Importance Perioperative immunotherapy has improved clinical outcomes for patients with early-stage non–small cell lung cancer (NSCLC). The influence of immune checkpoint inhibitor in combination with chemotherapy on surgical outcomes remains to be explored. Objective To evaluate perioperative toripalimab in combination with chemotherapy on surgical outcomes. Design, Setting, and Participants This multicenter, double-blind, placebo-controlled phase 3 randomized clinical trial (Neotorch study) enrolled patients with resectable stage III NSCLC and took place at 50 centers in China. Patients who had histologically confirmed resectable stage IIIA or IIIB NSCLC were eligible. These data were analyzed from July 2024 to March 2026. Interventions Patients were randomized (1:1) to receive toripalimab (240 mg) plus platinum-based chemotherapy or placebo plus platinum-based chemotherapy for 3 cycles before surgery and 1 cycle after surgery, followed by maintenance with toripalimab or placebo alone for 13 cycles. Main Outcomes and Measures Surgical outcomes, including perioperative complications, tumor downstaging, and lymph node downstaging, and their association with event-free survival (EFS), were studied in this post hoc analysis. Results Among 404 patients enrolled, 314 patients (median [SD] age 60 [6.82] years; 90% of patients were male and 10% were female) underwent surgery (166 in toripalimab group and 148 in placebo group). Percentage of patients canceling surgery (17.8% vs 26.7%; P = .03) was significantly lower in the toripalimab group. Proportions of minimally invasive surgery, R0 resection, and lobectomy were slightly higher in the toripalimab group. Surgical complications were similar between the 2 groups. Rates of postsurgery tumor (80.7% vs 50.7%; P < .001) and lymph node downstaging (67.5% vs 48.6%; P = .001) were both significantly higher with toripalimab than placebo. With a median follow-up of 18.3 months, a better EFS was noticed in the toripalimab group. Tumor and lymph node downstaging in the toripalimab group were both associated with better EFS than nondownstaging (median EFS, not estimable [NE] vs 17.5 months; P = .004 and NE vs 19.2 months; P = .001, respectively), and were also associated with even better EFS than tumor and lymph node downstaging in the placebo group (median EFS, NE vs 22.0 months; P = .002 and NE vs NE; P = .009, respectively). Conclusions and Relevance In this study, perioperative toripalimab plus chemotherapy showed comparable perioperative outcomes, as with chemotherapy alone without new safety signals, and could help improve survival through effective tumor downstaging in patients with resectable stage III NSCLC. Trial Registration ClinicalTrials. gov Identifier: NCT04158440

Lung cancer incidence among never-smoking women in Xuanwei, China, is among the highest worldwide and is primarily attributed to household air pollution (HAP) from smoky (bituminous) coal combustion, with early-life exposure identified as playing a critical role. We conducted epigenome-wide DNA methylation (DNAm) analyses of HAP exposure and its polycyclic aromatic hydrocarbon (PAH) constituents across exposure windows. Leukocyte DNAm was measured in 106 never-smoking women, including 23 individuals with repeated measurements. Cooking fuel use and stove type was obtained through questionnaire, and comprehensive personal and environmental air monitoring was conducted. Validated exposure models estimated 43 HAP constituents, predominantly PAHs, across childhood, current, and cumulative exposure windows, and PAH clusters were derived via hierarchical clustering. Generalized estimating equations were used to identify CpG sites associated with HAP exposure and PAH clusters, including 5-methylchrysene, a methylated PAH previously linked to lung cancer. We identified several differentially methylated CpG sites, predominantly hypomethylated with higher HAP exposure. Although some DNAm signatures overlapped with those observed in smoking, the majority were distinct. Notably, higher current exposure to 5-methylchrysene was significantly associated with hypomethylation at cg05575921 (AHRR; p = 2.05x10-06), an established smoking marker. Life-course analyses indicated lasting DNAm variations with both childhood and cumulative PAH exposures at loci such as SLC43A2. Within the PAH clusters, 5-methylchrysene was a key contributor to DNAm variations. Top CpG sites were linked to immune regulation, G-protein coupled signaling, and molecular mechanisms of cancer and other disease pathways. These findings provide novel insight into HAP-induced DNAm changes and their potential health implications.

Lung adenocarcinoma (LUAD) is the most common type of lung cancer and seriously threatens the lives of many people worldwide. The difficulty in early diagnosis of lung cancer has always been a difficulty in lung cancer treatment, and basic leucine zipper nuclear factor 1 (BLZF1) has been shown to promote the occurrence and development of various cancers. This study used 505 LUAD patients in TCGA (TCGA dataset) and 60 LUAD patients in Yunnan Cancer Hospital (Clinical dataset) as research subjects to explore the role of BLZF1 in LUAD. The study found that the expression levels of mRNA and protein of the BLZF1 gene in cancer tissues were significantly higher than those in para-cancer tissues in the TCGA dataset and clinical dataset (P < 0.001). Receiver operating characteristic (ROC) curves analysis found that the AUC value of BLZF1 was 0.759 (95% CI = 0.7049-0.8140, P < 0.0001) in the TCGA dataset, and the AUC value was 0.9985 (95% CI = 0.9954-1.0000, P < 0.0001) in the clinical dataset. Moreover, the BLZF1 gene expression level in the two data sets was significantly correlated with the patient's T stage, and survival analysis showed that high BLZF1 gene expression levels were associated with decreased recurrence-free survival (RFS) (HR = 1.510, 95% Cl = 1.095-2.083, P = 0.012) and overall survival (OS) (HR = 1.472, 95% Cl = 1.099-1.973, P = 0.010). Protein-protein interaction (PPI) and enrichment analysis showed that the BLZF1 gene was closely associated with biological processes such as Golgi function, vesicle transport and cell membrane system maintenance. The expression correlation of BLZF1 with glycolysis-related genes indicated that BLZF1 may play a role in LUAD by participating in the sugar metabolism pathway. In addition, this study downregulated the expression of BLZF1 by small interfering RNA (si-BLZF1), and downregulation of BLZF1 expression significantly inhibited the proliferation, cloning, migration and invasion of LUAD cells. Therefore, BLZF1 may be involved in the occurrence and development of lung adenocarcinoma, which can be a potential diagnostic biomarker in clinical practice.

[This retracts the article DOI: 10.21037/jtd.2020.03.103.].

Importance:Perioperative immunotherapy has improved clinical outcomes for patients with early-stage non-small cell lung cancer (NSCLC). The influence of immune checkpoint inhibitor in combination with chemotherapy on surgical outcomes remains to be explored. Objective:To evaluate perioperative toripalimab in combination with chemotherapy on surgical outcomes. Design, Setting, and Participants:This multicenter, double-blind, placebo-controlled phase 3 randomized clinical trial (Neotorch study) enrolled patients with resectable stage III NSCLC and took place at 50 centers in China. Patients who had histologically confirmed resectable stage IIIA or IIIB NSCLC were eligible. These data were analyzed from July 2024 to March 2026. Interventions:Patients were randomized (1:1) to receive toripalimab (240 mg) plus platinum-based chemotherapy or placebo plus platinum-based chemotherapy for 3 cycles before surgery and 1 cycle after surgery, followed by maintenance with toripalimab or placebo alone for 13 cycles. Main Outcomes and Measures:Surgical outcomes, including perioperative complications, tumor downstaging, and lymph node downstaging, and their association with event-free survival (EFS), were studied in this post hoc analysis. Results:Among 404 patients enrolled, 314 patients (median [SD] age 60 [6.82] years; 90% of patients were male and 10% were female) underwent surgery (166 in toripalimab group and 148 in placebo group). Percentage of patients canceling surgery (17.8% vs 26.7%; P = .03) was significantly lower in the toripalimab group. Proportions of minimally invasive surgery, R0 resection, and lobectomy were slightly higher in the toripalimab group. Surgical complications were similar between the 2 groups. Rates of postsurgery tumor (80.7% vs 50.7%; P < .001) and lymph node downstaging (67.5% vs 48.6%; P = .001) were both significantly higher with toripalimab than placebo. With a median follow-up of 18.3 months, a better EFS was noticed in the toripalimab group. Tumor and lymph node downstaging in the toripalimab group were both associated with better EFS than nondownstaging (median EFS, not estimable [NE] vs 17.5 months; P = .004 and NE vs 19.2 months; P = .001, respectively), and were also associated with even better EFS than tumor and lymph node downstaging in the placebo group (median EFS, NE vs 22.0 months; P = .002 and NE vs NE; P = .009, respectively). Conclusions and Relevance:In this study, perioperative toripalimab plus chemotherapy showed comparable perioperative outcomes, as with chemotherapy alone without new safety signals, and could help improve survival through effective tumor downstaging in patients with resectable stage III NSCLC. Trial Registration:ClinicalTrials. gov Identifier: NCT04158440.

Lung cancer is the malignant tumor with the highest incidence and mortality rate worldwide. The current treatment methods have limited efficacy, and the prognosis of patients is poor. There is an urgent need to explore new therapeutic targets and strategies. Epigenetic modification disorders are closely related to the occurrence and development of tumors. Among them, histone deacetylase 1 (HDAC1), as a key epigenetic regulatory molecule, participates in the regulation of biological processes such as cell proliferation, differentiation, and apoptosis. HDAC1 is highly expressed in lung cancer, and its expression level is closely related to the malignancy degree, clinical stage, and poor prognosis of lung cancer. Abnormal activation of HDAC1 is also one of the core factors for the resistance of lung cancer to chemotherapy, targeted therapy, and immunotherapy. The development of HDAC1 inhibitors provides a new direction for the treatment of lung cancer, and the combination with chemotherapy, targeted therapy, and immunotherapy can significantly enhance the synergistic anti-tumor effect. This article systematically reviews the structural characteristics and physiological functions of HDAC1, deeply explores its regulatory mechanism in lung cancer, elaborates on its association with lung cancer resistance, and summarizes the research and development progress, clinical trial status, and challenges of HDAC1 inhibitors, with the aim of providing new ideas for the precise treatment of lung cancer.

Capsular contracture, a common complication following breast implant surgery, is driven by fibroblast-to-myofibroblast transition and excessive collagen deposition. Although bacterial biofilm and TGF-β signaling are implicated, the molecular mechanisms linking infection to fibrosis remain unclear. Using in vitro fibroblast models and in vivo rat capsular contracture assays, we combine transcriptomics, protein interaction analysis, and targeted mutagenesis to identify Spata13 as a critical mediator of TGF-β/Smad signaling. Functional assays assess collagen synthesis (hydroxyproline content), fibroblast proliferation (CCK-8), and myofibroblast markers (α-SMA). A competitive peptide (PT637) is designed to disrupt Spata13-TGFβRI binding. Staphylococcus epidermidis biofilm synergizes with silicone implants to upregulate Spata13, activates TGF-β/Smad signaling, and promotes fibroblast activation. Spata13 binds to TGF-β receptor I (TGFβRI) via Ser637, and its knockdown suppresses α-SMA expression and collagen deposition. The TGFβRI inhibitor LY2157299 attenuates fibrosis in vivo. Strikingly, PT637 disrupts the Spata13-TGFβRI interaction and reduces both fibrosis markers and capsular thickness in biofilm-challenged rats. We define Spata13 as a novel regulator of infection-associated fibrosis and demonstrate that targeted disruption of Spata13-TGFβRI binding by PT637 offers a precision therapeutic strategy for capsular contracture.

TRAILBLAZER is a proof-of-concept phase 2 study (ClinicalTrials.gov, NCT04580498) of neoadjuvant retlirafusp alfa (an anti-PD-L1/TGF-β bifunctional agent) in unresectable stage III non-small cell lung cancer (NSCLC) not harboring EGFR or ALK alterations. During induction, retlirafusp alfa was administered either with chemotherapy or as monotherapy, followed by surgery or radiotherapy as assessed by a local multidisciplinary team and consolidation retlirafusp alfa. Patients without high PD-L1 expression were allocated to retlirafusp alfa plus chemotherapy (arm A; n = 88); patients with high PD-L1 expression were randomly allocated at a 1:1 ratio to retlirafusp alfa combination (arm B; n = 9) or monotherapy (arm C; n = 10). In this updated analysis (data cutoff, March 24, 2025), the median follow-up was 39.4 months. The event-free survival (EFS) rate at 3 years was 50.5% (95% CI 39.0-61.0) in arm A + B and 77.1% (34.5-93.9) in arm C; the corresponding overall survival (OS) rates at 3 years were 68.3% (95% CI 57.5-77.0) and 87.5% (38.7-98.1), respectively. Among 27 patients who underwent surgery, the 3-year EFS and OS rates were 69.5% (95% CI 48.1-83.5) and 84.9% (64.5-94.0), respectively, versus 50.8% (36.5-63.4) and 70.4% (56.7-80.5), respectively, in radiotherapy-treated patients. The safety data were consistent with those in a previous report. With extended follow-up, the study regimen showed sustained survival benefits with no new safety signals. Patients who underwent surgery after induction treatment achieved clinically meaningful survival gains. Our findings support the use of neoadjuvant immunotherapy with a response-adapted surgical strategy as a promising approach for unresectable stage III NSCLC.

Household coal smoke was evidenced to cause the uniquely high lung cancer mortalities in Xuan Wei, China. Lung cancer screening in local villagers found concurrently high prevalence of interstitial pneumonia. What could be the shared hazard linking those pathologies? Could it be some coal-derived mineral deposit in lungs that causes both fibrotic and malignant changes? A case-control study was conducted by recruiting 50 lung cancer cases and 30 pseudotumor controls among non-smoking women from Xuan Wei, China. The severity of interstitial lung abnormalities (ILAs) was compared between cases and controls by high-resolution computed tomography (HRCT) and histopathological analysis; mineral deposits in lung tissues were examined by light microscopy and electron microscopy techniques. The lung cancer case group and the pseudotumor group share this characteristic of abundant ILAs while the fibrotic changes are more severe in lung cancer than pseudotumor cases. Fibrotic changes are more severe in peribronchial lymph nodes than in lung parenchyma. Mineral deposits embedded in the anthracotic pigments are visible under polarized light microscopy (PLM) due to their birefringence. The morphology of this birefringent mineral resembles that of acicular berthierine-chamosite identified in Late Permian coal from Xuan Wei, China. These preliminary findings underscore the need for further investigation into the mineralogical factors contributing to the high incidence of lung cancer in this region.

Lung cancer is the world's leading cause of cancer deaths. Early detection through low-cost metabolite screening approaches could reduce lung cancer mortality. Here we report the results of a large-scale, quantitative metabolomics study aimed at identifying plasma biomarkers for lung cancer detection in a Chinese population. A cohort of 410 patients, including 137 healthy controls, 189 biopsy-confirmed individuals with stage I/II lung cancer, and 84 individuals with biopsy-confirmed stage III/IV cancer, were studied. Plasma samples were collected and analyzed using an in-house-developed, targeted liquid chromatography-mass spectrometry (LC-MS) metabolomics method that detects and quantifies 138 metabolites. Logistic regression was used to develop an optimal biomarker panel that could distinguish all-stage lung cancer patients from healthy controls. The resulting six-metabolite panel achieved an area under the curve (AUC) of 95.0

Surgical resection constitutes the cornerstone of treatment for lung cancer, a disease with high global incidence. Among postoperative complications, delayed fatal hemorrhage occurring beyond 30 days postoperatively has garnered scant attention in clinical and research settings. Notably, there are no documented cases of vascular rupture and bleeding induced by chronic mechanical friction between the bronchial stump and pulmonary artery trunk to date. Following pulmonary lobectomy, the anatomical proximity between the bronchial stump and pulmonary artery trunk creates a potential risk of delayed pulmonary artery hemorrhage secondary to bronchial stump-related pathology. Herein, we report a case of a 53-year-old male patient who presented with sudden massive hemoptysis on the 40th day after right upper lobectomy. Bronchial artery embolization was initially performed but failed to control the bleeding. Emergency thoracotomy revealed a 3-mm rupture with active bleeding in the right pulmonary artery trunk, accompanied by a 2-mm fistula at the right upper lobe bronchial stump. Intraoperatively, the vascular rupture was repaired using a pericardial patch, and both the repaired vessel and the bronchial stump were wrapped with an intercostal muscle flap, achieving successful hemostasis. The patient experienced an uneventful postoperative recovery and remained alive and well at the 3-month follow-up. Written informed consent was obtained from the patient for the publication of this case report and the accompanying clinical images.

Background: ASTRUM-002 met the primary endpoint of progression-free survival (PFS) with the combination of serplulimab plus HLX04 (bevacizumab biosimilar) and chemotherapy at interim analysis. Here, we report the results of the final survival analysis. Methods: A total of 636 patients with treatment-naïve, locally advanced or metastatic nonsquamous non-small cell lung cancer (nsq-NSCLC) without epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK)/ROS proto-oncogene 1 receptor tyrosine kinase (ROS1) genetic alterations were randomized 1:1:1 to receive serplulimab plus HLX04 and chemotherapy (group A), serplulimab plus HLX04 placebo and chemotherapy (group B), or double placebo plus chemotherapy (group C). Patients and the investigators were blinded to the group assignments. The primary endpoint was blinded independent central review-assessed PFS. Overall survival (OS) was the key secondary endpoint. Results: At the final analysis, median OS was 23.7 (95% confidence interval [CI] 20.5 to 27.5) months, 26.8 (95% CI 21.2 to 30.9) months, and 20.3 (95% CI 16.2 to 24.6) months in groups A (n = 212), B (n = 214), and C (n = 210), respectively. A significant reduction in risk of death for group B compared to group C was observed (hazard ratio [HR] = 0.66, 95% CI 0.52 to 0.83; P < 0.001). A total of 79 (37.6%) patients in group C had crossed over to serplulimab plus HLX04 treatment. Median OS in group C adjusted by the 2-stage model was 14.2 months (95% CI 11.9 to 17.0), corresponding to an adjusted HR of 0.53 (95% CI 0.42 to 0.68; P < 0.001) for group B versus group C. Using the rank-preserving structural failure time model, the adjusted median OS in group C was 17.9 months (95% CI 14.2 to 20.3), with a corresponding adjusted HR of 0.65 (95% CI 0.51 to 0.83; P < 0.001). No statistical difference in median OS for group A compared to group B (HR = 1.12, 95% CI 0.88 to 1.42; P = 0.363) was found. Conclusions: Serplulimab plus chemotherapy significantly prolonged OS and maintained PFS benefit compared to chemotherapy; however, the addition of bevacizumab biosimilar HLX04 did not yield further improvement for the first-line treatment of nsq-NSCLC without EGFR or ALK/ROS1 genetic alterations. Trial registration: This trial was registered at ClinicalTrials.gov (NCT03952403, date of registration: 2019 May 14).

Molecular residual disease (MRD), detected through circulating tumor DNA, has emerged as a promising biomarker for surveillance in patients with early-stage non-small cell lung cancer (NSCLC) following curative-intent resection. Here we report the MRD analysis from the phase 3 EVIDENCE trial, which includes patients with stage II-IIIA resected EGFR-mutated NSCLC who have received either adjuvant icotinib or chemotherapy. A total of 1,352 plasma samples from 175 patients are analyzed using the MinerVa Prime assay, a personalized tumor-informed MRD platform. At the landmark timepoint, MinerVa Prime detects MRD positivity in 35.8% (38/106) of patients with stage III disease and 14.7% (10/68) of patients with stage II disease, with a longitudinal positivity rate of 47.4%. MRD-positive status is significantly correlated with inferior disease-free survival (DFS), both at landmark (hazard ratio [HR]: 4.44, P < 0.001) and during longitudinal monitoring (HR: 7.82, P < 0.001). Icotinib confers DFS benefits over chemotherapy in both MRD subgroups, enhancing MRD clearance in MRD-positive patients while reducing molecular recurrence in landmark MRD-negative patients. Longitudinal MRD shows a 91.3% negative predictive value, with a median lead time of 169 days prior to clinical recurrence. Among serial monitoring timepoints, MRD status at 24 weeks post-randomization demonstrates the highest prognostic value.

Inherited genomic susceptibility and associated transcriptomic patterns are crucial players in lung cancer etiology. Lung cancer susceptibility is getting rising attention in carcinogenesis. The present study aimed to investigate unique clinical features and transcriptomic profile in patients with familial lung cancer (FLC) in Yunnan-Guizhou Plateau, Wumeng-Mountain area of China. 1,823 local lung cancer patients were enrolled (762 FLC, 1061 Sporadic). Clinicopathologic parameters were analyzed and summarized. 43 lung tissue samples (the adjacent nonmalignant tissue) were selected for Transcriptome/RNA-seq, the differential gene expression patterns were analyzed, significant functions and pathways were enriched and studied. Our FLC cohort showed unique characters: younger age; increased rate of adenocarcinoma, and early-stage cases; unbalance in blood types, anatomic sites and co-existing diseases; highlighted with significantly elevated comorbidity and early-onset of hypertension in FLC + population. Notably, our FLC + group exhibited a higher rate of bilateral lung cancers and multiple pulmonary nodules; beside, were more likely to develop different cysts, polyps, hyperplasia at a younger age. The transcriptome found that immune-related functions pathways were significantly enriched in the familial cohort. E.g. “immune cells recruitment” with higher Neutrophils/ lower CD4 memory T cells. Collectively, these transcriptomic differences suggested: individuals with FLC may have baseline alterations in immune regulation, which could reflect a compromised immune surveillance or dysregulated inflammatory tone in their normal lung tissue. For the key gene, MUC16 may contribute to this process by influencing the assembly, structure dynamical functions of pulmonary epithelial cilium; which could potentially impair mucociliary clearance, leading to prolonged retention of pollutants and carcinogens in the lung microenvironment. Hereditary factors likely contribute to the susceptibility to both lung cancer and hypertension in this population, while chronic exposure to local air pollution may further promote their early-onset and comorbidity. Our findings highlighted the potential significance of MUC16 in familial lung cancer or even early-onset lung cancer; and provided useful data for early screening and personalized treatment strategies for lung cancer.

Purpose:This study aimed to create a nomogram model to predict the spread through air spaces (STAS) in patients diagnosed with stage IA lung adenocarcinoma, utilizing a substantial sample size alongside a blend of clinical and imaging features. This model serves as a valuable reference for the preoperative planning process in these patients. Materials and methods:A total of 1244 individuals were included in the study. Individuals who received surgical intervention between January 2022 and May 2023 were categorized into a training cohort (n=950), whereas those treated from June 2023 to October 2023 were placed in a validation cohort (n=294). Data from clinical assessments and CT imaging were gathered from all participants. In the training cohort, analyses employing both multivariate and univariate logistic regression were performed to discern significant clinical and CT characteristics. The identified features were subsequently employed to develop a nomogram prediction model. The evaluation of the model's discrimination, calibration, and clinical utility was conducted in both cohorts. Results:In the training cohort, multivariate logistic regression analysis revealed several independent risk factors associated with invasive adenocarcinoma: maximum diameter (OR=2.459, 95%CI: 1.833-3.298), nodule type (OR=4.024, 95%CI: 2.909-5.567), pleura traction sign (OR=2.031, 95%CI: 1.394-2.961), vascular convergence sign (OR=3.700, 95%CI: 1.668-8.210), and CEA (OR=1.942, 95%CI: 1.302-2.899). A nomogram model was constructed utilizing these factors to forecast the occurrence of STAS in stage IA lung adenocarcinoma. The Area Under the Curve (AUC) measured 0.835 (95% CI: 0.808-0.862) in the training cohort and 0.830 (95% CI: 0.782-0.878) in the validation cohort. The internal validation conducted through the bootstrap method yielded an AUC of 0.846 (95% CI: 0.818-0.881), demonstrating a robust capacity for discrimination. The Hosmer-Lemeshow goodness-of-fit test confirmed a satisfactory model fit in both groups (P > 0.05). Additionally, the calibration curve and decision analysis curve demonstrated high calibration and clinical applicability of the model in both cohorts. Conclusion:By integrating clinical and CT imaging characteristics, a nomogram model was developed to predict the occurrence of STAS, demonstrating robust predictive performance and providing valuable support for decision-making in patients with stage IA lung adenocarcinoma.

This study aims to establish a hypoxia-immune-related gene signature within the tumor microenvironment (TME) to reliably predict prognosis in non-small cell lung cancer (NSCLC). Transcriptomic profiles and clinical data of lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases (GSE74777, GSE68465). Hypoxia- and immune-related genes were curated from MSigDB, ImmPort, and INATDB. Prognostic genes were identified via Cox and LASSO regression analyses, and a risk model was constructed. Model validity was assessed through Kaplan-Meier survival analysis, receiver operating characteristic (ROC) curves, and external validation. An eight-gene prognostic signature (AKAP12, MT2A, SERPINE1, CD1E, CD79A, CXCL13, XCL2, ANGPTL4) was established. The model demonstrated significant predictive accuracy for NSCLC survival (AUC: 0.643/0.649/0.620 at 1/3/5 years in TCGA cohort). Patients with high immune activity exhibited superior survival outcomes compared to those with low-immune counterparts (log-rank P < 0.001). Multivariate Cox regression confirmed the risk score as an independent prognostic factor (HR = 1.82, 95

BackgroundEsophageal squamous cell carcinoma (ESCC) is a common and aggressive form of esophageal cancer, particularly prevalent in East Asia. This study aimed to investigate the impact of sex on clinical outcomes, including survival and postoperative complications, in elderly ESCC patients following esophagectomy.MethodsWe conducted a retrospective cohort study using data from the Sichuan Cancer Hospital & Institute Esophageal Cancer Case Management Database, involving patients aged 70 years and older who underwent esophagectomy from May 2016 and August 2021. Patients were grouped by sex, and subgroup analyses were performed on non-smoking, non-drinking patients. OS and DFS were analyzed using the Kaplan-Meier method, and between-group comparisons were conducted using the log-rank test. Propensity score matching (PSM) was applied to adjust for potential confounders.ResultsAlthough females showed a longer median OS (60.2 months) compared to males (40.0 months), the difference was not statistically significant after PSM (HR = 0.885, P = 0.573). Similarly, no significant differences were observed in DFS between sexes. In non-smoking, non-drinking subgroups, OS and DFS remained higher but without significant sex-based differences. Postoperative adverse events such as pulmonary infection and anastomotic leakage were common across groups.ConclusionsWhile sex does not significantly affect OS and DFS in elderly ESCC patients, male patients may experience higher rates of certain postoperative complications, such as abnormal liver function and pneumothorax.