Translating trial findings to real-world cure rates for resectable oesophageal and gastroesophageal junction (GEJ) adenocarcinoma is critical. Standard endpoints like disease-free survival (DFS) may not distinguish durable cures from delayed recurrences. This analysis of the AGAMENON-SEOM registry (NCT04958720) compared perioperative chemotherapy versus neoadjuvant chemoradiotherapy (nCRT). We estimated cure rates and analysed DFS and overall survival (OS) using mixture cure models and Cox proportional hazards models. In 500 patients, perioperative FLOT improved DFS (HR 0.60; p = 0.01) and OS (adjusted HR 0.63; p = 0.015) compared to CROSS-based nCRT. Notably, cure models confirmed a higher cure fraction for FLOT in high-risk subgroups (e.g., stage III, high neutrophil-to-lymphocyte ratio). While platinum-fluoropyrimidine-based nCRT ± immunotherapy yielded higher R0 and pathological complete response rates, its estimated cure rate was comparable to FLOT, both overall and across all subgroups. Cure is an informative endpoint in localised oesophageal cancer. In this registry analysis, perioperative FLOT was associated with higher cure rates than CROSS, particularly in high-risk subgroups. Exploratory findings suggest that alternative neoadjuvant strategies, such as those incorporating ICIs or FOLFOX, warrant further investigation.

Previous observational studies have suggested a protective effect of Helicobacter pylori (HP) infection against the incidence of esophageal adenocarcinoma(EAC). To further validate this perspective at the genetic level, we employed Mendelian randomization (MR) to analyze the correlation between HP infection-related serological antibodies and EAC in the European population. This study employed a two-sample MR analysis method, utilizing GWAS data on seven serological antibodies related to HP infection selected from European populations as instrumental variables. The outcome data comprised GWAS data from 16,790 cases of EAC. Three analytical techniques were employed: inverse variance weighting, Egger -MR, and weighted median method. Additionally, Cochran's Q test, Egger -MR intercept test, MR-Presso method, and leave-one-out analysis were utilized for sensitivity analyses. The results of analysis indicated no clear relationship between the seven serological antibodies related to HP infection and the incidence of EAC in European populations(all p > 0.05). The secondary outcomes further validated the previously mentioned results (p > 0.05), with analyses of heterogeneity (p > 0.05) and pleiotropy (p > 0.05) confirming the robustness of the MR results. No significant association was detected between various serological antibodies related to HP infection and the incidence of EAC in the European population. This may, to some extent, negated the protective role of HP infection against EAC.

Barrett's esophagus (BE) is the replacement of normal squamous epithelium in the distal esophagus by columnar epithelium. The prognosis of esophageal adenocarcinoma (EAC) depends largely on the stage at diagnosis. Advances in endoscopic imaging and quality standards have significantly improved the early detection of BE-associated neoplasia. This review summarizes current classification systems, sampling protocols, and adjunct tools for diagnosing early neoplasia in BE in Western practice. In Western practice, the diagnosis of Barrett's esophagus (BE) relies on consensus criteria requiring endoscopic evidence and histological confirmation of columnar epithelium proximal to the gastroesophageal junction. However, there are discrepancies regarding the minimum BE extent and the necessity of intestinal metaplasia for diagnosis. Detecting early neoplasia in BE is challenging due to the flat and subtle nature of dysplastic lesions. High-definition white light endoscopy (HD-WLE) is the standard modality for BE surveillance and is used to assess for characteristic features of neoplasia, including nodularity, surface irregularity, color changes, and demarcated areas. Image-enhancing techniques-such as virtual chromoendoscopy (e.g., Narrow-Band Imaging [NBI], Texture and Color Enhancement Imaging [TXI], Blue Light Imaging [BLI], Linked Color Imaging [LCI]), and acetic acid chromoendoscopy-have improved dysplasia detection when applied alongside validated classification systems. Despite technological advances, random four-quadrant biopsies (4QBs) remain the standard for dysplasia detection. Estimating lesion depth is based primarily on HD-WLE, with limited contribution from chromoendoscopy and ancillary imaging techniques (i.e. endoscopic ultrasound [EUS], confocal laser endomicroscopy [CLE], optical coherence tomography [OCT]). Early Barrett's neoplasia is challenging to detect. HD-WLE and image-enhancing techniques improve visualization, but random 4QBs remain central to the diagnostic process. Lesion depth is primarily assessed using endoscopic features and, to a limited extent, ancillary techniques.

Oesophageal adenocarcinoma (OAC) and its precursor condition, Barrett oesophagus, are characterized by phenotypic and molecular intertumoural and intratumoural heterogeneity. This heterogeneity arises in space and time through a complex and still poorly understood interplay between cancer-cell-intrinsic factors, the tumour microenvironment and external influences, such as exposure to anticancer therapies. Together, these elements contribute to a high degree of resistance to therapy while limiting the development of novel targeted therapies and the identification of predictive biomarkers. This situation is exacerbated both in Barrett oesophagus and OAC by a historical clinical reliance on biopsy samples that reflect disease status only at a single location and timepoint. A better understanding of heterogeneity is therefore vital to improve efforts to intercept the development of and optimize treatments for OAC. In this Review, we provide an overview of current and future directions of research on the heterogeneity of Barrett oesophagus and OAC, summarizing our knowledge of the factors that influence heterogeneity, and its consequences across the spectrum of these diseases.

Background/Objectives: Despite the introduction of targeted therapies such as Nivolumab, survival outcomes for patients with esophageal adenocarcinoma remain poor. During tumorigenesis, some tumors develop auxotrophy by downregulation of Argininosuccinate Synthetase-1 (ASS1), making them reliant on external arginine supply and thus potentially susceptible to arginine deprivation therapy. Arginine deprivation therapy with agents such as pegargiminase has shown improved survival in patients with pleural mesothelioma exhibiting ASS1 loss in tumor cells. Therefore, we investigated the prevalence of ASS1 loss in esophageal adenocarcinoma. Methods: First, we compared the staining patterns of three antibodies for ASS1 with RNA in situ Scope analysis results to identify the most reliable antibody for ASS1 immunohistochemical staining in esophageal adenocarcinoma. Subsequently, we performed ASS1 immunohistochemical staining on samples from 97 patients who underwent curative resection. The staining results were classified into three categories based on expression levels: negative, low-positive, and positive. Results: Among all included patients, 6.2% exhibited an ASS1 loss, and 6.2% showed low ASS1 expression. Notably, patients with an ASS1 loss did not demonstrate a response to neoadjuvant therapy. Patients with ASS1 loss or low expression were significantly younger. Conclusions: Our findings indicate that approximately 12.4% of patients with esophageal adenocarcinoma may be eligible and could potentially benefit from arginine deprivation therapy. This underscores the urgent need for clinical trials evaluating the efficacy of pegargiminase in this patient population. Additionally, incorporating ASS1 immunohistochemical staining into pre-neoadjuvant biopsy assessments should be considered to optimize neoadjuvant treatment strategies and advance the implementation of personalized cancer therapy.

IntroductionEsophageal and gastric cancers account for nearly 1.5 million new cases and 1.1 million deaths annually worldwide. In western countries, the incidence of esophageal cancer is rising while that of gastric cancer has decreased, although the pattern varies between the morphological types and subsites. We aim to describe the burden of esophageal and gastric cancers in Norway by providing national trends in incidence and mortality, separately for esophageal squamous cell carcinoma (SCC) and adenocarcinoma (AC), and for gastric ACs by gastric subsites.MethodsWe extracted information about all esophageal (ICD10 C15) and gastric cancer (ICD10 C16) patients diagnosed 1993‒2022 from the Cancer Registry of Norway. Age-standardized (European standard population) rates and performed joinpoint regression analyses were calculated to examine trends in incidence and mortality over time, for esophageal cancer SCC and AC and by subsite for gastric AC (cardia: ICD10 C16.0 and non-cardia: ICD10 C16.1–9). We used annual percent change (APC) and weighted average APC (AAPC), stratified by sex, age group, and stage at diagnosis.ResultsDuring 1993–2022, 6,433 esophageal cancers (2,616 SCC, 3,817 AC) and 14,453 gastric AC were diagnosed, and 4,683 esophageal and 10,421 gastric AC deaths occurred. The incidence and mortality of esophageal ACs increased whereas the rates for esophageal SCC declined in men and were stable in women. The highest AC incidence and mortality increases were seen in men (incidence AAPC = 2.8) and ages ≥70 years (incidence AAPC = 5.9). In contrast, the incidence and mortality of gastric cancer decreased over time, most pronounced for non-cardia gastric AC (incidence AAPC men =−5.3, women =−3.9).ConclusionThe incidence and mortality of esophageal AC has increased in Norway during the last decades, most pronounced in men, ages ≥70 years. The rates of SCCs decreased, although trends differed between sex and age groups. The incidence and mortality of gastric AC decreased in all age-groups for both sexes, especially for non-cardia gastric cancer.

While multimodality therapy for locally advanced esophageal cancer evolves, neoadjuvant chemoradiation has been a longstanding treatment paradigm. Pathologic complete response (pCR) rates vary by histology: 25% for adenocarcinoma (AC) and up to 50% for squamous cell carcinoma (SCC). Long-term outcomes after pCR remain poorly understood but important to define as multiple treatment options emerge. We analyzed patients with cT2+/N+M0 esophageal AC or SCC treated with neoadjuvant chemoradiation and resection from an institutional database. Recurrence-free survival (RFS) and overall survival (OS) were assessed using Kaplan-Meier and multivariable Cox models. A risk score for recurrence was developed and validated using National Cancer Data Base data. Of 830 patients, 37.1% achieved pCR (n = 250/720, 34.2% for AC and n = 58/100, 58.0% for SCC). pCR was associated with prolonged OS (5-year OS: 56.2% versus 35.0% for residual disease, p < 0.001). pCR remained an independent predictor of OS after adjustment for known predictors of OS (HR 0.58, p < 0.001). Recurrence typically occurred within 2 years then plateaued, with 5-year RFS of 72.6% for AC and 83.0% for SCC. Clinical T3/T4, cN+, fewer lymph nodes examined, and AC histology were independently associated with worse RFS. A weighted risk score for recurrence was developed, which externally predicted OS after pCR in the NCDB (HR 1.12 per point, p < 0.001). Median OS was 7.8 years for cases with score 0-3 versus 5.7 years for cases with score 4-5. pCR after neoadjuvant chemoradiotherapy is a strong predictor of survival, but recurrence remains common. Further investigation into adjuvant therapies for high-risk pCR patients is needed.

Objectives Oesophageal adenocarcinoma (OAC) has a poor prognosis as patients typically present with late-stage disease. Gastro-oesophageal reflux disease (GORD) can lead to Barrett’s oesophagus (BO), the only known precursor to OAC. Detecting patients with BO allows interventions to prevent development of late-stage OAC and improve survival. Non-endoscopic devices, such as EndoSign, coupled with biomarkers trefoil factor 3, atypia and p53 have demonstrated performance for diagnosis of BO. The CYTOPRIME 2 Study was designed to assess the feasibility of implementing this test in a real-world community care setting. Methods Patients with chronic GORD identified from general practitioner electronic records were invited to have a capsule sponge test (ie, EndoSign) in the community, of which 1815 completed the test. Results 266 (14.7%) had a subsequent endoscopy based on a positive test. 97 patients (5.3%) of the total group, or 36% of those endoscoped, had BO confirmed at endoscopy of whom 90 (93%) had intestinal metaplasia on histology and 3 had low-grade dysplasia (3%). In addition, 6 patients (0.3%), or 2.2% of those endoscoped, had cancer—4 with OAC, 1 squamous cell oesophageal tumour and 1 early stage gastric cancer. Patients’ and clinicians’ acceptability of the test was high. Conclusions Non-endoscopic capsule sponge testing can be used successfully in community settings to diagnose BO and minimally symptomatic oesophagogastric cancer in a target population of patients with GORD. Patients diagnosed with BO can be offered prospective surveillance to detect precancerous changes and allow endoscopic therapies to prevent late-stage oesophageal cancer.

FOXP3 is a favourable prognostic indicator in oesophageal adenocarcinoma.

Precision Medicine in Thoracic Surgery: Esophageal Cancer.

Barrett's Oesophagus Surveillance Versus Endoscopy at Need Study (BOSS): A Randomized Controlled Trial.

AGA Clinical Practice Guideline on Surveillance of Barrett's Esophagus.

In the Western world, esophageal adenocarcinomas account for 85% of all esophageal cancers, with most located in the infracarinal area, making adequate infracarinal dissection with mediastinal lymphadenectomy followed by intrathoracic anastomosis (the Ivor Lewis procedure) the standard operative technique. Esophagectomy is a complex procedure due to the intricate anatomy of the mediastinum, and understanding this complexity requires knowledge of the embryological development of the posterior mediastinum to interpret the interrelation of mediastinal organs and the planes between them. To this end, we conducted a study on the embryogenic development and beyond of the posterior mediastinum, focusing on the infracarinal mesoesophagus, a pivotal structure for performing an adequate infracarinal dissection. We examined the posterior mediastinum of five embryos (stages 15 to 23) and one twelfth-week fetus, analyzing the region from the carina to the esophageal hiatus. Along with a general description of the esophagus, the vascular system, and the vagus nerves, we provided a detailed account of the development of these structures, specifically the infracarinal mesoesophagus, which is a mesenteric-like bilayer extending from the descending aorta to the infracarinal esophagus and incorporating vessels, lymphatics, and nerves. Our findings show that the infracarinal mesoesophagus is well developed at all stages of embryogenesis, initially appearing short and broad proximally, and gradually elongating and thinning distally toward the hiatus, resembling its adult anatomical counterpart in later stages. This study describes the formation of the infracarinal posterior mediastinum and highlights significant changes in the development of mediastinal structures, including the esophagus, the vascular system, the vagus nerve, and the primordium of the lungs, while also offering insight into the evolution of the infracarinal mesoesophagus. A thorough understanding of the development of the infracarinal posterior mediastinum is essential for upper gastrointestinal surgeons to enhance their comprehension of surgical anatomy, ultimately improving the adequacy and reproducibility of esophageal surgery.

Purpose Barrett’s esophagus (BE) is the main precursor to esophageal adenocarcinoma, a cancer with a significantly rising incidence. While proton-pump inhibitors (PPIs) are the standard therapy for managing BE, the chemopreventive role of aspirin is an area of growing interest with inconclusive evidence, particularly regarding its use in combination with PPIs. This study aimed to assess whether adding aspirin to PPI therapy reduces the incidence of esophageal cancer in patients with BE more than PPIs alone. Methods A nationwide retrospective cohort study was conducted using the TriNetX database. Adult patients with BE were divided into two cohorts: those receiving aspirin plus a PPI and those receiving a PPI only. Propensity score matching was used to balance baseline demographics and clinical comorbidities. The primary outcome was the incidence of malignant neoplasm of the lower third of the esophagus. Subgroup analyses were also performed for low-dose (81 mg) and high-dose (300–325 mg) aspirin. Results After matching, each cohort included 88,184 patients. The cohort receiving aspirin and PPIs had a lower risk of developing esophageal cancer compared to the PPI-only cohort (odds ratio [OR] 0.799, 95% CI: 0.679–0.941). The protective association was observed in both high-dose (OR 0.643) and low-dose (OR 0.664) aspirin subgroups, suggesting a potential dose-dependent effect. Conclusion This large, real-world analysis suggests that the concurrent use of aspirin with PPIs is associated with a reduced risk of esophageal cancer in patients with BE.

Background and Clinical Significance: Barrett’s esophagus (BE) is the precursor to esophageal adenocarcinoma (EAC). Accurately predicting which patients with BE are at the highest risk of progressing to EAC is a significant clinical challenge. This article discusses how the tissue systems pathology test (TSP-9, TissueCypher) can help guide risk-aligned care for patients with BE. TSP-9 is an AI-driven prognostic test that stratifies patients with BE for risk of progression to high-grade dysplasia (HGD)/EAC. Case Report Presentation: Three clinically low-risk patients had esophageal biopsies tested by TSP-9. The real-world utility of TSP-9 is demonstrated through a brief discussion of how the test was utilized to assess each patient’s personalized risk of BE progression to HGD/EAC and inform risk-aligned care. Conclusions: The use of validated AI-powered tools such as TSP-9 is poised to become standard practice in gastroenterology clinical settings and will help improve health outcomes for patients with BE to prevent EAC-related mortality.

Endoscopic resection (ER) is curative for early-stage oesophageal adenocarcinoma (OAC) without high-risk features. Piecemeal endoscopic mucosal resection (pEMR) prevents assessment of lateral margins, complicating risk estimation for neoplastic recurrence. We investigated the risk factors for residual and recurrent OAC post-pEMR. We performed a longitudinal study of two independent patient cohorts: the test cohort who underwent piecemeal or en-bloc ER (n=140) and the validation cohort who underwent pEMR only (n=89). Inclusion criteria were: OAC stage T1a or low-risk T1b, no lympho-vascular invasion, and R0 resection. The primary outcome was residual OAC at first post-ER endoscopy, and secondary outcomes were residual neoplasia (high-grade dysplasia and/or OAC), recurrence of neoplasia at any post-ER endoscopy, and remission of neoplasia, dysplasia and metaplasia at most recent endoscopy. In the test cohort, the incidence of neoplastic recurrence was higher in patients treated with pEMR (n=54, 49%) versus en-bloc ER (n=7, 23%) (p=0.021). The percentage of pEMR specimens with OAC was an independent risk factor for residual OAC at the first post-pEMR endoscopy (OR for a 10% increase=1.24, CI=1.03-1.51, p=0.025). A 50% cut-off of pEMR specimens with OAC was optimal to predict residual OAC (specificity=0.68, sensitivity=0.63). Rates of residual (p=0.039) and recurrent (p=0.0052) OAC were higher when >50% of pEMR specimens were involved by OAC. In the validation cohort, recurrent OAC was also more frequent when cancer burden was >50% (p=0.013). High cancer burden on pEMR specimens correlates with the risk of residual OAC. Post-pEMR site check before endoscopic ablation is recommended if more than 50% of pEMR specimens show OAC.

BackgroundAs the major subtypes of esophageal cancer (EC), esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC) exhibit distinct etiological mechanism, epidemiology, tumor biology, and prognoses. We performed bioinformatics analysis on specific genes related to pathological subtypes to identify potential biomarkers and therapeutic targets.MethodsDifferentially expressed genes (DEGs) between tumor and normal tissues were identified from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO). Weighted gene co-expression network analysis (WGCNA) was subsequently employed to screen genes associated with pathological subtypes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotations, along with gene set enrichment analysis (GSEA), were performed to elucidate the biological roles of these DEGs. A protein‒protein interaction (PPI) network was constructed to explore the hub genes. Furthermore, the prognostic genes were identified via LASSO Cox regression. The differences between EAC and ESCC in terms of immune cell infiltration, somatic mutations, copy number variations (CNVs), and drug sensitivity were subsequently analyzed.ResultsA total of 131 genes were identified as EAC-specific DEGs, whereas 49 genes were recognized as ESCC-specific DEGs. Enrichment analysis revealed significant enrichment of the extracellular matrix (ECM)-related pathway, along with the cell cycle, epithelial‒mesenchymal transition (EMT), and hypoxia signaling pathways, in ESCC. Conversely, EAC was associated with alterations in tumor metabolism, particularly glycolysis and gluconeogenesis. For EAC, a prognostic risk model was constructed, including RHOV, SYTL1, MT1X, PRRG4, KCNK5, and CCL20, which demonstrated robust predictive capabilities for patient outcomes. In ESCC, TUSC3 was identified as a prognostic biomarker and was validated in tissue samples. Furthermore, an in-depth analysis revealed distinct patterns in immune cell infiltration, somatic mutations, CNVs, and drug sensitivity between EAC and ESCC.ConclusionsIn this study, pathologically specific genes were identified in EAC and ESCC. These findings might provide valuable insights into the molecular mechanisms and potential therapeutic targets for these two distinct subtypes.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12885-025-15090-z.

Body weight loss (BWL) is frequently observed after esophagectomy in patients with esophageal cancer (EC). We conducted a retrospective study to evaluate the clinical impact of BWL at recurrence on oncological outcomes in patients with recurrent EC who underwent esophagectomy and chemotherapy after recurrence. We retrospectively reviewed the medical records and collected data from consecutive patients with recurrent EC who received systemic chemotherapy after recurrence at Yokohama City University from 2005 to 2022. Patients included in this study met the following criteria: histological diagnosis of esophageal adenocarcinoma, adenosquamous carcinoma, or squamous cell carcinoma based on a histological examination, and an imaging-based diagnosis of stage IV disease. Sixty-eight patients were included in this study. The median BWL was 12% (range=-26% to 41.1%). According to the 1- and 3-year OS rates, we set the cutoff value of BWL at 15% in the present study. Among the 68 patients, 49 were classified into the BWL-low group and 19 were classified into BWL-high group. The median OS was 22.2 months in the BWL-low group, while the median OS was 14.2 months in the BWL-high group (p=0.005). In addition, the 1- and 3-year OS rates were 69.6% and 43.9%, respectively in the BWL-low group and 51.7% and 0.0% in the BWL-high group. In the univariate and multivariate analyses for OS, BWL was selected as an independent prognostic factor (hazard ratio=2.111; 95% confidence interval=1.109-4.018, p=0.023). The best overall response rate was 52.6% in the BWL-low group and 34.7% in the BWL-high group (p=0.178). BWL at recurrence was an independent prognostic factor in patients with recurrent EC who underwent esophagectomy. In addition, BWL at recurrence may affect first-line treatment after recurrence. Therefore, patients with EC after esophagectomy require careful attention for BWL, even when curative treatment and nutritional management or care are needed to maintain body weight.

Amaranthus viridis L. belongs to the Amaranthaceae family. It is a rich source of numerous phytochemicals and amino acids. The objective of this work was to optimize Ultrasound-Assisted Extraction (UAE) based on the extraction yield and Thin-Layer Chromatography (TLC) profile under different conditions, to compare the optimized UAE to the Soxhlet extraction method and evaluate the cytotoxic effects of the ethyl acetate fraction of the 80 % ethanolic extract on the SKGT-4 (human esophageal adenocarcinoma), AGS (human gastric adenocarcinoma) and A431 (human epidermoid carcinoma). A one-factor at a time experiment was carefully designed to assess the influence of the following factors on the extraction: time, frequency, solid-to-solvent ratio and aqueous ethanol concentration. Soxhlet extraction using 80 % aqueous ethanol was done for defatted plant material, then fractionation using chloroform, ethyl acetate and n-butanol. Cytotoxicity of ethyl acetate fraction was evaluated using the MTT assay on AGS, A431 and SKGT-4 cell lines. The results indicated that in the UAE, the solid-to-solvent ratio has the most significant effect on yield. Soxhlet extraction proved to be more efficient than UAE in terms of TLC profiles. The cytotoxicity of the ethyl acetate fraction exhibited cytotoxic activity against the tested cell lines in a concentration-dependent manner. Thus, selecting a particular extraction method depends on the target compounds. Soxhlet is preferred for gaining certain compounds that require heat for their extraction. The ethyl acetate fraction showed a cytotoxic effect on various cell lines related to cell components and their interactions with phytochemicals present in this fraction.

The prevalence of sarcopenia exhibits considerable variation depending on patient age, definitions, diagnostic techniques, and classifications. Previous studies showed that sarcopenia in patients with esophageal cancer might increase the risk of postoperative complications. However, its impact on overall (OS) and disease-free survival (DFS) is unclear. Retrospective multicenter study (January 2014 to December 2024), including patients with resectable Siewert I-II esophageal adenocarcinoma who underwent Ivor-Lewis esophagectomy. Sarcopenia was assessed by using the Psoas Muscle Index (PMI), calculated at the level of the third lumbar vertebra on preoperative CT scan. Overall, 338 patients were included; 79.5% were male, and the median age was 66 years. The prevalence of sarcopenia was 39.7%. Anastomotic leak (21.6% vs. 10.8%; p = 0.02), pneumonia (14.9% vs. 6.4%; p = 0.02), and 90-day mortality (7.5% vs. 1.9%; p = 0.03) were significantly higher in sarcopenic patients. On multivariate analysis, sarcopenia was an independent predictor of anastomotic leak (oddsratio [OR] 1.41, 95% confidence interval [CI] 1.12-1.87), pneumonia (OR 1.84, 95% CI 1.24-2.15), and 90-day mortality (OR 1.21, 95% CI 1.05-1.55). The 60-month DFS (32% vs. 52%; p = 0.001) and OS (47% vs. 61%; p = 0.008) were significantly reduced in sarcopenic patients. Sarcopenia was an independent predictor of poor survival in the regression analysis (hazard ratio [HR] 1.84, 95% CI 1.36-2.78). Sarcopenia is a highly prevalent condition among patients with esophageal adenocarcinoma. Patients with sarcopenia have lower DFS and OS rates compared with those without sarcopenia. Sarcopenia was independently associated with postoperative anastomotic leak, pneumonia, 90-day mortality, and poor long-term survival.