BACKGROUND:CCT7 is a chaperonin containing tailless complex polypeptide 1 subunit. The study focused on investigating its prognostic significance for lung adenocarcinoma (LUAD). METHODS:CCT7 expression in LUAD and matched non-carcinoma lung samples was examined via TCGA database. Besides, we utilized the GEO database and RT-qPCR for validating differential CCT7 expression. The relation with clinical factors and its functions in diagnosis and prognosis prediction were determined. GO, KEGG, along with GSEA were conducted for exploring CCT7's functions. We also performed CIBERSORT, ssGSEA, and ESTIMATE for examining the LUAD immune microenvironment. By analyzing tumor mutational burden (TMB) and immune checkpoints, the relationship between CCT7 and immunotherapy was explored. RESULTS:CCT7 expression significantly increased within LUAD relative to matched non-carcinoma lung samples. As revealed by GO, KEGG, as well as GSEA results, CCT7 was mostly related to cell movement and regulation of multiple biological processes. Furthermore, CCT7 expression varied significantly among different immune cells, and those having increased CCT7 expression showed greater TMB. CONCLUSIONS:An increase in CCT7 expression carries significant implications for diagnosing and predicting LUAD prognosis.

Metastasis remains a leading cause of mortality in esophageal squamous cell carcinoma (ESCC) patients, underscoring the urgent need to elucidate the molecular mechanisms driving disease progression. In this study, we delineated that ZBED2, a zinc finger protein, correlates with inferior survival outcomes and metastasis in ESCC patients. ZBED2 formed phase-separated nuclear condensates that functionally promote tumor metastasis, and integrin-linked kinase (ILK) was pinpointed as a critical downstream effector in mediating the pro-metastatic function of ZBED2. Mechanistically, ZBED2 enhanced the transcription of HSP90AA1, promoted the physical interaction between HSP90AA1 and ILK, and consequently stabilized ILK by suppressing its ubiquitination. Subsequently, ILK promoted PD-L1 transcription and CD8+ T cell exhaustion, thereby creating an immunosuppressive microenvironment that facilitates cancer metastasis. Collectively, these findings establish the pivotal role of ZBED2 in driving ESCC metastasis and immune evasion, thereby validating it as a promising therapeutic target for this aggressive malignancy.

Lung metastasis (LM) imposes a substantial burden on the management of solid tumors. Although local surgical interventions remain controversial, particularly for lung-limited metastasis (LLM), pan-cancer evidence on surgery-associated survival outcomes remains limited. This study aimed to delineate the epidemiological landscape of LLM and evaluate cancer-type-specific associations between surgical interventions and overall survival using large-scale population-based data. Data were obtained from the Surveillance, Epidemiology, and End Results database (2010-2022). A total of 157,365 patients with synchronous LM were identified among 3,621,017 cases of solid tumors. Temporal trends were analyzed using a Joinpoint regression. To improve balance in measured baseline covariates and mitigate observed treatment-selection imbalance, overlap weighting based on propensity scores was employed. Kaplan-Meier and Multivariable Cox regression analyses were conducted to estimate the associations of primary tumor resection (PTR), pulmonary metastasectomy (PM), and combined surgery with overall survival (OS) across 24 primary cancer types. The absolute number of synchronous LM cases increased over time, whereas the utilization of PTR remained relatively stable. Among patients with LLM, PTR was associated with lower all-cause mortality in 16 cancer types after adjustment for measured covariates (e.g., breast and colorectal cancers; hazard ratio [HR] < 1.00, p < 0.001), whereas no statistically significant association was observed in anal, biliary, bladder and ureter, esophageal, prostate cancers, small intestine, or testis cancers (p > 0.05). PM showed consistent associations with lower all-cause mortality in 11 cancer types, including colorectal, soft tissue, and liver cancers, with HRs ranging from 0.40 to 0.77 (p < 0.05). Combined surgery (PTR plus PM) was associated with lower all-cause mortality than PTR alone in bladder and ureter, breast, colorectal, soft tissue, skin, and thyroid cancers (HR range, 0.52-0.80; p < 0.05). Collectively, the overall disease burden of LM remains substantial, with highly heterogeneous underlying drivers. In patients with LLM, surgery-associated survival patterns varied markedly by cancer type, supporting cancer-type-specific evaluation of PTR and PM within multidisciplinary decision-making. These population-based findings warrant prospective validation and should be interpreted in light of residual confounding and treatment selection bias.

Ablation (AL) and laser excision (LE) have shown broad application prospects in treating pulmonary malignant tumor (PMT). This study is the first to directly explore the differences in outcomes between AL and LE in treating patients with PMT at III–IV stages. The study included 157 PMT patients from the Surveillance, Epidemiology, and End Results (SEER) database. Propensity score matching (PSM) was used to minimize the impact of clinical feature imbalances on confounding factors between the AL and LE groups. Kaplan-Meier curves, cumulative incidence function, univariable Cox regression analysis, and multivariable Cox regression analysis were used to explore prognostic factors for overall survival (OS)/cancer-specific survival (CSS). Before PSM, a trend was observed indicating poorer OS, crude CSS, and net CSS in the AL group compared to the LE group (p = 0.019–0.071). After PSM, the LE group demonstrated significantly longer OS (median: 18.00 months) than the AL group (median: 13.00 months; p = 0.048). Similarly, crude CSS (p = 0.017) and net CSS (p = 0.028) were superior in the LE group. In the post-PSM multivariable analysis, LE remained associated with improved OS (adjusted HR = 0.52 [95

Objective: To describe temporal trends and metastatic patterns of brain metastases (BMs) and to assess the associations of primary site surgery (PSS) and metastatic site surgery (MSS) with overall survival (OS) among patients with brain-limited metastases (BLMs) at diagnosis across primary cancer types. Methods: Using SEER-17 (2010-2022), we identified 65,861 patients with BMs at diagnosis among 3,540,748 solid tumors. The analytic cohort included 23,394 patients with BLMs (no extracranial distant metastases) with known PSS/MSS status. Propensity score-based overlap weighting was used to reduce measured confounding in cancer-specific Cox models of OS. Results: BMs were identified in 1.9% of solid tumors, with lung cancer accounting for 80.0% of cases. BM counts increased from 4459 (2010) to 5330 (2022), while the overall proportion among solid tumors remained at approximately 2%. BLMs accounted for 35.5% of patients with BMs. Among patients with BLMs, median OS was 7.0 months, and 5-year OS was 9.4%, varying widely by primary site (23-24 months for thyroid/prostate vs. 3 months for pancreatic/liver primaries). PSS was uncommon and declined modestly (8.5% to 7.0%), whereas MSS increased (22.1% to 29.1%). In fully adjusted overlap-weighted models, PSS and MSS were associated with lower mortality for most cancer types; in lung cancer, PSS (HR, 0.52) and MSS (HR, 0.74) were associated with lower mortality, with both associations remaining significant after Benjamini-Hochberg false discovery rate adjustment (adjusted p < .05). Conclusions: Prognosis and surgery-associated survival in BLMs vary by primary site and may help inform cancerspecific multidisciplinary decision-making and the design of future prospective studies.

This study aimed to identify clinical parameters influencing treatment efficacy during neoadjuvant chemotherapy (NAC) for esophageal cancer (EC) patients, with a particular focus on demographic and clinical variables, to establish predictive biomarkers for chemotherapeutic response. A total of 194 EC patients undergoing NAC were retrospectively included. Significant predictors of pathological response were identified through univariate and multivariate logistic regression analyses, followed by the construction of a predictive nomogram. The model’s discriminative performance was validated using receiver operating characteristic (ROC) curve analysis, while calibration accuracy and clinical utility were assessed using bootstrap-corrected calibration curves (1,000 resamples) and decision curve analysis (DCA), respectively. External validation was performed on an independent cohort of 74 EC patients. Both univariate and multivariate logistic regression analyses identified abnormal transaminase levels, average cycle cost, and hair loss as significant risk factors affecting the effectiveness of NAC (p < 0.05). The constructed nomogram model demonstrated strong predictive performance, with a concordance index (C-index) and area under the curve (AUC) of 0.735. Calibration curves showed a high degree of fit between predicted and observed outcomes, while DCA confirmed the clinical utility of these predictive factors. External validation yielded an AUC of 0.865, further supporting the model’s predictive accuracy. By incorporating the indicators of abnormal transaminase levels, average chemotherapy cycle cost, and the occurrence of hair loss, the developed nomogram effectively identifies EC patients who are more likely to benefit from NAC.

The study aimed to investigate the role of SLC2A14 in hepatoblastomaHB,a prevalent pediatric liver tumor.Through RNA-seq analysis of public and in-house datasets,we found SLC2A14 upregulated in HB and linked to ferroptosis.Our analysis revealed SLC2A14s potential as a diagnostic marker and its association with tumor metabolism,suggesting it may be a therapeutic target.The study concludes that SLC2A14s role in HB should be further explored for clinical applications.

The role of thymic epithelial cells (TECs) in eliminating self-reactive T cells through the presentation of self-antigens is well-established. However, it remains unclear whether TECs can eliminate tumor-reactive CD8+ T cells by presenting tumor antigens. In this study, we observed that CD73+ Granzyme B+ peripheral activated CD8+ T cells undergo apoptosis in the medullary region of the thymus in DEN-CCL4-induced spontaneous HCC mice, but not in the naïve control group. Mechanistically, HCC cells manipulate the thymus to recruit peripheral activated CD8+ T cells through the CCL19/CCL21-CCR7 axis. Additionally, TECs capture antigens from HCC cells for subsequent antigen presentation instead of de novo expressing tumor antigens. When tumor-associated CD8+ T cells homing to the thymus recognize the same tumor antigen presented by TECs, activation-induced cell death (AICD) is initiated in these T cells. Thymectomy redistributes CD8+ T cells into the tumor focus to suppress HCC growth. Alternatively, both inhibiting CCL19/CCL21 expression of thymic cells using an AMPK activator and blocking CCR7 on CD8+ T cells binding with ligands using Cmp2105 significantly reduces tumor-educated thymus dependent immune evasion. Our findings collectively demonstrate that HCC manipulates the thymus to trigger immune escape; pharmacologically targeting CCL19/CCL21-CCR7 axis to inhibit thymus homing can increase CD8+ T cells in the tumor microenvironment.

Cardiac calcification, often seen in age-related diseases, impairs heart function, yet its association with malignant tumors remains largely overlooked. Our study revealed that pericardial calcification (PC) occurs in up to 80% of breast cancer patients with pulmonary metastasis. We demonstrate a reciprocal relationship where breast cancer drives PC, which in turn accelerates cancer progression in humans and mice. Lung metastases increase monocyte-derived macrophage and mesenchymal stem cell (MSC)-derived osteoblast infiltration in the pericardial tissue, triggering inflammation and calcification. Mechanistically, metastatic cancer cells in the lungs highly express and secrete asparagine endopeptidase (AEP), which cleaves IGF2BP3 to free IGF2. AEP and IGF2 contribute to PC by promoting osteoblast differentiation in heart tissue through integrin αvβ5 and IGF1R activation, respectively. Pharmacological blockade of integrin αvβ5 and IGF1R, especially when combined, effectively inhibits ectopic osteogenesis and disrupts the feedback loop between PC and cancer progression. These findings elucidate the interplay between metastatic breast cancer and PC and suggest therapeutic strategies to hinder breast cancer progression.

Prostate cancer (PCa), the most common male malignant tumor worldwide, is associated with high morbidity and mortality, particularly when it progresses to metastatic disease. Ferroptosis, an iron-dependent form of cell death, has been implicated in various cancers. This study investigated the role of NADPH oxidase 4 (NOX4) in PCa and its potential connection to ferroptosis. By analyzing mRNA expression data from TCGA and GEO, NOX4 was found to be significantly upregulated in PCa tissues compared to non-cancerous tissues (SMD = 0.75, 95% CI: 0.41–1.10) and exhibited a moderate diagnostic accuracy (AUC = 0.79, 95% CI: 0.75–0.82). A total of 464 differentially co-expressed genes (DCEGs) were identified, including the hub genes BUB1, CCNB1, and CCNB2. Furthermore, NOX4 expression showed significant correlations with ferroptosisrelated genes such as ALOX15, UBC, FTH1, and SLC2A6. Functional enrichment analyses (GO and KEGG) revealed that NOX4-associated DCEGs were enriched in metabolic pathways, cell cycle regulation, mitotic nuclear division, chromatin binding, and centromeric regions. These results suggest that NOX4 may contribute to ferroptosis regulation in PCa through its involvement in meta-bolic and cell cycle pathways, highlighting its potential as a therapeutic target.

This study examined the expression and clinical significance of pituitary tumortransforming gene 1 (PTTG1) in prostate cancer (PCa) and metastatic prostate cancer (MPCa). Analysis of 19 PCa and 10 MPCa public datasets showed that PTTG1 expression was significantly upregulated in PCa (SMD=0.55, 95% CI: 0.29, 0.83) and MPCa (SMD=2.28, 95% CI: 1.38, 3.19). PTTG1 also demonstrated moderate discriminatory ability for PCa (AUC=0.75, 95% CI: 0.71, 0.79) and high discriminatory potential for MPCa from localized PCa (AUC=0.97, 95% CI: 0.95, 0.98). Differential co-ex-pressed gene (DCEG) analysis identified 314 PTTG1-related genes, with CCNA2, CCNB1, and CDK1 emerging as key hub genes positively correlated with PTTG1. While most clinical parameters showed no correlation with PTTG1 expression, data from The Cancer Genome Atlas (TCGA) revealed an association between PTTG1 and both M-stage and recurrence. Enrich-ment analyses indicated that PTTG1 DCEGs were involved in cell division, nucleoplasm, protein binding, and the cell cycle pathway. These findings suggest that PTTG1 may serve as a marker for distinguishing MPCa from localized PCa and provide insights into its potential role in prostate cancer progression.

There is limited research on the impact of surgery on the cancer-specific survival (CSS) of patients with malignant thymoma and concurrent or previous extrathymic malignancies (PMTEMs). This retrospective analysis evaluated the prognostic value of surgery in PMTEMs. Data were sourced from the SEER database, encompassing PMTEMs aged 20–90 with confirmed diagnoses and comprehensive clinical information. Patients were categorized into surgical (n = 105) and nonsurgical (n = 25) groups. Propensity score matching (PSM) was employed to mitigate selection bias, resulting in well-balanced baseline characteristics between the groups. Kaplan–Meier curves and the log-rank test were used to investigate the prognostic value of surgery in PMTEMs. Using PSM, the matching of characteristics between the surgical and nonsurgical groups was well-balanced, ensuring the reliability of subsequent analyses. Pre-PSM, the CSS in the surgical group was significantly better than that in the nonsurgical group (p <.001). Similarly, according to the post-PSM data, the CSS for PMTEMs in the surgical group remained superior to that in the nonsurgical group, which indicates that the survival advantage of the surgical group persisted after PSM (p =.030). Additionally, PMTEMs with smaller thymomas (≤ 5 cm) had a significant advantage in CSS compared to those with larger thymomas (p = .046). In conclusion, this study shows that surgery may significantly improve the survival rate of PMTEMs.

ABSTRACTBackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most prevalent and lethal malignancies worldwide. Despite progress in immunotherapy for cancer treatment, its application and efficacy in ESCC remain limited. Therefore, there is an ongoing need to explore potential molecules and therapeutic strategies related to tumor immunity in ESCC.MethodsIn this study, we integrated high‐throughput sequencing data, gene chip data, single‐cell sequencing data, and various bioinformatics analysis methods along with experimental approaches to identify key genes involved in immune infiltration in ESCC and investigate their relationship with immune cell development, as well as the potential of these key genes in immunotherapy.ResultsWe discovered and validated a positive correlation between macrophage infiltration and ITGB2 expression in ESCC. ITGB2 is overexpressed in ESCC and has potential as a prognostic biomarker for the disease. We present for the first time the finding that the expression of ITGB2 in infiltrating macrophages increases as these macrophages polarize toward a tumor‐promoting phenotype in ESCC. Moreover, during the progression of ESCC, ITGB2 expression in infiltrating macrophages is upregulated. The higher the expression of ITGB2, the more feasible it is to target macrophages. Additionally, we found that evaluating immune therapy responses in ESCC patients through ITGB2 expression is a viable approach. Furthermore, we identified three miRNAs associated with abnormal ITGB2 expression, providing insights into the upstream molecular interactions of ITGB2.ConclusionsMacrophage infiltration in ESCC is closely associated with ITGB2, which holds significant potential for immunotherapy applications in ESCC. Based on our findings and prior studies, we propose a novel hypothesis: inducing M1 macrophages in vitro, knocking out ITGB2, and then reinfusing these ITGB2‐knockout M1 macrophages into ESCC patients may represent a promising new immunotherapy strategy, providing a new avenue for ESCC immunotherapy.

BACKGROUND:The association between platelet count (PLTC) and the risk of lung squamous cell carcinoma (LUSC) remains unclear. METHODS:We analyzed 19 223 samples from public and internal cohorts to investigate the relationship between high PLTC and the risk of developing LUSC using the retrospective analysis and Mendelian randomization analysis (MRA). RESULTS:Elevated PLTC were detected in the population with lung cancer compared to healthy individuals (odds ratio [OR] = 1.41 [per 1-SD], 95% CI 1.13-1.75, p < 0.05). Furthermore, there is a significant association between elevated PLTC and an increased risk of LUSC based on an in-house cohort (OR = 1.63 [per 1-SD], 95% CI 1.08-2.45, p < 0.05). Individuals with high PLTC had an increased risk of developing LUSC using the inverse-variance weighting method (OR = 1.62 [per 1-SD], 95% CI 1.14-2.31, p < 0.05), an outcome that was directionally consistent across the weighted median, MR Egger, simple mode, and weighted modes methods (OR > 1.00). No pleiotropy (the MRA pleiotropy residual sum and outlier test p = 0.553) or heterogeneity (Cochran's Q statistic p = 0.777) was found in the MRAs. Besides PLTC, age and five other hematological parameters (e.g., red blood cell count) were identified as independent factors associated with the incidence of lung cancer or its subtype LUSC (p < 0.05). CONCLUSIONS:High circulating PLTC may serve as a risk factor for lung squamous cell carcinoma.

Catalytic hairpin assembly (CHA) offers significant potential for point-of-care nucleic acid detection due to its enzyme-free, isothermal amplification. However, its clinical translation is hindered by critical limitations: background leakage, matrix interference in complex samples like serum, and insufficient quantitative accuracy. To address these challenges, we developed a novel Digital TNA-CHA-TR-FRET platform for ultrasensitive miRNA detection. Firstly, we introduced Threose Nucleic Acid (TNA) modifications at the stem ends of the hairpin DNA probes (TNA-CHA). This modification significantly increased probe thermal stability, effectively suppressing background leakage caused by transient DNA breathing while maintaining catalytic efficiency, with optimal performance achieved using two TNA base pairs. Secondly, to overcome serum autofluorescence interference, we integrated TNA-CHA with Time-Resolved Fluorescence Resonance Energy Transfer (TR-FRET). The time-delayed measurement window of TR-FRET effectively filtered out short-lived background fluorescence, achieving an impressive limit of detection of 1 aM in serum. Thirdly, to resolve the poor linearity and repeatability inherent to CHA kinetics, we incorporated a microfluidic digital partitioning strategy (digital-TNA-CHA-TR-FRET). Partitioning the reaction into nanoliter droplets significantly improved linear correlation (R2 = 0.986) and repeatability (CV <5 % across concentrations). Clinically validated for early esophageal cancer diagnosis using serum miRNAs (miRNA21, miRNA25, miRNA93) on 100 samples (50 patients, 50 controls), our platform demonstrated high diagnostic performance using a "two-positive-out-of-three" miRNA logic gate: 96 % sensitivity, 90 % specificity, and 93 % accuracy. This integrated platform provides a powerful tool for non-invasive, early cancer diagnosis.

Background: Previous studies have underscored the significance of hematocrit (HCT) in different tumors. However, further research is needed to explore its causal relationship with various tumors. Research design and methods: A retrospective analysis and a Mendelian randomization analysis were conducted on a sample of 3,580,275 samples to investigate the causal relationships between high HCT levels and the risks of developing the 15 prevalent malignant tumors. Additionally, using an in-house cohort, Kaplan-Meier curves were utilized to examine the relationship between HCT levels and the prognosis of patients with prostate cancer (PCa). Results: An elevated HCT level was identified as a protective factor against six types of cancers, including PCa (odds ratio [OR] < 1.000, p < 0.05), and a risk factor for cervical cancer, melanoma, and non-melanoma skin cancer (OR > 1.000, p < 0.05). A potential causal association was found between high HCT levels and decreased risks of developing PCa (OR = 0.887, p < 0.05) and breast cancer (OR = 0.893, p < 0.05). HCT was identified as a protective factor against PCa (p < 0.05). Conclusions: This study identified significant associations between HCT and nine tumors. HCT levels may serve as a protective factor against PCa.

This study focuses on the significant role between gut microbiota and lymph node metastasis (LNM) in colorectal cancer (CRC). By conducting 16S rRNA sequencing on fecal samples from 147 CRC patients and combining it with the linear discriminant analysis effect size algorithm, we successfully identified significant differences in the gut microbiota between patients with LNM and those with no lymph node metastasis (NLNM). Furthermore, using transcriptome data from 23 CRC patients, we constructed an immune cell infiltration matrix to deeply explore the biological functions associated with LNM. Eventually, using the characteristics of the gut microbiota associated with LNM, we developed random forest (RF) and multilayer perceptron (MLP) machine learning models to predict the LNM status of CRC patients. We identified 21 differentially abundant gut microbes between the two groups, among which Bacteroides plebeius, significantly enriched in the LNM group, is closely related to the upregulation of neutrophils and chemokine CXCL8 expression, and this bacterial species is also positively correlated with the enhancement of inosine monophosphate metabolism. The RF and MLP models constructed based on the LNM-associated gut microbiota showed good predictive efficacy in predicting LNM status in CRC. This study reveals that Bacteroides plebeius may play an important role in the progression of CRC, with its mechanism potentially involving changes in immune modulation and metabolic pathways. The classification model constructed based on gut microbiota characteristics can predict LNM status of CRC, providing a new perspective for personalized and precision treatment of CRC patients.IMPORTANCEThis study highlights the pivotal role of gut microbiota in lymph node metastasis (LNM) of colorectal cancer (CRC), identifying key microbial differences between LNM and NLNM groups. Our findings implicate Bacteroides plebeius in CRC progression via immune modulation and metabolic alterations. Moreover, machine learning models based on gut microbiota predict LNM status accurately, offering a novel approach for personalized CRC treatment.

BACKGROUND:This study aimed to elucidate the causal relationship between Omega-6/Omega-3 fatty acid ratio and the risk of lung cancer by using Mendelian randomization (MR) analyses. METHODS:Omega-6/Omega-3 fatty acid ratio data from the IEU database and lung cancer patient data from the International Lung Cancer Consortium were collected for this MR analyses. Single nucleotide polymorphisms (SNPs) associated with Omega-6/Omega-3 fatty acid ratio were collected as instrumental variables (IVs) with criteria of P < 5E-8, linkage disequilibrium R2 > 0.001 and clump distance < 10,000 kb. We used the inverse variance weighted (IVW) method as the primary method of MR analyses to evaluate the causal relationship between Omega-6/Omega-3 fatty acid ratio and lung cancer risk. Heterogeneity of the analyses was assessed by Cochran's Q test. Horizontal pleiotropy was evaluated by the intercept with the MR-Egger test. RESULTS:28 SNPs related to Omega-6/Omega-3 fatty acid ratio were selected as IVs in total. The MR analyses results showed that higher Omega-6/Omega-3 fatty acid ratio was associated with lower risk of lung cancer (P = 0.009). No statistical significance was observed for MR-Egger and simple mode methods (P > 0.05). No significant horizontal pleiotropy was detected by MR-Egger regression test (P = 0.73). Conclusion: Higher Omega-6/Omega-3 fatty acid ratio was associated with lower lung cancer risk.

ObjectiveThis study aimed to explore the risk factors of hypokalemia after radical resection of esophageal cancer (EC) and establish a nomogram risk prediction model to evaluate hypokalemia risk after esophagectomy. Thus, this study provides a reference for the clinical development of intervention measures.MethodsClinical data of EC patients who underwent radical surgery from January 2020 to November 2022 in the First Affiliated Hospital of Guangxi Medical University were retrospectively collected. The relevant variables were screened using multivariate logistic regression analysis with IBM SPSS 25.0 and R 4.2.0 software, and a nomogram for predicting hypokalemia risk was established. The established nomogram was evaluated by receiver operating characteristic (ROC), calibration, and decision curves. The model was also internally validated by 1000 bootstrap resampling methods.ResultsAfter radical EC resection, the incidence rate of hypokalemia in 213 patients was 19.2% (41/213). The hemoglobin levels, total serum protein, serum albumin, calcium ion concentration, direct bilirubin, prothrombin time (PT), and activated partial thromboplastin time (APTT) were related (p < 0.05). The multivariate logistic analysis showed that the white blood cell count, serum albumin level, direct bilirubin, and operation time were risk factors for hypokalemia after radical EC resection (p < 0.05). The area under the ROC curve (AUC) was 0.764, demonstrating the good discriminative ability of the established nomogram for hypokalemia prediction. The calibration curve showed a good fit between the predicted and actual observed probabilities. The model maintained a high C-index in the internal validation (C-index = 0.758), supporting that the nomogram can be widely used for hypokalemia prediction.ConclusionThe prediction model for hypokalemia risk with individualized scores based on the patient's white blood cell count, serum albumin level, direct bilirubin, and operation time can screen out high-risk patients who might develop hypokalemia. It is of certain reference value for clinicians to screen and follow up with patients with emphasis and to formulate preoperative and postoperative intervention strategies.