crossing96/oncoscreening huggingface dataset:
Lymph node ratio predicts adjuvant chemotherapy benefit in esophageal squamous cell carcinoma.	BACKGROUND: The lymph node ratio (LNR) has emerged as an important prognostic factor in various cancers, including esophageal squamous cell carcinoma (ESCC). This study aimed to evaluate the utility of LNR in guiding decisions for adjuvant chemotherapy in ESCC patients following resection. MATERIALS AND METHODS: A retrospective analysis was conducted on 2267 patients who underwent potentially curative surgery for ESCC at Sichuan Cancer Hospital and Institute between January 2010 and December 2017. Univariate and multivariate Cox proportional hazards regressions were used to assess factors influencing overall survival (OS), with LNR analyzed using restricted cubic splines (RCS) to explore its relationship with treatment and survival outcomes. Propensity score matching (PSM) was employed to adjust for biases between treatment groups. RESULTS: Among the patients, 1416 underwent surgery alone (S group) and 851 received surgery plus adjuvant chemotherapy (S + CT group). The median LNR was 3%, with an interquartile range of 0%-12%. RCS analysis identified an LNR threshold of 11%, below which patients showed a significant OS benefit from adjuvant chemotherapy (hazard ratio [HR]: 0.57; 95% CI: 0.46-0.71; P < 0.001). However, patients with an LNR above 11% did not derive any OS benefit from chemotherapy (HR: 0.87; 95% CI: 0.70-1.09; P = 0.238). CONCLUSION: These findings suggest that LNR is a valuable marker for identifying ESCC patients who would benefit from postoperative adjuvant chemotherapy. A threshold LNR of 11% can help personalize treatment strategies, and patients with higher LNRs may require more intensive approaches like chemoradiotherapy to improve survival. Further prospective studies are needed to validate these results.	esophagus
Acetyl-CoA carboxylase 1 knockdown promotes esophageal squamous cell carcinoma metastasis via the CXCL8-NET axis.	Esophageal squamous cell carcinoma (ESCC) is associated with variable clinical outcomes, even among tumours with similar characteristics, complicating treatment. Here, we identify acetyl-CoA carboxylase 1 (ACC1), a key lipogenic enzyme, as a factor influencing this variability. Specifically, ACC1 knockdown in ESCC cells induces histone acetylation, activating c-Fos and C-X-C motif chemokine ligand 8 (CXCL8) transcription, which in turn promotes epithelial-mesenchymal transition (EMT) and enhances migration and invasion via CXCL8-C-X-C motif chemokine receptor 1/2 (CXCR1/2)-mediated PI3K/AKT and MEK/ERK signalling. Additionally, ACC1 knockdown stimulates neutrophil recruitment and neutrophil extracellular trap (NET) formation through CXCL8-dependent paracrine signalling, further enhancing tumour cell migration and invasion. In ESCC xenografts, ACC1 knockdown increases neutrophil infiltration and NET formation, accelerating metastasis. Clinically, low ACC1 expression and high CXCL8 levels are linked to poor prognosis in patients with ESCC, while NET formation further correlates with reduced survival. These findings highlight the ACC1-CXCL8-NET axis as a potential therapeutic target and prognostic marker in ESCC.	esophagus
5-FU Resistance Facilitates Immune Evasion in Esophageal Squamous Cell Carcinoma Through ADAM10-Mediated PD-L1 Shedding and Tumour Microenvironment Remodelling.	Chemoresistance remains a major challenge in esophageal squamous cell carcinoma (ESCC) therapy, particularly resistance to 5-Fluorouracil (5-FU). This study uncovers how 5-FU resistance reprograms the tumour microenvironment, primarily through the up-regulation of ADAM10 and the release of soluble PD-L1, which collectively facilitate immune evasion. Using a 5-FU-resistant AKR mouse ESCC cell line (5-FU-AKR) and its parental counterpart, we applied third-generation DNA sequencing, proteomic analysis, and single-cell RNA sequencing to unravel the resistance-associated molecular and cellular shifts. We found that ADAM10 is significantly up-regulated in 5-FU-AKR cells, promoting soluble PD-L1 release, thereby limiting CD8+ T cell infiltration. Xenograft models further demonstrated enhanced tumourigenicity and immune exclusion in 5-FU-resistant tumours. These findings highlight a novel mechanism of immune suppression driven by ADAM10, suggesting that targeting the ADAM10-PD-L1 axis may restore anti-tumour immunity and improve treatment outcomes for 5-FU-resistant ESCC.	esophagus
NCAPD2 stimulates glycolysis and esophageal cancer metastasis through Wnt5A-dependent Notch activation.	BACKGROUND: Although non-SMC condensin I complex subunit D2 (NCAPD2) is a significant player in multiple tumors, its role in esophageal cancer (EC) remains poorly defined. This study aimed to investigate the molecular mechanisms by which NCAPD2 influenced EC metastasis. METHODS: The mechanism of NCAPD2 in EC cells was analyzed through transcriptome sequencing. The extracellular acidification rate (ECAR), oxygen consumption rate (OCR), lactate production, and glucose consumption were measured using assay kits to evaluate the level of glycolytic metabolism. Western blot was used to validate the expression of critical glycolytic enzymes, EMT markers, and Notch signaling components. Cell migration and invasion were assessed through scratch and Transwell assays. In vivo experiments included the establishment of subcutaneous tumors in BALB/c nude mice to monitor tumor growth and assess invasiveness via H&E staining. The expression of NCAPD2, Wnt5A, Notch pathway, and EMT-related proteins was detected by immunohistochemistry. RESULTS: NCAPD2 overexpression in EC cells enhanced their ability to migrate and invade by promoting glycolysis-a process tightly linked to the activation of Wnt5A. Specifically, NCAPD2 drove up Wnt5A levels, which in turn boosted glycolytic flux. This metabolic shift relied on the activation of the Notch pathway by Wnt5A, ultimately fueling the metastatic potential of EC. CONCLUSION: NCAPD2 enhanced the proliferation and metastasis of EC cells by promoting glycolysis through Wnt5A-mediated activation of the Notch pathway. This finding not only revealed the critical role of the NCAPD2/Wnt5A axis in EC but also provided a potential therapeutic target for EC treatment.	esophagus
USP4-Deubiquitinated PGAM5 Regulates Mitochondrial Dynamics in the Progression of Esophageal Squamous Cell Carcinoma.	This study explored the effect of ubiquitin-specific protease 4 (USP4) on mitochondrial dynamics in esophageal squamous cell carcinoma (ESCC). USP4 and phosphoglycerate mutase 5 (PGAM5) expression in ESCC tissues was measured. ESCC cells were subjected to gain- and loss-of-function experiments, followed by examinations of proliferation, invasion, migration, apoptosis, light chain 3 (LC3), P62, Bcl2-associated X (Bax), B-cell lymphoma 2 (Bcl2), Cytochrome c (CytC), caspase3, mitochondrial membrane potential (MMP), mitochondrial reactive oxygen species (mtROS), and ROS. An in vivo tumor formation model of ESCC was established for in vivo verification. The relationship between USP4 and PGAM5 was analyzed. USP4 and PGAM5 expression was high in ESCC tissues. Mechanistically, USP4 eliminated K48-linked ubiquitin chains to maintain PGAM5 stability. PGAM5 knockdown impaired malignant behaviors of ESCC cells, reduced LC-3I-to-LC-3II conversion, increased mtROS, ROS, and P62 levels, activated the caspase-dependent mitochondrial pathway, and decreased MMP. Overexpressing USP4 increased MMP and Bcl2 expression while lowering Bax, CytoC, cleaved caspase3, and mtROS levels in ESCC cells, which was nullified by PGAM5 knockdown. Ectopic USP4 accelerated tumor growth in mice, which was reversed by PGAM5 knockdown. Collectively, USP4 promotes cell growth and excessive mitophagy in ESCC by stabilizing PGAM5.	esophagus
Neoadjuvant Radio-Chemo-Immunotherapy Impact on Postoperative Patient-Reported Outcomes in Oesophageal Cancer.	OBJECTIVES: Clinical trials have shown promising clinical and safety outcomes of neoadjuvant chemoradiotherapy combined with immunotherapy (nICRT) in patients with resectable oesophageal cancer. However, knowledge of the impact of nICRT on symptomatic improvement and quality of life (QOL) remains scarce. Therefore, this study compared postoperative patient-reported outcomes in patients with oesophageal cancer receiving nICRT and those receiving neoadjuvant chemoradiotherapy alone (nCRT). METHODS: Among 92 patients, 25 were selected from each group after propensity score matching. Repeated-measures analysis of variance was used to assess differences in QOL, symptoms, anxiety, and depression using the M.D. Anderson Symptom Inventory, Quality of Life Questionnaire Core 30, and Hospital Anxiety and Depression Scale. RESULTS: After matching, no significant differences were observed in overall health status or functional scores (P > .05). However, the nICRT group reported better nausea, vomiting, and pain scores (P < .05). Over time, both groups showed significant improvements in overall health (F = 5.222, P < .01) and functional subscale scores (physical, role, emotional, and cognitive; all P < .001). The nICRT group demonstrated significantly better pain, fatigue, nausea, and vomiting scores (P < .05). Anxiety and depression improved significantly in both groups (P < .001), with greater anxiety reduction in the nICRT group (P < .05). CONCLUSIONS: The nICRT group exhibited better QOL, fewer adverse symptoms, and lower anxiety and depression levels postoperatively, suggesting that nICRT may enhance recovery.	esophagus
Prognostic Value of UBE2S, HIF-1α, and FOXM1 Expression in Esophageal Squamous Cell Carcinoma.	OBJECTIVE: The present investigation was aimed to examine ubiquitin-conjugating enzyme E2S (UBE2S), hypoxia-inducible factor (HIF)-1α, and factor forkhead box M1 (FOXM1) levels in esophageal squamous cell carcinoma (ESCC) and esophageal low-grade intraepithelial neoplasia (LIN), high-grade intraepithelial neoplasia (HIN). Additionally, the investigation explored the correlation between these levels and clinicopathological features in addition to prognosis. METHODS: To investigate the expression patterns of UBE2S, HIF-1α, and FOXM1, immunohistochemical staining was performed on tissue samples, including LIN, HIN, ESCC, and healthy controls. Subsequently, the chi-square test was applied to analyze the correlations between the expression levels of the three proteins and the clinicopathological features of ESCC. The impact of UBE2S, HIF-1α, and FOXM1 on ESCC prognosis was evaluated using survival analysis. Spearman correlation analysis was employed to analyze the correlation of three proteins in ESCC, HIN, and LIN, respectively. RESULTS: UBE2S overexpression was related to ethnicity (p < 0.001) and the place of the tumor (p = 0.021). Overexpression of HIF-1α (p = 0.017) and FOXM1 (p = 0.015) was connected to metastasis of the lymph node. Individuals with elevated levels of UBE2S, HIF-1α, and FOXM1 had reduced overall survival (OS) and progression-free survival (PFS). CONCLUSION: The expression levels of UBE2S, HIF-1α, and FOXM1 are closely associated with the incidence and progression of ESCC. UBE2S, HIF-1α, and FOXM1 have potential as prognostic indicators for ESCC.	esophagus
Research Communication: Prevalence of Asymptomatic Premalignant Oesophageal Lesions in Patients With Fanconi Anaemia.	Fanconi anaemia (FA), a rare genetic disorder of DNA repair, predisposes to squamous cell carcinomas of head, neck and oesophagus. We assessed the value of screening esophagogastroduodenoscopy (EGD) in 20 asymptomatic adults (median age 23.5, 65% female) with FA, compared to age-and sex-matched non-FA patients enrolled at a 3:1 ratio. Among 11 FA patients with abnormal oesophageal mucosa, 15% had low-grade dysplasia, nodular high-grade dysplasia or squamous carcinoma in situ, 10% had non-dysplastic Barrett's oesophagus and 30% had columnar epithelium without goblet cells, compared to none in the controls (p < 0.001). Our findings support routine EGD screening of asymptomatic FA patients.	esophagus
Enhanced prognosis prediction model in esophageal cancer via lymph node assessment post-neoadjuvant.	Develop an improved lymph node evaluation system for prognosis prediction in esophageal squamous cell carcinoma (ESCC) patients receiving neoadjuvant therapy. METHODS: Studied 282 ESCC patients who underwent neoadjuvant chemoradiotherapy (NCRT) and surgery. Evaluated lymph node factors like number, size, location, and intra-nodal cancer status. Developed and validated a prognostic model using these factors. RESULTS: Cases with a clearance of 17-30 lymph nodes during surgery showed improved overall survival (OS) compared to those with fewer than 17 or more than 30 cleared nodes. Patients with a lower tumor regression grade of lymph nodes (LN-TRG) experienced improved OS and recurrence-free survival (RFS). Patients with LN extracapsular invasion had worse OS and RFS. Abdominal lymph nodes showed the highest ratio of residual cancer, highest hazard ratio (HR), and the largest number and proportion of positive cases. The five most relevant factors for prognosis, as revealed by Lasso regression and Cox univariate analysis, were LN-TRG, LN total tumor diameter, the clearance of 17-30 lymph nodes, the proportion of positive lymph nodes, and LN extracapsular invasion. The predictive model, based on these factors, achieved good risk stratification for OS and RFS (AUC = 0.705, 0.679), surpassing pathology N (pN) staging. CONCLUSION: A comprehensive lymph node assessment using a predictive model enables improved prognosis prediction and risk stratification compared to pN staging for patients undergoing neoadjuvant therapy. This approach contributes to the accurate evaluation of clinical prognosis and assists in guiding treatment strategies.	esophagus
Overexpression of LINC01354 predicts well prognosis and suppresses esophageal cancer progression.	Long non-coding RNA (lncRNA) LINC01354 is involved in the progression of some cancer types, but the expression profile and prognostic value of this lncRNA in most tumor types, as well as its role and mechanism in esophageal cancer (ESCA), remain poorly characterized. Here, we identify LINC01354 as a tumor-suppressive lncRNA that inhibits ESCA progression by disrupting cell division signaling. Clinically, a pan-cancer analysis revealed widespread downregulation of LINC01354 in tumors compared to normal specimens, including ESCA and breast cancer (BRCA). Low tumor LINC01354 expression correlated with poor overall survival (OS) in ESCA and BRCA patients. In addition, the low expression of LINC01354 in tumors was validated again by two ESCA cohorts, and LINC01354 showed promising diagnostic potential. Moreover, tissue microarray (TMA) staining based on fluorescence in situ hybridization (FISH) once again confirmed the down-regulation of LINC01354 expression in ESCA. Functionally, enrichment analysis of LINC01354's co-expressed genes indicated its critical role in ESCA cell cycle regulation, and its tumor suppressive effect was verified by an in vivo tumor-bearing mouse model. The inhibition of OE-LINC01354 on ESCA cell-cycle progression was further demonstrated by flow cytometry. Mechanistically, high-depth proteomic profiling revealed that overexpression of LINC01354 alters key cell division regulators, including AURKA, AURKB, BRCA2, CCND1, CDC20, and SOX9, etc. Thus, these findings establish the LINC01354-cell division axis as a novel tumor-suppressive mechanism in ESCA and highlight its therapeutic potential.	esophagus
Guiding esophagectomy with intraoperative NIR-II fluorescence video imaging and rapid computation.	Preclinical shortwave infrared/near-infrared II (SWIR/NIR-II, 1,000 to 3,000 nm) fluorescence imaging has shown superior contrast, resolution, and penetration depth compared to traditional near-infrared I (NIR-I, 700 to 900 nm) imaging, owing to reduced light scattering and tissue autofluorescence. Here, we carried out clinical translation of NIR-II fluorescence imaging to guide esophagectomy through intraoperative video imaging and rapid analysis of blood perfusion in the gastric conduits (GC) of esophageal cancer patients, following intravenous administration of indocyanine green (ICG). Within <1 min, NIR-II video imaging clearly visualized the spatial and temporal blood flow features, and importantly, intraoperative principal component analysis (PCA) of the video revealed distinct perfusion patterns in GC. This led to rapid, subjective decision-making for targeted resection of poorly perfused tissue and informed reconstruction of the GC to reduce the risk of life-threatening anastomotic leakage. This approach enhances surgical precision and improves outcomes by providing operator-independent intraoperative guidance.	esophagus
Surgery versus chemoradiotherapy in patients with stage T1bN0M0 esophageal cancer: a retrospective cohort study.	To compare survival outcomes between surgery and chemoradiotherapy in patients with stage T1bN0M0 esophageal cancer. Stage T1bN0M0 esophageal cancer patients treated with either surgery or chemoradiotherapy were extracted from the Surveillance, Epidemiology, and End Results database between 2000 and 2020. Included patients were divided into two groups: surgery and chemoradiotherapy. Cancer-specific survival (CSS) and overall survival (OS) were compared between the two groups. Among the 515 patients included in the study, 55 (10.7%) underwent chemoradiotherapy and 460 (89.3%) received surgery. Surgery showed better 5-year CSS (73.2% vs. 31.0%; hazard ratio [HR] = 0.27, 95% confidence interval [CI] 0.19-0.39; P < 0.001) and OS (60.0% vs. 21.5%; HR = 0.35, 95% CI 0.25-0.48; P < 0.001) compared to chemoradiotherapy. Subgroup analysis indicated that surgery remained associated with superior 5-year CSS (61.3% vs. 40.6%; HR = 0.51, 95% CI 0.26-0.99; P = 0.049) and OS (48.9% vs. 23.8%; HR = 0.52, 95% CI 0.29-0.91; P = 0.021) compared to chemoradiotherapy in squamous cell carcinoma patients. Similarly, surgery showed better 5-year CSS (76.0% vs. 27.1%; HR = 0.22, 95% CI 0.14-0.34; P < 0.001) and OS (62.7% vs. 20.6%; HR = 0.31, 95% CI 0.21-0.46; P < 0.001) compared to chemoradiotherapy in adenocarcinoma patients. Surgery is associated with superior survival outcomes compared to chemoradiotherapy in stage T1bN0M0 esophageal cancer and should be considered the preferred treatment for eligible patients, particularly in settings where consistent follow-up and salvage therapy may be limited.	esophagus
A case report of lymphoma presenting initially with tracheoesophageal fistula and literature review.	RATIONALE: Extranodal involvement in non-Hodgkin lymphoma most commonly occurs in the gastrointestinal tract, whereas direct esophageal invasion by lymphoma is rare. The coexistence of a tracheoesophageal fistula (TEF) in such cases is even more exceptional, typically indicating a poor prognosis. This case report describes a female patient with advanced-age, large B-cell lymphoma involving both the lungs and esophagus, complicated by a TEF. Following treatment, the patient demonstrated improved physical strength and nutritional status, surviving more than 15 months post-diagnosis. PATIENT CONCERNS: An 81-year-old female patient presented with a 2-month history of progressively worsening dysphagia, accompanied by cough and expectoration of white sticky sputum, along with marked weight loss and declining physical strength. DIAGNOSES: The patient was definitively diagnosed with extranodal metastasis of large B-cell lymphoma involving the esophagus and complicated by TEF combined imaging studies and endoscopic biopsy. Concurrently, the patient presented with multiple comorbidities, including pulmonary fungal infection, viral hepatitis, moderate aortic valve regurgitation, and atrial fibrillation. INTERVENTIONS: The patient received 2 cycles of standard chemotherapy, concurrently supported by aggressive nutritional intervention via a jejunal feeding tube. This approach led to improved physical strength, stabilization of body mass index, and elevated serum albumin levels compared to baseline. A 1-year follow-up plain computed tomography scan demonstrated no further tumor progression. OUTCOMES: The patient's physical strength increased and nutritional status improved, with a post-diagnosis survival period exceeding 15 months. LESSONS: This case underscores that individualized, effective symptomatic treatment can prolong survival and enhance quality of life in high-risk, frail oncology patients, while highlighting the critical role of nutritional support in comprehensive cancer care.	esophagus
Knowledge, attitudes, and practices of esophageal cancer patients regarding pulmonary rehabilitation training.	INTRODUCTION: This study aimed to assess the knowledge, attitudes, and practices (KAP) of esophageal cancer patients concerning pulmonary rehabilitation training. METHODS: A cross-sectional study was conducted at the Henan Cancer Hospital from July 1, 2024, to August 31, 2024. Data were collected through questionnaires that gathered demographic information and KAP scores. RESULTS: A total of 530 esophageal cancer patients participated, including 197 (37.17%) regular smokers and 145 (27.36%) regular alcohol consumers. The mean ± SD scores were 7.78 ± 4.56 for knowledge (range: 0-20), 40.42 ± 4.66 for attitudes (range: 10-50), and 21.13 ± 3.08 for practices (range: 5-25). Correlation analyses showed positive relationships between knowledge and attitude scores (r = 0.335, p < 0.001), knowledge and practice scores (r = 0.323, p < 0.001), and attitude and practice scores (r = 0.567, p < 0.001). Structural Equation Modeling (SEM) indicated significant effects of knowledge on attitude (β = 0.420, p < 0.001) and attitude on practice (β = 0.711, p < 0.001). CONCLUSION: Esophageal cancer patients showed inadequate knowledge but positive attitudes and proactive practices regarding pulmonary rehabilitation. These findings highlight the need for targeted educational interventions to improve patient knowledge, enhancing overall engagement in rehabilitation practices.	esophagus
Regulatory role of ezrin in esophageal cancer progression via the PI3K-AKT signaling pathway.	BACKGROUND: The progression of esophageal cancer (EC) has been associated with aberrant activation of oncogenes and suppression of tumor suppressor genes. The EZR gene encodes ezrin, which is highly activated and upregulated in cancer cells, contributing to their invasive potential. This study aimed to elucidate the role of ezrin in EC progression, with a specific focus on the PI3K-AKT signaling pathway. METHOD: Expression of the EZR gene was silenced in ECA109 cells to assess changes in the phosphorylation levels of multiple kinases Bioinformatics analyses were conducted to identify ezrin-associated signaling pathways. In vitro functional assays were performed to investigate the effects of EZR silencing on cell proliferation, apoptosis, migration, and invasion. RESULTS: Cells with EZR knockdown demonstrated markedly decreased phosphorylation of AKT1/2/3 (S473), EGFR (Y1086), PLC-γ1 (Y783), Src (Y419), STAT5a/b (Y694/Y699), Yes (Y426), and β-Catenin, relative to control cells. These findings indicate that the PI3K-AKT signaling pathway is a critical downstream mediator of ezrin activity. The inhibition of AKT phosphorylation resulting from EZR knockdown was reversed upon treatment with an AKT pathway activator, confirming the involvement of this signaling axis. Functionally, EZR silencing significantly reduced EC cell proliferation, migration, and invasion, and increased apoptosis. These effects were attenuated, in part, by concurrent activation of the AKT pathway. Collectively, the data suggest that ezrin modulates key oncogenic processes in EC through the PI3K-AKT signaling pathway. CONCLUSION: Ezrin contributes to the progression of EC through modulation of the PI3K-AKT signaling cascade, influencing cellular proliferation, apoptosis, migration, and invasion.	esophagus