crossing96/oncoscreening huggingface dataset:
Diagnosing Complete Response to Preoperative Chemoradiation in Esophageal Cancer Using Dynamic Contrast-Enhanced MRI Response Criteria.	OBJECTIVE: To assess the performance of novel qualitative diagnostic criteria using dynamic contrast-enhanced (DCE) magnetic resonance imaging (MRI) to identify the pathologic complete response (pCR) of primary tumors in esophageal cancer after neoadjuvant chemoradiation (nCRT). MATERIALS AND METHODS: Patients who underwent nCRT, subsequent MRI, positron emission tomography/computed tomography (PET/CT), endoscopy, or esophagectomy for esophageal cancer between October 2021 and October 2023 were retrospectively analyzed. The DCE-MRI response of primary tumors was interpreted using five grades by thoracic radiologists as follows: G1 (compatible with CR), G2 (probable CR), G3 (probable partial response [PR]), G4 (compatible with PR), and G5 (stable or progressive disease). The performances of MRI, PET/CT, endoscopy, and their combinations in diagnosing pCR in primary tumors were calculated. RESULTS: A total of 52 patients (male:female, 46:6; age, 61.2 ± 8.0 years) were included. Surgical specimens revealed pCR (ypT0) in 34 patients. G1 as the MRI criterion for pCR of primary tumors yielded a positive predictive value (PPV), specificity of 100% (18/18), and low sensitivity (23.5% [8/34]). Combining G1 and G2 as the MRI criteria increased the sensitivity to 73.5% (25/34), with a specificity of 88.9% (16/18), accuracy of 78.8% (41/52), and PPV of 92.6% (25/27). Adding the DCE-MRI results (G1-2) significantly improved accuracy for both PET/CT (from 65.4% [34/52] to 80.8% [42/52], P = 0.03) and endoscopy (from 55.8% [29/52] to 76.9% [40/52], P = 0.005), with increase in sensitivity (from 55.9% [19/34] to 82.4% [28/34] for PET/CT-based evaluation [P = 0.008] and from 47.1% [16/34] to 82.4% [28/34] for endoscopy-based evaluation [P = 0.001]). CONCLUSION: DCE-MRI-based grading shows high diagnostic performance for identifying pCR in primary tumors, particularly in terms of PPV and specificity, and enhances response evaluation when combined with PET/CT and endoscopy.	esophagus
A multicenter prospective clinical trial reveals cell-free DNA methylation markers for early esophageal cancer.	BACKGROUNDCurrent methods for detecting esophageal cancer (EC) are generally invasive or exhibit limited sensitivity and specificity, especially for the identification of early-stage tumors.METHODSWe identified potential methylated DNA markers (MDMs) from multiple genomic regions in a discovery cohort, and a diagnostic model was developed and verified in a model-verification cohort of 297 participants. The accuracy of the MDM panel was validated in a multicenter, prospective cohort (n = 1,429). The clinical performance of identified MDMs were compared with current tumor-associated protein markers.RESULTSFrom 31 significant differentially methylated EC-associated regions identified in the marker discovery, we trained and validated a 3-MDM diagnostic model that could discriminate among patients with EC and volunteers without EC in a multicenter clinical prospective cohort with a sensitivity of 85.5% and a specificity of 95.3%. This panel showed higher sensitivity in diagnosing early-stage tumors, with sensitivities of 56% for stage 0 and 77% for stage I, compared with the performance of current biochemical markers. In population with high risk for EC, the sensitivity and specificity were 85.68% and 93.61%, respectively.CONCLUSIONThe assessment of tumor-associated methylation status in blood samples can facilitate noninvasive and reliable diagnosis of early-stage EC, which warrants further development to expand screening and reduce mortality rates.TRIAL REGISTRATIONChiCTR2400083525.FUNDINGScience and technology funds of Beijing Municipal Science & Technology Commission, Administrative Commission of Zhongguancun Science Park. Project number: Z201100005420007.	esophagus
An integrated prognosis prediction model based on real-word clinical characteristics for immunotherapy in advanced esophageal squamous cell carcinoma.	INTRODUCTION: Immune checkpoint inhibitors (ICIs) benefit only a subset of patients in advanced esophageal squamous cell carcinoma (ESCC). Our study aims to develop and validate a clinically accessible model to better identify those who may respond to ICIs. METHODS: This study enrolled advanced ESCC patients treated with ICIs at Peking University Cancer Hospital from January 14, 2016, to January 26, 2024 for the training cohort and at Harbin Medical University Cancer Hospital between January 10, 2019, and July 6, 2022 for the validation cohort. Combined positive score (CPS) was recorded to assess the predictive value of programmed cell death ligand-1 (PD-L1). Baseline clinical and laboratory characteristics were identified as predictors through Akaike information criterion (AIC) and Cox proportional hazards regression. The prediction model underwent internal validation through bootstrapping and was externally validated in the validation cohort. RESULTS: The training cohort consisted of 430 patients, while the validation cohort included 184 patients. PD-L1 expression failed to discriminate survival outcomes. The prediction model incorporates 10 variables: stage, bone metastasis, line of therapy, treatment, lactate dehydrogenase, carcinoembryonic antigen, carbohydrate antigen 199, systemic immune-inflammation index, lymphocyte count and prognostic nutritional index. The model achieved a C-index of 0.725 in the training cohort, 0.722 following bootstrapping, and 0.691 in the external validation cohort. An interactive online prediction tool ( https://escc-survival.shinyapps.io/shiny_app/ ) was subsequently developed. CONCLUSIONS: This is the first large-scale, real-world model for individualized survival prediction for advanced ESCC patients treated with ICIs, offering a practical tool for optimizing clinical decisions.	esophagus
Evaluating Postoperative Morbidity and Outcomes of Robotic-Assisted Esophagectomy in Esophageal Cancer Treatment-A Comprehensive Review on Behalf of TROGSS (The Robotic Global Surgical Society) and EFISDS (European Federation International Society for Digestive Surgery) Joint Working Group.	BACKGROUND: Esophageal cancer, the seventh most common malignancy globally, requires esophagectomy for curative treatment. However, esophagectomy is associated with high postoperative morbidity and mortality, highlighting the need for minimally invasive approaches. Robotic-assisted surgery has emerged as a promising alternative to traditional open and minimally invasive esophagectomy (MIE), offering potential benefits in improving clinical and oncological outcomes. This review aims to assess the postoperative morbidity and outcomes of robotic surgery. METHODS: A comprehensive review of the current literature was conducted, focusing on studies evaluating the role of robotic-assisted surgery in esophagectomy. Data were synthesized on the clinical outcomes, including postoperative complications, survival rates, and recovery time, as well as technological advancements in robotic surgery platforms. Studies comparing robotic-assisted esophagectomy with traditional approaches were analyzed to determine the potential advantages of robotic systems in improving surgical precision and patient outcomes. RESULTS: Robotic-assisted esophagectomy (RAMIE) has shown significant improvements in clinical outcomes compared to open surgery and MIE, including reduced postoperative pain, less blood loss, and faster recovery. RAMIE offers enhanced thoracic access, with fewer complications than thoracotomy. The RACE technique has improved patient recovery and reduced morbidity. Fluorescence-guided technologies, including near-infrared fluorescence (NIRF), have proven valuable for sentinel node biopsy, lymphatic mapping, and angiography, helping identify critical structures and minimizing complications like anastomotic leakage and chylothorax. Despite these benefits, challenges such as the high cost of robotic systems and limited long-term data hinder broader adoption. Hybrid approaches, combining robotic and open techniques, remain common in clinical practice. CONCLUSIONS: Robotic-assisted esophagectomy offers promising advantages, including enhanced precision, reduced complications, and faster recovery, but challenges related to cost, accessibility, and evidence gaps must be addressed. The hybrid approach remains a valuable option in select clinical scenarios. Continued research, including large-scale randomized controlled trials, is necessary to further establish the role of robotic surgery as the standard treatment for resectable esophageal cancer.	esophagus
The Kinesin Eg5 Inhibitor K858 Enhances Radiosensitivity in Esophageal Squamous Cell Carcinoma and Affects the Expression of Epithelial-mesenchymal Transition Related Markers: In vitro and In vivo Studies.	BACKGROUND: Radioresistance is the primary cause of treatment failure in esophageal squamous cell carcinoma, emphasizing the importance of identifying effective radiosensitizers. OBJECTIVES: This study aimed to explore the effects and potential mechanisms of Eg5 inhibitor K858 on the radiosensitivity of esophageal squamous cell carcinoma TE-1 and KYSE150 cell lines, as well as xenografts (TE-1 cells). METHODS: Cellular function was assessed using CCK8, wound healing, and transwell invasion assays. Radiosensitivity parameters were derived from colony formation assays. Cell apoptosis and cell cycle were assessed using flow cytometry, whereas protein expression levels were detected using western blotting and immunohistochemistry. The xenograft model was used to observe the growth of tumors. RESULTS: K858 inhibited the malignant functions of TE-1 and KYSE150 cell lines. Radiosensitivity parameters were reduced after K858 treatment. The combination of K858 and irradiation markedly suppressed cell proliferation, induced apoptosis, and stimulated cell cycle arrest during the irradiation-sensitive phase. Additionally, K858, combined with irradiation, significantly increased the expression of the epithelial-mesenchymal transition marker E-cadherin and decreased the expression of N-cadherin, vimentin, MMP2, and MMP9. K858, combined with irradiation, significantly inhibited tumor growth in xenograft models. CONCLUSION: K858 enhanced the radiosensitivity of esophageal squamous cell carcinoma and affected the expression of epithelial-mesenchymal transition-related markers.	esophagus
Developing a health education program for home enteral nutrition after esophageal cancer surgery based on the Delphi method.	To develop a health education program for home enteral nutrition (HEN) after Esophageal cancer (EC) surgery based on Delphi method, providing reference opinions for clinical nursing education and patient home care. The health education program for HEN after EC surgery was constructed through literature research, theoretical analysis and group discussion. From February to June 2024, experts in clinical nursing, clinical medicine, and nutrition of EC were invited to conduct 2 rounds of Delphi expert consultation to initially determine the items of the program. The weight and assignment of each items were determined through analytic hierarchy process (AHP), and then the final health education program for HEN after EC surgery was established. The authoritative coefficients of the 2 rounds consulting experts were 0.918 and 0.929 and the positive coefficients were 100% and 95%, respectively; The mean range of importance assignment for the second round of consultation indicators was 4.26 to 5.00 points, with a full score range of 40.90% to 95.45%. The mean harmony coefficients for expert opinions from 2 rounds were 0.206 and 0.218 (P < .01), respectively. The final health education program for postoperative HEN in EC includes 6 primary items, 27 secondary items, and 18 tertiary items. The results of the AHP showed that the consistency coefficients (CR values) of each matrix for the tertiary items were all < 0.1, meeting the requirements of consistency testing. The constructed health education program for postoperative HEN patients with EC in this study has high scientific and practical value, and can provide reference for the health education of postoperative HEN patients with EC.	esophagus
Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma and its Clinical Implications in Systemic Chemotherapy.	Esophageal cancer is a significant global health concern, with esophageal squamous cell carcinoma being the predominant subtype in high-incidence regions like China. Despite advances in multidisciplinary treatments, the prognosis for ESCC remains poor, with systemic chemotherapy facing the challenge of drug resistance. Epigenetic alterations, particularly DNA methylation, play a crucial role in ESCC carcinogenesis and therapeutic response. Aberrant DNA methylations, including global hypomethylation and promoter-specific hyper-methylation, disrupt critical pathways such as cell cycle regulation, apoptosis, and DNA repair, contributing to chemoresistance. Several studies have identified methylation markers that predict treatment response, particularly for chemotherapy, targeted therapy and immunotherapy, such as p16 and GPX3 for cisplatin, MTHFR for 5-FU, CHFR for paclitaxel. DNA methyltransferase inhibitors and other epigenetic therapies are being explored to reverse these methylation changes and enhance therapeutic efficacy. However, the clinical utility of these markers remains limited due to the lack of large-scale validation and concerns over off-target effects. This review aims to summarize all aberrant methylation alterations in ESCC and the clinical implications of aberrantly methylated candidate genes identified in ESCC systemic chemotherapy, with the goal of further understanding the underlying molecular mechanisms, refining methylation-targeting therapies, and integrating them with conventional treatments to improve patient outcomes.	esophagus
Postoperative complications and health-related quality of life after oesophageal cancer surgery: a national, population-based cohort study.	BACKGROUND AND PURPOSE: Surgical resection for oesophageal cancer is technically challenging and associated with a high incidence of complications. This study aimed to assess whether complications influence long-term health-related quality of life (HRQL) in oesophageal cancer survivors. MATERIALS AND METHODS: This nationwide cohort study included 617 patients who underwent oesophagectomy for cancer in Sweden between 2013 and 2021 with a 1-year follow-up. Complications within 30 days of surgery were categorised into (1) with or without, (2) medical or surgical and (3) according to the Clavien-Dindo classification (0-1, 2-3a, 3b-4). HRQL was assessed with European Organisation for Research and Treatment questionnaires and analysed using multivariable linear regression models, proving mean score differences (MSD) with 95% confidence intervals. The MSDs were adjusted for age, sex, education level, comorbidity, tumour histology, tumour stage, surgical technique and neoadjuvant therapy. RESULTS: The cohort included 406 patients who survived at least 1 year after oesophageal cancer surgery. Of these, 273 (68%) had at least one complication in the first 30 postoperative days. Long-term HRQL was comparable between patients with or without complications, with or without medical and surgical complications and between different grades of complication severity. INTERPRETATION: This study suggests that the influence of complications within 30 days of oesophageal cancer surgery on HRQL is minor after 1 year.	esophagus
Postoperative Adjuvant Therapy Benefits Non-pCR Patients Rather Than pCR Patients for Locally Advanced ESCC: A Multicenter Real-World Study.	BACKGROUND: There is no unified standard in adjuvant therapy (AT) for patients with esophageal squamous cell carcinoma (ESCC) after neoadjuvant therapy and surgery. We evaluated the significance of AT for these patients and explored its influencing factors. METHODS: ESCC patients who underwent neoadjuvant therapy and surgery from 2019 to 2022 at three centers were divided into AT (n = 227) and non-AT groups (n = 435). Baseline characteristics were balanced using propensity score matching (PSM). Primary endpoints were disease-free survival (DFS) and overall survival (OS), assessed using the Kaplan-Meier method. Subgroup analyses and univariate and multivariate Cox regression analyses were conducted to identify the prognostic factors. RESULTS: The median follow-up period is 36 (2-72) months. After PSM, the total population had 1-, 2-, and 3-year OS rates of 71.3%, 66.0%, and 64.1%, respectively. There were no statistically significant differences in DFS (HR: 0.79; 95% CI: 0.55-1.14, p = 0.21) or OS (HR: 0.75; 95% CI: 0.49-1.13, p = 0.17) between AT and non-AT groups. Subgroup analysis revealed that non-pCR patients benefited from AT in DFS (p = 0.042) and OS (p = 0.033). Moreover, in non-pCR patients who received AT, BMI ≥ 21.5 kg/m(2) and ypN0 were independent protective factors of DFS. ypN0 was an independent protective factor of OS. In terms of AT regimens, the Kaplan-Meier analysis revealed that adjuvant immunochemotherapy (AICT) provided superior survival benefits than adjuvant radiotherapy and adjuvant chemotherapy. CONCLUSIONS: Postoperative AT benefited ESCC patients with non-pCR, while AICT may be a relatively better AT regimen in real-world data, which deserves further exploration.	esophagus
Atractylenolide I Inhibits the Growth of Esophageal Cancer Cells by Inhibiting the Wnt/β-Catenin Pathway.	BACKGROUND: Esophageal cancer is a highly lethal cancer with a rapidly increasing incidence and a poor prognosis. Atractylenolide I is a natural sesquiterpene lactone extracted from the rhizome of the Asteraceae plant, which has a variety of pharmacological effects, such as anti-inflammatory and immunomodulatory. Still, its impact on esophageal cancer has not been reported. Therefore, this study investigated the in vitro and in vivo effects of Atractylenolide I on the growth and proliferation of esophageal cancer and explored its possible mechanisms. METHODS: To evaluate the effect of atractylenolide I on esophageal cancer cells, apoptosis assay and cell cycle assay tests were performed. Atractylenolide I was used to treat esophageal cancer cells for 48 hours, and flow cytometry detects apoptosis and cell cycle. The Wnt/β-catenin-related pathway proteins were then detected by Western blotting. For in vivo studies, an esophageal cancer graft tumor model was established subcutaneously in BALB/c nude mice, which were given Atractylenolide I treatment for 2 weeks. RESULTS: The result shows that Atractylenolide I inhibited the proliferation and induced apoptosis of esophageal squamous carcinoma and adenocarcinoma cells. Further research shows that Atractylenolide I inhibited the Wnt/β-catenin signaling pathway, decreased the expression of CCND1, MYC, and FN1 genes, and thus increased the apoptosis of esophageal cancer cells and blocked the cell cycle in G(0)/G(1) phase, hence exerting the role of inhibiting esophageal cancer cells in vivo and in vitro. CONCLUSION: This study indicates that Atractylenolide I is an efficient lead compound for the treatment of esophageal cancer, providing a theoretical basis for further clinical development and application of Atractylenolide I.	esophagus
Post-esophagectomy aortogastric-tube fistula treated successfully with TEVAR: case report and review of the literature.	BACKGROUND: Aortogastric-tube fistula is a rare but fatal complication of esophagectomy, most commonly induced by anastomotic leakage and peptic ulcer formation. METHODS: We report a rare case of a 55-year-old male patient presenting with an aortogastric-tube fistula located in the gastric conduit due to a recurrence of esophageal carcinoma. RESULTS: The patient was treated successfully with Thoracic Endovascular Aortic Repair (TEVAR) followed by esophageal stent placement to relieve dysphagia. CONCLUSION: Although aortogastric-tube fistula is an extremely rare entity, the advent of esophageal cancer surgery, has led to the recognition of aortogastric-tube fistula with increasing frequency in the literature. Herein, we provide a comprehensive review of the literature, focusing on the pathophysiology, time interval between surgery and presentation, type of treatment and survival of reported cases with post-esophagectomy aortogastric-tube fistula.	esophagus
Angiotensin II and AGTR1 in ESCC Proliferation and Invasion: Insights from the JAK/STAT3 Pathway.	BACKGROUND: Angiotensin II (Ang II) and its receptor, Angiotensin II receptor type 1 (AGTR1), have been implicated in the proliferation of cancer cells across various tumor types. This study aims to examine the impact of Ang II and AGTR1 on esophageal squamous cell carcinoma (ESCC) cells. METHODS: The clonogenicity and proliferation of tumor cells were evaluated through Clone Formation and Cell Counting Kit-8 (CCK-8) assays. Cell migration and invasion were determined utilizing Transwell assays. Flow cytometry was employed to analyze the cell cycle. Additionally, to investigate the expressions of genes associated with cell growth, migration, infiltration, and Janus kinase-signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathways, quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were utilized. RESULTS: In the current study, it was observed that increasing the concentration of Ang II significantly augmented the proliferation of ESCC cells. However, with the addition of its inhibitor losartan, the proliferative activity of ESCC cells was significantly reduced with the increase of losartan concentration (p < 0.05). The inhibition of AGTR1 also markedly reduced the proliferative activity of ESCC cells, counteracting the effect induced by Ang II treatment (p < 0.05). Additionally, Ang II was found to stimulate the migration and invasion of ESCC cells, facilitate the transition of these cells from the first gap (G1) to the synthesis (S) phase, and impede apoptosis (p < 0.05). However, treatment with losartan and AGTR1 inhibition significantly diminished the number of migratory and invasive cells, inhibited the transition from G1 to S phase, and promoted apoptosis in ESCC cells (p < 0.05). Regarding the mechanism, our research team found that Ang II and AGTR1 can enhance the proliferation and invasion of ESCC cells and inhibit their apoptosis via the JAK/STAT3 signaling pathway. Nevertheless, the AGTR1 blocker, losartan, effectively obstructed this process. CONCLUSION: The activation of the JAK/STAT3 signaling pathway by Ang II and AGTR1 promotes the advancement of ESCC tumors. Consequently, targeting Ang II and AGTR1 could potentially emerge as a promising strategy for ESCC treatment.	esophagus