotypes (e.g., PD-L1 expression, T-cell exhaustion) in lung cancer patients. Analyze the impact of sleep disturbances on immunotherapy efficacy (e.g., PD-1 inhibitors) and prognostic outcomes. Explore underlying mechanisms, including hypoxia-inducible factor (HIF-1α) signaling and sympathetic nervous system activation

Sex

All

Minimum age

20 Years

Maximum age

70 Years

Inclusion Criteria:

1. NSCLC or SCLC was diagnosed.
2. Patients have received immunotherapy (e.g., PD-1/PD-L1 inhibitors) or standard treatment (chemotherapy/radiotherapy).
3. Sleep disorder diagnoses and immune-related biomarkers fully recorded in medical records.

Exclusion Criteria:

1. The patient had a history of other malignant tumors.
2. Key clinical data lacking.
3. The presence of a serious psychiatric or neurologic condition.