crossing96/oncoscreening huggingface dataset:
RNF185 promotes esophageal squamous cell carcinoma progression by regulating BAK1 ubiquitination and activating the cGAS-STING-IRF3 pathway.	OBJECTIVE: RNF185 is a mitochondrial RING-type E3 ubiquitin ligase known to regulate mitochondrial homeostasis, apoptosis, and innate immune signaling through ubiquitination of substrates such as BNIP1, JWA, and cGAS. Although dysregulation of RNF185 has been reported in several cancers, its role in esophageal squamous cell carcinoma (ESCC) remains unclear. The present study aimed to investigate the function of RNF185 in ESCC progression and assess its potential as a therapeutic target. METHODS: We analyzed RNF185 expression in the TCGA-ESCA dataset and ESCC cell lines. RNF185 knockout cell lines were generated using CRISPR/Cas9. Functional assays including CCK-8, colony formation, apoptosis analysis, transmission electron microscopy (TEM), and ELISA were performed. Activation of the cGAS-STING pathway and downstream transcription factors was assessed by Western blot, qPCR, luciferase assays, and ChIP-qPCR. BAK1 ubiquitination and interaction with RNF185 were evaluated using immunoprecipitation. In vivo tumor growth inhibition was tested using a subcutaneous mouse xenograft model with Honokiol treatment. RESULTS: RNF185 was significantly overexpressed in ESCC tissues and correlated with worse patient outcomes. RNF185 knockout suppressed cell proliferation, induced apoptosis, and caused mitochondrial damage and mtDNA release, activating the cGAS-STING-IRF3 pathway. Mechanistically, RNF185 mediated BAK1 ubiquitination to maintain mitochondrial integrity. Loss of RNF185 led to BAK1 accumulation and IRF3-dependent transcriptional upregulation of BAK1, forming a positive feedback loop promoting apoptosis. Knockdown of BAK1 or IRF3 rescued mitochondrial structure and cell survival. Honokiol, identified via molecular docking, targeted RNF185, reduced BAK1 ubiquitination, activated innate immune signaling, and inhibited tumor growth in vivo. CONCLUSION: RNF185 sustains mitochondrial homeostasis and ESCC cell survival by promoting BAK1 ubiquitination and limiting cGAS-STING-IRF3-mediated immune activation. Targeting RNF185 with small molecules like Honokiol may represent a promising therapeutic approach in ESCC.	esophagus
Immunotherapy combined with definitive chemoradiotherapy for locally advanced unresectable esophageal squamous cell carcinoma.	BACKGROUND: The clinical value of immune checkpoint inhibitors (ICIs) in the treatment of unresectable locally advanced esophageal squamous cell carcinoma (LA-ESCC) remains under investigation in large-scale randomized clinical trials. In this study, we aimed to assess the efficacy and safety of concurrent ICIs in combination with definitive chemoradiotherapy (dCRT) in a relatively large cohort of patients with unresectable LA-ESCC. METHODS: Between January 2019 and December 2023, this retrospective study included patients with LA-ESCC who received ICIs concurrently with dCRT at Jiangsu Cancer Hospital. The primary endpoints were overall survival (OS) and progression-free survival (PFS), while secondary endpoints included clinical response and safety. RESULTS: A total of 165 patients with LA-ESCC were included in this study, with a median age of 66 years (IQR 60-70 years), and 163 (98.8%) had stage III or IVA disease. After a median follow-up of 24 months (IQR 16-33 months), the 2-year OS was 64.3% (95%CI 57.2%-72.3%), and the 2-year PFS was 50.2% (95%CI 42.9%-58.8%). It is noteworthy that induction therapy before dCRT did not improve OS (HR = 1.09, 95% CI: 0.61-1.93, P = 0.770) or PFS (HR = 1.00, 95% CI: 0.59-1.72, P = 1.000). The objective response rate (ORR) was 70.9% and disease control rate (DCR) was 86.7%. The most common adverse event was grade 3 or worse lymphopenia, observed in 60.0% of the patients (90/165). CONCLUSION: ICIs combined with concurrent dCRT demonstrated promising efficacy and manageable safety in patients with unresectable LA-ESCC.	esophagus
Decoding intratumoral cyclooxygenase-2 signaling through multi-omics: insights from esophageal cancer and beyond.	Cyclooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis, was significantly upregulated in various cancers, including esophageal cancer (ESCA). This study investigated the role of COX-2 in cancer progression and its potential as a therapeutic target, utilizing multi-omics approaches, including single-cell RNA sequencing, spatial transcriptomics, protein docking analysis and experimental validation. We found that COX-2 expression was significantly elevated in ESCA and other cancers, correlating with malignant phenotype and poor prognosis. Enrichment analyses revealed that COX-2 was involved in key oncogenic signaling pathways, including TNF/NF-κB and IL-17, which promoted cell proliferation, migration, and invasion. Additionally, COX-2 facilitated a pro-inflammatory microenvironment by enhancing immune cell infiltration, particularly macrophages, monocytes, and mast cells. Functional assays demonstrated that celecoxib, a selective COX-2 inhibitor, effectively reduced ESCA cell proliferation, migration, and invasion in a dose-dependent manner. Pan-cancer analysis confirmed that COX-2 was a poor prognostic indicator across various cancers, highlighting its broader clinical relevance. This study underscored COX-2 as a critical regulator of inflammatory microenvironment and cancer progression in ESCA, supporting its potential as both a prognostic biomarker and therapeutic target. The use of COX-2 inhibitors, such as celecoxib, holds promise for improving patient outcomes in ESCA and other COX-2-associated cancers.	esophagus
Retrospective Analysis of Risk Factors and Prediction Model of Cervical Anastomotic and Intrathoracic Anastomotic Leakage After Radical Esophagectomy.	BACKGROUND: Esophagogastric anastomotic leakage is a common complication after esophageal cancer surgery. Therefore, how to treat and predict is the focus of clinicians' research. AIMS: To analyze the risk factors of cervical and intrathoracic anastomotic leakage after radical resection of esophageal cancer and establish a prediction model to provide a basis for early clinical prevention and treatment. METHODS: We retrospectively analyzed the clinical data of 776 esophageal squamous cell carcinoma patients who underwent Sweet (n=115), Ivor-Lewis (n=278), and McKeown (left neck anastomosis) (n=383) esophagectomy at Yancheng First People's Hospital from August 2019 to December 2021. Univariate and logistic regression models were used to analyze the independent risk factors of anastomotic leakage after esophageal cancer surgery, and a nomogram prediction model was established. RESULTS: Of the 776 patients, 95 experienced postoperative anastomotic leakage, with an incidence of 12.2%. There were 63 cases of cervical anastomotic leakage and 32 cases of intrathoracic anastomotic leakage. The multivariate logistic regression analysis showed that BMI, high blood pressure, chronic bronchitis, peptic ulcer, operation way, anastomotic location, and postoperative albumin were independent risk factors for postoperative anastomotic leakage of esophageal cancer (p < 0.05). Our nomogram prediction model yielded a high predictive value, with an area under the receiver operating characteristic curve of 0.765 (95% CI 0.716-0.814). CONCLUSION: The occurrence of anastomotic leakage after esophageal cancer surgery is related to various factors, including BMI, hypertension, chronic bronchitis, peptic ulcer, operation way, anastomotic way, postoperative albumin, and anastomotic location. The clinical prediction model can promote the early detection, diagnosis, intervention, and treatment of anastomotic leakage and shorten the hospitalization time of patients.	esophagus
[Application of esophageal-tubular gastric asymmetric anastomosis in esophageal and esophagogastric junction cancer].	Objective: To evaluate the anti-reflux effect of digestive tract reconstruction using esophageal-tubular gastric asymmetric anastomosis after radical resection of esophageal and esophagogastric junction cancer. Methods: The main steps were as follows:(1)oblique incision of the lower esophagus;(2)curved incision of the tubular anterior gastric wall;(3)the lower end of the esophagus was anastomosed to the tubular gastric incision with a 90-degree torsion; (4)The anterior wall of the anastomosis was reinforced with a transverse-inverted suture,the posterior wall with a folded suture,and the corners of the gastric stump were buried with sutures.The anastomosis operation time,postoperative complications and postoperative hospital stay were recorded;the reconstructed structure and anti-reflux effect of the anastomosis were observed by digestive tract radiography,gastroscopy and follow-up investigation. Results: The Department of Gastrointestinal and Thoracic Surgery of Huaian First People's Hospital, affiliated to Nanjing Medical University, treated 5 patients of esophagogastric junction cancer and 20 esophageal cancer cases between August 2022 and November 2024, including 19 men and 6 women, with a mean age of (66.7±7.4) years. The mean anastomosis time was (35.4±5.9) minutes, the intraoperative blood loss was (117.6±33.4) ml and the mean postoperative hospital stay was(16.6±5.2) days, with no complications such as anastomotic leakage and bleeding. Postoperative digestive tract radiography (Trendelenburg position)showed that all the patients had no contrast reflux,gastroscopy showed no signs of reflux esophagitis and bile reflux gastritis, the anastomosis showed an inverted whiskers valve-like structure. The median follow-up time was (16.8±6.3) months, and all patients had no reflux symptoms such as acid reflux and belching,and no acid suppressive medication was needed. Conclusion: The esophageal-tubular gastric asymmetric anastomosis is a safe and effective antireflux reconstruction technique.	esophagus
Study on the anticancer mechanism of hydroxygenkwanin in esophageal cancer via the ESRRA signaling pathway.	OBJECTIVE: To explore the role of ESRRA in esophageal squamous cell carcinoma (ESCC) progression and evaluate the antitumor effects of hydroxygenkwanin (HGK), focusing on its interaction with ESRRA and the underlying molecular mechanisms. METHODS: Cell viability, apoptosis, invasion, and proliferation were assessed in EC109 and TE-1 cells treated with HGK using CCK-8, Hoechst staining, Transwell, and colony formation assays. ESRRA expression was analyzed via qPCR and Western blot. An ESCC mouse model was established, with treatment groups receiving HGK. Serum IL-10 and IL-12 levels were measured by ELISA; tumor growth and toxicity were evaluated by histology. EMT marker expression was analyzed by IHC and RT-qPCR. TCGA database analysis explored ESRRA-related pathways and its link to the tumor microenvironment and patient survival. RESULTS: HGK inhibited EC109 and TE-1 cell proliferation and migration, especially in EC109 cells, by downregulating ESRRA in a dose-dependent manner. In vivo, HGK reduced tumor growth with minimal toxicity, though high doses showed possible renal effects. IL-12 levels decreased, and EMT markers were altered. ESRRA was overexpressed in ESCC tissues and correlated with EMT-related genes. TCGA analysis confirmed ESRRA's association with poor survival in ESCC patients. CONCLUSION: HGK effectively suppresses ESCC with low toxicity, primarily by inhibiting ESRRA and blocking EMT, highlighting its therapeutic potential.	esophagus
Comparative analysis of robotic Ivor Lewis, McKeown, and transhiatal esophagectomy: a comprehensive systematic review and meta-analysis of perioperative outcomes, complication profiles, oncologic efficacy, and long-term survival.	Robotic-assisted minimally invasive esophagectomy (RAMIE) has been increasingly adopted, yet the comparative outcomes of its three principal approaches-Ivor Lewis, McKeown, and transhiatal-remain inadequately defined. This study aims to provide a comprehensive comparison to guide surgical decision-making. A systematic review and meta-analysis were conducted following PRISMA guidelines. Databases were searched from January 2010 to December 2023 for studies comparing robotic Ivor Lewis, McKeown, and transhiatal esophagectomy. Primary outcomes included perioperative parameters, complication rates, and oncologic efficacy. Sixteen studies (7,339 patients) were included in the systematic review, with eight studies (3,015 patients) eligible for meta-analysis. Robotic Ivor Lewis esophagectomy demonstrated superior outcomes compared to robotic McKeown, including significantly lower rates of recurrent laryngeal nerve palsy (OR = 0.13, 95% CI = 0.06-0.31, P < 0.00001), reoperation (OR = 0.60, 95% CI = 0.41-0.89, P = 0.01), anastomotic leak (OR = 0.47, 95% CI = 0.28-0.78, P = 0.003), and respiratory complications (OR = 0.53, 95% CI = 0.39-0.71, P < 0.0001). Compared to transhiatal esophagectomy, transthoracic approaches (Ivor Lewis and McKeown) yielded significantly more lymph nodes (mean difference 8.3 nodes, P < 0.001) but were associated with higher pulmonary complications. Transhiatal esophagectomy had shorter operative times and reduced blood loss but higher anastomotic leak rates compared to Ivor Lewis. R0 resection rates and 5-year overall survival were comparable among the approaches. Robotic Ivor Lewis esophagectomy offers an optimal balance of perioperative safety and oncologic efficacy, with lower complication rates while maintaining equivalent long-term survival. The surgical approach should be individualized based on tumor location, patient comorbidities, and surgical expertise. These findings support the tailored adoption of robotic technology in esophageal cancer surgery.	esophagus
Study on symptom cluster and core symptoms of esophageal cancer patients discharged from hospital under accelerated rehabilitation surgery mode.	Esophageal cancer is a common malignant tumor of the gastrointestinal tract worldwide, and surgery remains the main treatment modality. With the promotion of the enhanced recovery after surgery concept, length of hospital stay has been shortened significantly, but postoperative symptom burden may not be adequately identified and managed due to early discharge. At present, research on the discharge-time symptom clusters and core symptoms among enhanced recovery after surgery-managed esophageal cancer patients is scarce, which hinders the development of precise intervention measures. To investigate the symptom cluster and core symptoms of esophageal cancer patients at discharge under the accelerated rehabilitation surgery model, so as to provide a reference for the formulation of accurate and efficient symptom management scheme. A convenience sampling method was used to select 263 patients with esophageal cancer surgery for investigation. General information questionnaire and esophageal cancer perioperative symptom assessment scale were used. R language was used to construct the synchronous network layout, describe the relationship between symptoms, and calculate the central index. Postoperative esophageal cancer patients under the accelerated rehabilitation surgery model exhibited 3 symptom clusters at discharge: an eating-related symptom cluster, a pain-fatigue symptom cluster, and a somatic-psychological symptom cluster. These accounted for a total variance contribution rate of 67.84%. Weight loss was the most frequently occurring symptom. In the symptom network, fatigue (strength centrality, rs = 2.10) and globus sensation (rs = 2.06) exhibited the highest centrality strengths, indicating they are the most influential symptoms within the network. Under the accelerated rehabilitation surgery model, postoperative esophageal cancer patients face multiple symptom burdens. These symptoms interact to form 3 symptom clusters, with fatigue and globus sensation serving as core symptoms. Healthcare professionals should closely monitor changes in patients' symptoms and integrate symptom clusters with network-centrality indicators. This approach enables targeted and efficient interventions on key symptom clusters and core symptoms, ultimately improving the quality of life for esophageal cancer patients.	esophagus
Risk stratification for stricture formation after endoscopic submucosal dissection for esophageal dysplasia.	We aimed to evaluate the demographic, clinical, procedural, and histopathologic factors associated with stricture development following esophageal endoscopic submucosal dissection (ESD). We conducted a retrospective cohort study of patients undergoing ESD for esophageal lesions from 2019 to 2024 at St. Michael's Hospital, in Toronto, Canada. The primary outcome was stricture formation, defined as a symptomatic luminal narrowing at the ESD site confirmed on follow-up endoscopy, requiring intervention. Strictures requiring dilation developed in 24% of patients, 85% of which were impassable with a standard gastroscope (9.9 mm diameter). Stricture rates increased with defect circumferential involvement: <50% (7.7%), 50%-74% (11.5%), 75%-89% (23.1%), and ≥90% (57.7%). Intraprocedural local triamcinolone acetate (LTA) injection was administered in 40 of 108 patients (37%), with a mean defect circumferential size of 87.5%. Among patients receiving LTA, stricture rates varied based on defect size: for <50% circumferential defect involvement (n = 1) and 50%-74% (n = 3), no strictures developed; for 75%-90% (n = 17), 6 patients (35%) developed strictures, 5 of which were impassable; and for 90%-100% (n = 19), 11 patients (58%) developed strictures, all of which were impassable. Patients selectively discharged on prophylactic steroids demonstrated varied stricture rates depending on the steroid regimen: prednisone (61.5%), oral budesonide (26.9%), and combination therapy (7.7%). Independent predictors of stricture formation included defect circumferential involvement (OR 1.07, 95% CI 1.03-1.12, p < 0.001), length of hospitalization (OR 1.88, 95% CI 1.11-3.16, p = 0.018), and presence of deep mural injury (OR 6.28, 95% CI 1.10-35.88, p = 0.039). Stricture formation post-ESD is strongly associated with lesion and procedural characteristics, including defect circumferential involvement, deep mural injury, and length of hospitalization.	esophagus
A clinical practice review: management strategies and emerging approaches for anastomotic leakage following radical surgery for esophageal cancer.	Radical esophagectomy remains the cornerstone of curative treatment for esophageal cancer, but is frequently complicated by postoperative events, most notably anastomotic leakage. Anastomotic leakage, occurring in up to 30% of cases, is multifactorial in origin and significantly increases morbidity and mortality. This review aims to summarize current management strategies, highlight emerging therapies, and identify persistent clinical challenges related to this complication. Relevant studies were identified through targeted literature searches of articles focusing on clinical management, therapeutic innovation, and reported outcomes related to anastomotic leakage, with an emphasis on recent and high-impact publications. This review synthesizes current strategies for the detection, prevention, and management of anastomotic leakage and evaluates emerging interventions. Early diagnosis through contrast-enhanced computed tomography (CT) and esophagography is critical for improving outcomes. Conservative measures such as broad-spectrum antibiotics, nutritional support, and image-guided drainage remain the first-line approach, while surgical revision and endoscopic techniques like stenting and vacuum therapy are increasingly employed in complex cases. Novel therapies, including tissue-engineered constructs and biodegradable stents, are under development but lack large-scale clinical validation. Despite these advancements, major clinical challenges persist, including limited predictive tools for risk stratification, variability in treatment algorithms across institutions, and unclear long-term efficacy of newer interventions. Furthermore, most novel strategies are supported by small cohort studies or preclinical data, limiting their immediate clinical application. Therefore, improved multidisciplinary collaboration, standardized treatment protocols, and integration of predictive diagnostics are essential for optimizing outcomes. Future research should focus on validating emerging therapies through randomized clinical trials and developing personalized management algorithms based on patient-specific risk factors and leak characteristics.	esophagus
Risk of fracture among esophageal cancer survivors: A population-based retrospective cohort study.	OBJECTIVE: Evidence regarding the occurrence of fracture in esophageal cancer (EC) survivors remains limited. We aimed to investigate the risk of fractures among EC survivors who received curative-intent surgery. METHODS: We conducted a population-based retrospective cohort study using the Korean National Health Insurance Service database (2009-2022), including patients who underwent surgery for EC (n = 4847) and their 1:3 propensity score matched controls (n = 14,541). We performed competing risk analyses to estimate the risk of fractures. RESULTS: We observed 305 incident fractures among EC survivors (24 [0.50 %], 119 [2.46 %], and 195 [4.02 %] at 1, 3, and 5 years post-surgery, respectively) and 980 fractures among matched controls (118 [0.81 %], 342 [2.35 %], and 557 [3.83 %]) during mean follow-up periods of 5.3 ± 3.7 and 8.1 ± 2.9 years, respectively. EC survivors had a significantly higher fracture risk than controls, with cause-specific hazard ratios of 1.46 (95 % confidence interval [CI] 1.28-1.66) for any fracture, 1.66 (95 % CI 1.31-2.10) for vertebral fracture, and 1.68 (95 % CI 1.28-2.21) for hip fracture, although risk was not significant within the first year after surgery. EC survivors are at a greater risk of fractures than controls regardless of treatment modality, with the highest fracture risk present among those receiving radiation therapy (RT) along with surgery. CONCLUSION: EC survivors had persistently higher risks of any, vertebral, and hip fracture than non-cancer controls, except for during the first year after surgery. The risk of fracture was prominent among EC survivors who received surgery combined with RT.	esophagus
Three-field lymph node dissection subsequent to neoadjuvant concurrent chemoradiotherapy in esophageal cancer.	BACKGROUND: In esophageal squamous cell carcinoma, three-field lymph node dissection (3FLND) is not commonly performed after neoadjuvant chemoradiotherapy (nCRT) due to the high morbidity associated with the procedure and the poor long-term survival of patients with cervical/supraclavicular lymph node metastasis. This study aims to evaluate the long-term survival outcomes of patients who underwent 3FLND combined with nCRT. METHODS: Between 2013 and 2021, patients who underwent esophagectomy and 3FLND after nCRT for advanced thoracic esophageal squamous cell carcinoma, either with (n = 41) or without (n = 65) clinical cervical/supraclavicular lymph node metastasis, were included in this study. RESULTS: The Ivor Lewis and McKeown procedures were performed in 22 patients (20.8%) and 84 patients (79.2%), respectively. The rates of major complications (Grade ≥ IIIb) and 90-day mortality were 6.6% and 2.8%, respectively. A pathological complete response was observed in 26 patients (24.5%), whereas residual cervical/supraclavicular lymph node metastasis was identified in 30 patients (28.3%). The five-year overall survival rates for patients with and without preoperative cervical/supraclavicular lymph node metastasis were 51.5% and 41.4%, respectively. Multivariable analysis of survival in patients with preoperative cervical/supraclavicular lymph node metastasis identified residual cervical/supraclavicular lymph node metastasis (hazard ratio [HR] = 7.885, P < 0.001) and major complications (HR = 74.581, P = 0.001) as significant risk factors for overall survival. CONCLUSIONS: 3FLND combined with nCRT can achieve favorable long-term survival even in patients with esophageal cancer and cervical/supraclavicular lymph node metastasis. Downstaging of cervical lymph node metastasis is a key factor in improving survival outcomes for these patients.	esophagus