crossing96/oncoscreening huggingface dataset:
Residual pattern of primary tumor and lymph node in ESCC treated with nCRT with or without pembrolizumab: an analysis from a prospective cohort.	BACKGROUND: Neoadjuvant chemoradiotherapy (nCRT) is recommended as the standard of care for locally advanced esophageal squamous cell carcinoma (ESCC). Adding immunotherapy to nCRT (nICRT) has gained attention in clinical practice. We evaluated the differences in clinicopathologic outcomes and the patterns of lymph node metastasis in patients receiving nCRT and nICRT for locally advanced ESCC. METHODS: A total of 208 ESCC patients who completed transthoracic esophagectomy after neoadjuvant treatment were enrolled. Clinicopathologic parameters and the rates of lymph node metastasis in each station classified using both the eighth edition of the American Joint Committee on Cancer (AJCC) esophageal cancer staging system and the 11th edition of the Japanese Classification of Esophageal Cancer (JCEC) standard were recorded and evaluated. RESULTS: The rates of pathological complete response (pCR) and major pathological response (MPR) were 44.9% in nICRT vs. 37.0% in nCRT (p = 0.263) and 79.5% in nICRT vs. 65.4% in nCRT (p = 0.024), respectively. The common sites of lymph node metastasis after neoadjuvant treatment were station 112pulL (8.3%), followed by station 104L (4.9%), station 7 (4.5%), and station 3a (4.3%), according to the 11th JCEC standard. Compared with nCRT, nICRT can significantly reduce the rates of lymph node metastasis in station 2R (0.8% vs. 4.6%, p = 0.039) classified using the AJCC system, and those in station 106recR (0.8% vs. 4.6%, p = 0.042) and station 20 (0 vs. 12.5%, p = 0.030) classified using the JCEC standard. CONCLUSION: nICRT followed by surgery may lead to a promising pathological response. For patients with lymph node metastasis in certain regions, nICRT should be considered as a better preoperative treatment option.	esophagus
Multiplex Digital PCR Assay Targeting DNA Methylation for Early Detection of Cancer.	Digital PCR has been demonstrated to enable the precise nucleic acid absolute quantification across a wide range of applications. Historically, dPCR technology was limited to two channels for fluorescence detection. Recent advances in digital PCR have made it possible to multiplex and allow for simultaneous analysis of multiple targets within a PCR reaction. Here, we describe a multiplex dPCR assay for the detection and quantification of methylated DNA (also known as DNA-methylation-specific multiplex digital PCR, or DNA-methylation specific dPCR). We also demonstrate the application of this technology for the development of a candidate DNA methylation-based biomarker panel for the early detection of high-grade dysplasia and esophageal adenocarcinoma. Further, we discuss common technical challenges and troubleshooting for performing successful DNA-methylation-specific MS-dPCR assays.	esophagus
[Hepatic Arterial Infusion Chemotherapy for Liver Metastasis after Esophagectomy for Esophageal Cancer].	The aim of this study was to evaluate the outcome and efficacy of hepatic arterial infusion chemotherapy for liver metastasis. Nineteen patients with liver metastasis after esophagectomy for esophageal squamous cell carcinoma underwent hepatic arterial infusion chemotherapy. Six patients(32%)received hepatic arterial infusion chemotherapy as the initial treatment, and the remaining 13 patients(68%)received hepatic arterial infusion chemotherapy after systemic chemotherapy. Of the 13 patients, 3 responders to the first systemic chemotherapy received as maintenance therapy, and 10 non-responders to the first systemic chemotherapy received as a second-line therapy. Response ratio was 37%, and 6 patients(32%)had a toxicity of Grade 3 or more. The median overall survival after liver metastasis was 10.8 months, and the 1-year overall survival rate was 42%. No patient survived more than 3 years after liver metastasis. The 1-year overall survival rate in patients received as the initial and maintenance therapy was 67%, while that in patients received as a second-line therapy was 20%(p=0.0291). Our findings suggested that hepatic arterial infusion chemotherapy for liver metastasis may be effective treatment as the initial therapy or the maintenance therapy for responders to the first systemic chemotherapy.	esophagus
Delayed Esophagectomy After Chemoradiation Is Not Associated With Increased Mortality or Recurrence.	OBJECTIVE: To evaluate the impact of delayed esophagectomy on the overall survival of esophageal cancer patients undergoing esophagectomy after CROSS. METHODS: A retrospective analysis was done of a prospective database of esophagectomy patients who underwent CROSS therapy and esophagectomy from May 2016 to January 2020. Preoperative characteristics, postoperative adverse events, recurrence rates, and survival rates were compared between patients who underwent surgery within 60 days of CROSS completion versus > 60 days. RESULTS: In total, 197 patients were included; 137 underwent surgery within 60 days (standard group, SG) versus 60 at > 60 days (delayed group, DG). Median time to surgery was 43 versus 76 days for the SG and DG groups. Median follow-up was 60 months. No differences were observed for gender, race, home state, Eastern Cooperative Oncology Group score, and tumor characteristics. DG patients were older; had higher Charlson Comorbidity Scores; and more history of myocardial infarction, stroke, and smoking, all p ≤ 0.05. DG had increased odds of major postoperative adverse events (odds ratio 2.26, 95% confidence interval 1.11-4.20). Overall survival and recurrence were similar. CONCLUSION: Following CROSS, a delay in esophagectomy beyond 60 days was not associated with worse recurrence or overall survival despite increased comorbidities and postoperative events.	esophagus
Whole exome sequencing identifies novel somatic variants in Xinjiang Kazak esophageal squamous cell carcinoma.	The incidence of esophageal squamous cell carcinoma (ESCC) is increasing globally. Notably, in Xinjiang, China, ESCC patients have garnered significant attention due to their unique epidemiological characteristics. Specifically, the mortality rate of Xinjiang Kazakh ESCC (referred to as XK ESCC) is substantially higher than the national average in China. This alarming disparity underscores the critical need for identifying new therapeutic targets. In this study, we aimed to elucidate the underlying genomic abnormalities in XK ESCC by conducting whole-exome sequencing on four matched pairs of esophageal squamous cell tumors and adjacent control tissues from Xinjiang Kazakh individuals. Comprehensive statistical analysis of the exome data revealed multiple somatic mutations, copy number variations (CNVs), and 14 potential cancer driver genes harbouring missense mutations. Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses were performed on 75 significantly mutated genes (SMGs). Intriguingly, we identified IFNA17 and NLRP6 as significantly mutated genes enriched in the NOD-like receptor signaling pathway. Subsequent functional studies on ESCC-derived IFNA17 and NLRP6 mutants demonstrated that these mutations enhance cellular invasion. To the best of our knowledge, this study represents the first comprehensive exome sequencing analysis specifically targeting XK ESCC. Our findings highlight novel mutation loci that may explain the aggressive nature of XK ESCC. These insights could contribute to the development of early diagnostic and prognostic markers, as well as therapeutic targets, tailored for XK ESCC.	esophagus
Metaplastic Barrett's oesophagus represents reversion to a developmental-like epithelial cell state.	In Barrett's oesophagus (BO), the precursor of oesophageal adenocarcinoma, the adult stratified squamous epithelium is replaced by a simple columnar phenotype. This has been considered metaplasia, i.e. the inappropriate conversion from one adult cell type to another. Alternatively, BO could represent reversion to an embryonic-fetal state when the early foregut is initially lined by simple columnar epithelium. Exploration of this hypothesis has been hampered by inadequate molecular details of human oesophageal development. Here, we adopted single-cell transcriptomic and epigenomic approaches to discover and de-code the cell types that constitute the initial primitive columnar, transitory and subsequently stratified lower oesophageal epithelium. Each stage comprises several previously undefined epithelial subpopulations. Importantly, early foregut columnar epithelial cells share core regulatory and gene expression programmes with BO. Among these, HNF4A is identified as a prominent transcriptional regulator that forms the core of a regulatory network in early foregut columnar cells. These regulatory networks are also central to programmes known to be reactivated in BO. Collectively, these data argue that the path to BO involves reactivation of pathways that define primitive embryonic and fetal epithelial cell states.	esophagus
Comparative analysis of robot-assisted minimally invasive esophagectomy versus conventional minimally invasive esophagectomy, a systematic review and meta-analysis.	Robot-assisted minimally invasive esophagectomy (RAMIE) may enhance visualization and lymph-node dissection compared with conventional minimally invasive esophagectomy (cMIE), but comparative effectiveness remains uncertain. We performed a PRISMA-compliant systematic review and meta-analysis of randomized controlled trials and propensity-matched cohort studies comparing RAMIE with MIE (from 2013 to August 26th, 2025). PubMed, Cochrane Library, Embase, and Web of Science were searched. Continuous outcomes were pooled as mean differences (MD) and dichotomous outcomes as risk ratio (RR) using randomized-effects models; heterogeneity was assessed with I(2). Risk of bias was evaluated with RoB-2 for trials and the Newcastle-Ottawa Scale for cohorts. Twenty-five studies (~ 8,900 patients; RAMIE ≈ 4,200; MIE ≈ 4,700) met eligibility criteria. Total operative time was longer with RAMIE (MD 38.91 min, 95% CI 16.05-61.76; p = 0.0008; I²=97%), while thoracic operative time alone was not significantly different (MD 16.18 min, 95% CI - 2.46 to 34.82; p = 0.09; I²=94%). Estimated blood loss was modestly lower with RAMIE (MD - 12.73 mL, 95% CI - 25.25 to - 0.21; p = 0.05; I²=86%). RAMIE achieved a higher total lymph node yield (MD 2.01 nodes, 95% CI 1.05-2.96; p < 0.001; I²=57%) and retrieved more left RLN lymph nodes (MD 0.60, 95% CI 0.13-1.08; p = 0.01), with no significant difference in right RLN nodes (MD 0.11, 95% CI - 0.02 to 0.24; p = 0.09; I² = 31%). In-hospital mortality (RR 0.76, 95% CI 0.42-1.39; p = 0.38; I²=0%) and 90-day mortality (RR 0.97, 95% CI 0.53-1.77; p = 0.91; I²=0%) were similar. Overall complications (RR 0.90, 95% CI 0.79-1.02; p = 0.09) and major complications (RR 0.80, 95% CI 0.63-1.01; p = 0.06) did not differ. Pulmonary complications trended lower (RR 0.88, 95% CI 0.76-1.02; p = 0.10), and recurrent laryngeal nerve palsy was borderline lower (RR 0.79, 95% CI 0.62-1.00; p = 0.05). Length of stay was shorter with RAMIE (MD - 1.28 days, 95% CI - 2.26 to - 0.34; p = 0.01; I²=84%), whereas ICU stay was longer (MD 2.68 days, 95% CI 0.51-4.84; p = 0.02; I²=98%). Publication bias signals for thoracic operative time and length of stay were driven by outlier on sensitivity analysis. RAMIE and cMIE are both safe. RAMIE involves a longer operative time but yields lower estimated blood loss, a higher total lymph nodes harvest-particularly along the left RLN- fewer pulmonary complications by trend, and a shorter length of stay, with no significant difference in anastomotic leak or early mortality. These results support patient-centered selection between RAMIE and cMIE, taking center experience and the learning curve into account. PROSPERO CRD420251134020.	esophagus
AL137246.1 inhibits esophageal squamous cell carcinoma cisplatin resistance by suppressing the transcriptional activity of GLI2 on ABCC1.	Esophageal squamous cell carcinoma (ESCC) is a malignant cancer. At present, platinum-based chemotherapy drugs are mainly used to treat ESCC patients. However, certain patients have developed significant resistance to cisplatin, which greatly limits the effectiveness of treatment. Hence, it is urgent to probe the mechanism of cisplatin chemotherapy resistance in ESCC. To clarify the association between AL137246.1 level and cisplatin resistance in ESCC patients, a total of 30 pairs of cisplatin-sensitive and cisplatin-resistant ESCC tissues were collected, and 30 non-cancerous tissues were used as controls. Survival analysis was used to detect the relationship between AL137246.1 level and ESCC prognosis. Then, Eca109 and Kyse70 cells were treated with cisplatin to induce the ESCC cisplatin resistance model. For understanding the detailed molecular process involving AL137246.1 in the development of cisplatin resistance in ESCC, the binding relationship between GLI2 and ABCC1 promoter was determined by dual luciferase and ChIP assays. RIP was applied to test the interaction between AL137246.1 and GLI2. Cell viability and proliferation were detected by CCK8 and Edu assays, respectively. Cell apoptosis was detected by flow cytometry. The results indicated that AL137246.1 level was reduced in ESCC and indicated a poor prognosis of ESCC. AL137246.1 overexpression was associated with increased sensitivity to cisplatin in ESCC cells, which was reversed by ABCC1 upregulation. Mechanistically, GLI2 led to the transcriptional activation of ABCC1 in ESCC. In conclusion, AL137246.1 inhibited the expression of ABCC1 by binding to GLI2, thereby enhancing the sensitivity of ESCC to cisplatin. This study suggested that AL137246.1, as a potential molecular target, has important application prospects in improving the sensitivity of ESCC to cisplatin chemotherapy.	esophagus
TNK2 promotes the EMT proliferation and invasion of esophageal squamous cell carcinoma by enhancing FOXO1 through the AKT pathway.	This study focuses on the function and molecular mechanisms of the tyrosine kinase non-receptor 2 (TNK2) in esophageal squamous cell carcinoma (ESCC). In this study, using ESCC as a model, techniques such as Western Blot, immunoprecipitation (IP), Transwell assay, and immunofluorescence staining, combined with lentiviral transfection experiments, were employed to analyze the molecular regulatory mechanism of TNK2. Analysis revealed a marked increase in TNK2 expression levels in clinical ESCC specimens and established ESCC cell lines. TNK2 promoted epithelial-mesenchymal transition (EMT), proliferation, and invasion of ESCC cells. Functional experiments demonstrate that TNK2 promotes EMT, proliferation, and invasive capacity in ESCC cells. Mechanistically, TNK2 interacts with AKT and promotes its phosphorylation, which in turn inhibits the ubiquitination and proteasomal degradation of FOXO1, ultimately leading to increased FOXO1 protein expression. This study reveals that TNK2 enhances FOXO1 expression via the AKT signaling axis, thereby driving ESCC malignant progression. Genipin targets TNK2 to inhibit the progression of ESCC. It provides new insights into the pathogenesis of ESCC and theoretical basis for positioning TNK2 gene as a potential therapeutic target.	esophagus
Disaggregating Asian American and Pacific Islander Subpopulations in Esophageal Cancer: Stage, Histology, and Survival.	BACKGROUND: Asian American/Pacific Islander (AAPI) patients are typically aggregated together in esophageal cancer (EC) research, which may mask differences in risk factors, histology, and survival. This study analyzed EC characteristics and outcomes in disaggregated AAPI groups. METHODS: Using the National Cancer Database (2009-2020), we compared aggregated AAPI patients, regional subgroups (East Asian, etc.), and subpopulations (Chinese, Vietnamese, etc.) to non-Hispanic White (NHW) patients. Advanced stage (III-IV) at diagnosis and squamous cell carcinoma (SCC) histology were analyzed. After adjusting for sociodemographic factors, 3-year overall survival (OS) was assessed. RESULTS: A total of 3,254 AAPI patients with EC were compared with 156,801 NHW patients. Aggregated AAPI patients had higher odds of advanced stage disease (adjusted odds ratio [aOR] 1.12, 95% confidence interval [CI] 1.03-1.21, p = 0.006), higher odds of squamous cell carcinoma (aOR 4.63, 95% CI 4.28-5.01, p < 0.0001), and better 3-year OS (hazard ratio [HR] 0.87, 95% CI 0.82-0.91, p < 0.001). For regional subgroups, only Southeast Asian (aOR 1.46, 95% CI 1.22-1.75, p < 0.0001) and Pacific Islander (aOR 1.62, 95% CI 1.19-2.23, p = 0.003) patients had higher odds of advanced stage disease. For subpopulations, Vietnamese patients had the highest odds of SCC (aOR 8.90, 95% CI 6.73-11.79, p < 0.0001) and worse 3-year OS (HR 1.29, 95% CI 1.09-1.51, p = 0.002), while Chinese (HR 0.66, 95% CI 0.60-0.74, p < 0.0001) and Korean patients (HR 0.70, 95% CI 0.59-0.84, p < 0.0001) showed better OS. CONCLUSIONS: Disaggregated analysis of AAPI patients revealed significant heterogeneity in EC characteristics and survival. Our findings emphasize collecting subpopulation-level data and tailoring interventions.	esophagus
Risk elements and diagnostic indicators for asymptomatic immune checkpoint inhibitor-associated myocarditis in esophageal cancer.	This article pertains to the study by Liu et al. Myocarditis caused by immune checkpoint inhibitors in patients with esophageal cancer is a concerning issue. This was found to be linked by increased levels of creatine kinase (CK) and CK isoenzymes, as well as older age and male gender. All these risk factors behind this phenomenon, which could be incorporated into a unified prediction model, have been briefly discussed. Several recommendations have been made to validate this prediction model for use in different clinical scenarios.	esophagus
[Inhibition of BRD4 promotes migration of esophageal squamous cell carcinoma cells with low ACC1 expression].	OBJECTIVES: To investigate the effect of BRD4 inhibition on migration of esophageal squamous cell carcinoma (ESCC) cells with low acetyl-CoA carboxylase 1 (ACC1) expression. METHODS: ESCC cell lines with lentivirus-mediated ACC1 knockdown or transfected with a negative control sequence (shNC) were treated with DMSO, JQ1 (a BRD4 inhibitor), co-transfection with shNC-siBRD4 or siNC with additional DMSO or C646 (an ahistone acetyltransferase inhibitor) treatment, or JQ1combined with 3-MA (an autophagy inhibitor). BRD4 mRNA expression in the cells was detected using RT-qPCR. The changes in cell proliferation, migration, autophagy, and epithelial-mesenchymal transition (EMT) were examined with CCK8 assay, Transwell migration assay, and Western blotting. RESULTS: ACC1 knockdown did not significantly affect BRD4 expression in the cells but obviously increased their sensitivity to JQ1. JQ1 treatment at 1 and 2 μmol/L significantly inhibited ESCC cell proliferation, while JQ1 at 0.2 and 2 μmol/L promoted cell migration. The cells with ACC1 knockdown and JQ1 treatment showed increased expresisons of vimentin and Slug and decreased expression of E-cadherin. BRD4 knockdown promoted migration of ESCC cells, and co-transfection with shACC1 and siBRD4 resulted in increased vimentin and Slug expressions and decreased E-cadherin expression in the cells. C646 treatment of the co-transfected cells reduced acetylation levels, decreased vimentin and Slug expressions, and increased E-cadherin expression. Treatment with JQ1 alone obviously increased LC3A/B-II levels in the cells either with or without ACC1 knockdown. In the cells with ACC1 knockdown and JQ1 treatment, additional 3-MA treatment significantly decreased the expressions of vimentin, Slug and LC3A/B-II and increased the expression of E-cadherin. CONCLUSIONS: BRD4 inhibition promotes autophagy of ESCC cells via a histone acetylation-dependent mechanism, thereby enhancing EMT and ultimately increasing cell migration driven by ACC1 deficiency.	esophagus
Neoadjuvant chemoimmunotherapy for esophageal squamous cell carcinoma with non-regional cervical lymph node metastasis: a retrospective pilot study.	BACKGROUND: Esophageal squamous cell carcinoma (ESCC) with non-regional cervical lymph node metastasis (CLNM) poses significant therapeutic challenges due to lack of consensus in guidelines and poor outcomes associated with conventional treatment modalities. Recent studies have demonstrated promising efficacy of combined immunotherapy, chemotherapy, and surgery in ESCC; however, the role of this multimodal approach in managing non-regional CLNM-historically considered inoperable-remains unclear. METHODS: This retrospective cohort study included 15 patients with thoracic ESCC and non-regional CLNM who underwent neoadjuvant chemoimmunotherapy (nCIT), followed by McKeown esophagectomy with three-field lymphadenectomy between 2020 and 2024. CLNM was confirmed via ultrasound-guided biopsy. Data on pathological response, safety, and survival outcomes were collected and analyzed. Survival analysis was performed using the Kaplan-Meier method. RESULTS: A pathological complete response (pCR) in CLNM was achieved in 93.3% of patients, while the Total pCR (ypT0N0M0) rate (clearance of both primary tumor and metastatic lymph node) was 33.3%. At a median follow-up of 18.0 months, the 1-year disease-free survival (DFS) rate was 91.7%. One patient died during the follow-up period. Postoperative complications occurred in 73.3% of patients, predominantly respiratory events such as atelectasis and pneumonia; only one patient experienced a grade 4 event. Treatment-related adverse events (TRAEs) were mild, with no grade ≥3 TRAEs observed; anemia was the most common TRAEs, occurring in 46.7% of patients. CONCLUSION: nCIT induces a high cervical nodal response in ESCC with non-regional CLNM and may redefine surgical eligibility for patients with non-regional metastases. The observed 1-year DFS of 91.7% is promising, though long-term outcomes require further validation through prospective studies.	esophagus
Pharmacological targeting of HDAC/BET pathway enhances 5-FU efficacy in esophageal squamous cancer cells.	5-Fluorouracil (5-FU) remains the most commonly used first-line chemotherapeutic agent for the treatment of esophageal cancer (EC), but its therapeutic efficacy is unsatisfactory. In this study, we found that 5% of ESCC cells survived the treatment with high doses of 5-FU for 5 days. Compared to the parental cells, the rapidly acquired drug-tolerant persister (DTP) cells showed enhanced expression of those genes associated with stemness and epithelial-mesenchymal transition. Once 5-FU was removed, the regrown cells regained their sensitivity to 5-FU. Additionally, the transcriptomic profiles analysis showed that the parental and the regrown cells had very similar gene expression profile, while DTP cells showed distinct changes. Significant changes in histone deacetylation pathway were observed in DTP cells. Knockdown of HDAC2/6/9 and BRD4 markedly reduced the formation of DTP cells. We screened our drug library and found that HDAC4/5/6/7 inhibitor TMP269 and BRD2/3/4 inhibitor ABBV-744 showed potent synergistic cytotoxic effects with 5-FU in the parental ESCC cells. Our team then synthesized a new HDAC inhibitor YFF-702 and BET inhibitor C-34, which showed synergistic effects with 5-FU in the parental ESCC cells. Moreover, ABBV-744 and YFF-702 showed synergistic cytotoxic effects with 5-FU in DTP cells. Animal experiments further demonstrated that YFF-702 significantly improved the efficacy of 5-FU in an in vivo tumor model. This current research demonstrates that combining HDAC/BET inhibition with 5-FU may be a promising therapeutic strategy for ESCC patients by targeting 5-FU indued DTP cells.	esophagus