crossing96/oncoscreening huggingface dataset:
The Burden of Esophageal Cancer and Its Correlation with Dietary, Metabolic, and Behavioral Risk Factors in 204 Countries and Territories: Results from the Global Burden of Disease Study 2021.	Background and Objectives: Esophageal cancer (EC) remains a major global public health challenge due to its aggressiveness and poor survival rates. Therefore, this study aims to summarize the incidence, mortality, prevalence, and global burden of EC based on sex, age, and geographical divisions and to investigate the correlation of some risk factors including the Sociodemographic Index (SDI) and important health indicators to identify high-risk populations. Materials and Methods: We extracted the number and age-standardized rates (ASRs) of EC incidence, mortality, disability-adjusted life years (DALYs), and targeted risk factors for 204 countries and territories from the Global Burden of Disease 2021 study. Correlations between the ASRs of incidence, death, and DALYs and risk factors were investigated using SPSS 22 with Spearman's correlation coefficient at a 0.05 significance level. Results: In 2021, the global age-standardized incidence rate (ASIR), death rate (ASDR), and DALY rate for EC were 6.65 (95% UI: 5.88-7.45), 6.25 (95% UI: 5.53-7.00), and 148.56 (95% UI: 131.71-166.82) per 100,000, respectively. Middle-SDI and high-middle-SDI regions showed the highest and lowest ASIR, ASDR, and DALY ASRs of EC. SDI correlated negatively with ASIR (-0.363), ASDR (-0.414), and DALY ASRs (-0.422). Male-to-female ratios for ASIR, ASDR, and DALY ASRs were 3.32, 3.37, and 3.51, respectively. As age increased, the incidence, death, and DALYs of EC also increased. East Asia recorded the highest incidence, death, and DALY values and ASRs of EC. The ASIR, ASDR, and DALY ASRs also increased with dietary risks, including the low intake of calcium, fruits, omega-6 polyunsaturated fatty acids, seafood omega-3 fatty acids, and vegetables. Conclusions: Considering the incidence, mortality, and high burden of EC in some regions, alongside the presence of modifiable risk factors, major interventions are needed to reduce these risks. Therefore, identifying high-risk areas and factors of EC, promoting lifestyle changes, and lowering the screening age could enable earlier detection and reduce the mortality of EC.	esophagus
Prognostic Significance of Preoperative Peripheral Circulating Eosinophils in Patients who Underwent Esophagectomy for Esophageal Cancer.	BACKGROUND/AIM: The relationship between peripheral eosinophil levels and prognosis or the tumor microenvironment (TME) in patients undergoing esophagectomy for esophageal cancer (EC) remains unclear. This study aimed to investigate the prognostic significance of preoperative peripheral eosinophils and their association with tumor-infiltrating immune cells. PATIENTS AND METHODS: A total of 243 patients who underwent curative esophagectomy for EC were retrospectively analyzed. Patients were classified into two groups based on a preoperative peripheral eosinophil cut-off value of 1.6%, determined using Youden's index. Survival outcomes were compared between the groups, and prognostic factors were identified using Cox proportional hazards modeling. In a subset of 96 patients with available data, correlations between preoperative eosinophil levels and tumor-infiltrating CD8(+) and CD163(+) cells in the TME were evaluated. RESULTS: Overall survival (OS) and relapse-free survival (RFS) in the preoperative peripheral eosinophil <1.6% group were significantly worse than those in the preoperative peripheral eosinophil ≥1.6% group. Multivariate analysis revealed that peripheral eosinophil <1.6% was an adverse prognostic factor for OS [hazard ratio (HR)=1.65; 95% confidence interval (CI)=1.03-2.64] and RFS (HR=1.63; 95%CI=1.06-2.49). Additionally, preoperative peripheral eosinophil count positively correlated with the number of TI CD8(+) cells (r=0.26), while peripheral eosinophils% and the number of TI CD163(+) cells had no correlation (r=-0.03). CONCLUSION: Preoperative low peripheral eosinophil count may be a prognostic factor in esophagectomized patients for EC. Additionally, peripheral eosinophil rate and the number of TI CD8(+) cells had positive correlation.	esophagus
Panaxadiol inhibits the proliferation and immune evasion of esophageal squamous cell carcinoma cells by suppressing HIF-1α/STAT3/PD-L1 pathway.	BACKGROUND: Several malignancies, including esophageal squamous cell carcinoma (ESCC), depend on immune evasion for growth and proliferation. This study aimed to determine whether panaxadiol can inhibit immune evasion and, hence, have anti-cancer effects in ESCC. METHODS: Human ESCC cell lines (EC109 and EC9706) were exposed to 3 or 10 μM panaxadiol dissolved in dimethyl sulfoxide. Colony formation and ethynyl deoxyuridine assays were performed to measure ESCC cell proliferation. After ESCC and CD8(+)T cell coculture, crystal violet staining and lactate dehydrogenase (LDH) assays were used to detect ESCC cell viability and death. An enzyme-linked immunosorbent assay was performed to measure the levels of inflammatory cytokines (interferon (IFN)-γ, interleukin (IL)-4, and IL-10). To establish a xenograft mouse model, 3 × 10(5) EC109 cells treated with or without panaxadiol were subcutaneously injected into mice. Western blotting was conducted to assess the protein expression of proliferation markers (cyclin D1, c-myc, and vascular endothelial growth factor), HIF-1α, programmed cell death 1 ligand 1 (PD-L1), and STAT3 phosphorylation in ESCC cells or mouse tumors. RESULTS: Both 3 and 10 μM panaxadiol significantly inhibited ESCC cell proliferation. After coculture with CD8(+)T cells, ESCC cell viability was markedly reduced, whereas IFN-γ, IL-10, and IL-4 levels were prominently elevated. LDH assays revealed that panaxadiol enhanced CD8(+)T cell-induced cytotoxicity toward ESCC cells. Moreover, panaxadiol effectively suppressed xenograft tumor growth in ESCC. The activities of STAT3, PD-L1, and HIF-1α in ESCC cells and mouse tumor tissues were significantly suppressed by panaxadiol. Additionally, FG-4592 (a factor that can stabilize HIF-1α) reversed the suppression of 10 μM panaxadiol-induced HIF-1α/STAT3/PD-L1 activity in ESCC cells. CONCLUSION: Panaxadiol suppresses cell proliferation, immunological evasion, and tumor formation in ESCC by inhibiting PD-L1 expression through the suppression of HIF-1α and STAT3.	esophagus
LncRNA HOXA11-AS promotes the cell proliferation, migration, invasion and inhibits cell apoptosis in esophageal squamous cell carcinoma.	This study aimed to investigate the expression and evaluate the function of long non-coding RNA (LncRNA) HOXA11-AS in Esophageal Squamous Cell Carcinoma (ESCC). HOXA11-AS expression was quantified in paired ESCC tumor tissues (n = 50) and adjacent histologically normal tissues (> 5 cm from tumor margin) (n=50) from surgical patients. The relationship between HOXA11-AS expression levels, clinical staging and patient survival was analyzed. Lentiviral transduction was employed to generate stable ESCC cell lines with HOXA11-AS overexpression (lv-HOXA11-AS) or knockdown (sh-HOXA11-AS), accompanied by negative control groups (lv-NC/sh-NC). The impact on malignant phenotype was assessed via CCK-8 proliferation assays, Transwell migration/invasion assays, wound healing assays, and flow cytometry for apoptosis. In vivo tumor growth was evaluated by subcutaneously injecting fluorescently labeled lv-HOXA11-AS or lv-NC cells into BALB/c-nu mice. RNA-sequencing and tissue qRT-PCR confirmed significantly higher HOXA11-AS expression in ESCC versus normal epithelium, and high HOXA11-AS expression was associated with advanced tumor stage and was identified as an independent predictor of poor prognosis. qRT-PCR validated the elevated expression of HOXA11-AS in ESCC cell lines too. HOXA11-AS overexpression promoted proliferation, migration, invasion, and suppressed early apoptosis in ESCC cells, HOXA11-AS knockdown exerted opposing effects. HOXA11-AS overexpression significantly enhanced tumor growth in mouse xenograft models. LncRNA HOXA11-AS is aberrantly overexpressed in ESCC and functions as an oncogene, driving tumor progression by enhancing proliferation, migration, invasion and suppressing apoptosis. Its association with poor prognosis identifies HOXA11-AS as a promising prognostic biomarker and potential therapeutic target for ESCC.	esophagus
Impact of indocyanine green fluorescence angiography on esophagogastric anastomotic leakage after Ivor Lewis esophagectomy.	PURPOSE: Esophagectomy for esophageal cancer involves high morbimortality when anastomotic leakage occurs. Optimal perfusion of the gastric tube can be assessed by indocyanine green fluorescence-angiography (ICG-FA). We evaluated whether locating the anastomosis in a zone enhanced within 60 s after ICG-FA injection reduced severe anastomotic leakage (Stage 2 or 3) within 30 days after esophagectomy. METHODS: ICG-FA was assessed in 69 patients and compared to 122 control patients undergoing minimally invasive Ivor Lewis esophagectomy. Whenever possible, the anastomosis was placed on gastric tissue enhanced within 60 s after ICG-FA injection, with resection of the gastric tip if needed. RESULTS: Severe anastomotic leakage occurred in 8.4% of cases, with 6 cases of anastomotic leakage (8.7%) in the ICG-FA group and 10 (8.2%) in the non-ICG-FA group (p = 1.000). There was no difference in postoperative outcomes between both groups, the main complications being pulmonary. ICG-FA enhancement level at 60 s was below the gastric tip in 33.8% of cases, with lowering of the anastomotic site in 18% of cases and resection of the gastric tip in 23% of cases. Overall, use of ICG-FA changed the surgical management in 29.9% of patients, with 2 patients presenting with anastomotic leakage. CONCLUSION: Our results were not statistically significant, possibly due to a lack of power. There was no trend indicating a decrease in anastomotic leakage using our ICG-FA method, therefore other studies must help determine an optimal quantitative ICG-FA method to reduce postoperative morbidity after esophagectomy.	esophagus
Immune checkpoint inhibitor-associated hypothyroidism, macular rash and adrenal insufficiency: case report and review of the literature.	BACKGROUND: Immune checkpoint inhibitors (ICIs) represent the most significant therapeutic advancement in oncology over the past decade, with sintilimab demonstrating efficacy as a programmed cell death-1 (PD-1) inhibitor. While these agents have markedly improved tumor response rates and overall survival across multiple malignancies, their use is complicated by a growing incidence of immune-related adverse events (irAEs), particularly endocrine toxicities. To our knowledge, this is the first case report of adrenal crisis during levothyroxine supplementation for ICI-induced hypothyroidism and undiagnosed adrenal insufficiency. CASE PRESENTATION: A 71-year-old male patient was admitted to our hospital with complaints of anorexia, fatigue, and weight loss. He had a confirmed diagnosis of esophageal squamous cell carcinoma 18 months prior and received systemic therapy, including sintilimab and esophagectomy (with normal thyroid and renal function at baseline). Sintilimab was administered for 10 treatment cycles. 4 months after completion of chemotherapy, the patient developed macular rash on the trunk and extremities and was treated with high-dose topical corticosteroids, and 1 month later, he began to suffer from anorexia and weight loss of 4.0 kg until this admission. At the same time, hypothyroidism and hyponatremia were detected, and levothyroxine (100 µg/day) was commenced. However, he worsened, with two episodes of fever, hypotension, and somnolence, as well as hyponatremia, hypoglycemia, anemia, and elevated serum creatinine. Cortisol and adrenocorticotrophic hormone (ACTH) levels decreased in the morning, and concurrent pericardial effusion and diffuse T-wave inversions were detected via electrocardiogram. He was diagnosed with secondary adrenal insufficiency and took prednisone (5 mg twice a day), and the symptoms improved rapidly. 1 week later, the serum electrolytes were normal, his weight increased by 3.5 kg, his physical activity improved, and the T wave on the electrocardiogram normalized. After taking prednisone for 18 days, his condition improved further. The morning cortisol level still decreased, while ACTH levels normalized, and pericardial effusion disappeared. CONCLUSION: This is a typical case of endocrine irAEs caused by ICIs, and the patient's macular rash may also be related to ICIs. For patients treated with ICIs, preventive monitoring of symptoms of irAEs and related hormones is crucial for timely diagnosis, treatment, and even prevention of endocrine crisis.	esophagus
Combining standard clinical blood values for improving survival prediction in patients with unresectable esophageal carcinoma: A retrospective study.	The prognosis for patients with esophageal squamous cell carcinoma (ESCC) is poor, with a 5-year survival rate of approximately 30%. There are significant differences in prognosis among patients, and some patients experience local recurrence and distant metastasis within 1 year after comprehensive treatment. Therefore, there is an urgent need for highly sensitive and specific biomarkers to assess the therapeutic risks and prognosis of patients with inoperable esophageal cancer. This study aimed to investigate the predictive value of the LabBM score in the survival of patients with inoperable ESCC. A single-center retrospective study was conducted, including 150 and 155 patients with unresectable ESCC who received concurrent chemoradiotherapy at our hospital between January 1, 2013, and June 30, 2018, and between July 1, 2018, and March 1, 2020, respectively, as the training and validation cohorts. Laboratory parameters, including lactate dehydrogenase, platelet count, C-reactive protein, and albumin, were collected 1 week prior to concurrent chemoradiotherapy. The LabBM score was calculated, and survival differences were analyzed across patients with different LabBM scores. Cox regression and Kaplan-Meier analyses were used to assess factors influencing progression-free survival (PFS) and overall survival (OS), aiming to clarify the prognostic value of the LabBM score for PFS and OS. In the training group, of the 150 patients enrolled, 123 were in the low LabBM group (0-1), 23 in the medium LabBM group (1.5-2), and 4 in the high LabBM group (2.5-3.5). The median survival was 33 months in the low LabBM group, 11 months in the medium LabBM group, and 6.5 months in the high LabBM group, with a significant difference in survival between the 3 groups (P = .000). Univariate Cox analysis showed that a higher LabBM score was associated with worse OS (P < .05). Multivariate Cox regression analysis revealed that a higher LabBM score (hazard ratios: 2.75, 95% CI: 1.08-7.03, P = .034) was an independent influencing factor for OS. In receiver operating characteristic analysis, the AUC area for OS and PFS predicted by the LabBM-based risk model was 0.92 (95% CI: 0.86-0.97, P = .00) and 0.956 (95% CI: 0.88-0.98, P = .000), respectively. The AUC for LabBM scores predicting OS and PFS were 0.63 (95% CI: 0.54-0.72, P = .011) and 0.61 (95% CI: 0.52-0.70, P = .039), respectively. The AUC area of the risk model was significantly higher than that of other single parameters. Subsequently, we re-enrolled 155 patients with inoperable esophageal cancer in different time periods for the above analysis, and the results were consistent with the experimental group. In inoperable ESCC patients, the LabBM score-based risk model is a novel and effective prognostic indicator.	esophagus
Effectiveness of Nutritional Screening Tools in Predicting the Impact of Malnutrition on Hospital and Intensive Care Unit Stay.	Malnutrition commonly occurs in patients with esophageal cancer (EC) and head and neck cancers (HNCs), adversely affecting clinical outcomes. The comparative effectiveness of nutritional screening tools in predicting prolonged length of stay (PLOS) and intensive care unit (ICU) admission in this population remains unclear. We aimed to investigate the effectiveness of various nutritional screening techniques in predicting the hospital and ICU LOS of patients with HNCs/EC. We retrospectively analyzed the data of 374 patients aged ≥18 years with EC/HNC who underwent first-time surgery between January 2013 and December 2023. Nutritional status was assessed using the Malnutrition Universal Screening Tool (MUST), Controlling Nutritional Status (COUNT), Geriatric Nutritional Risk Index (GNRI), and Prognostic Nutritional Index (PNI). Patients were classified into low-risk and high-to-moderate-risk groups. The outcomes included ICU stay >2 days and PLOS (>16 days). The COUNT, GNRI, and PNI were significantly associated with ICU stays >2 days and PLOS. The PNI had the highest predictive accuracy (ICU >2 days: adjusted odds ratio [aOR] = 8.44; area under the ROC curve [AUC-ROC] = 0.864; PLOS: aOR = 6.39; AUC-ROC = 0.859). The PNI, COUNT, and GNRI effectively predicted ICU stay and PLOS among surgical patients with EC and HNC.	esophagus
Inhibition of USP18 in the presence of IFN-α elevates apoptosis, autophagy, and chemosensitivity of oesophageal cancer cell lines.	Oesophageal cancer remains a poor-prognosis disease with a five-year survival of 20 %. Chemoresistance poses a significant challenge, and its mechanisms remain unclear. Our previous study found that the ISGylation network is differentially expressed in drug-sensitive and resistant oesophageal cancer cells. ISGylation involves conjugating Interferon-Stimulated Gene 15 (ISG15) to target proteins, regulated by E1, E2, and E3 enzymes, similar to ubiquitin. Ubiquitin Specific Peptidase 18 (USP18) removes ISG15 and negatively regulates the type I interferon (IFN) response. We investigated whether USP18 expression influences the chemosensitivity of two resistant oesophageal cancer cell lines. Treatment with IFN-α ( ± 5-fluorouracil (5-FU) or oxaliplatin) induces ISGylation network proteins, including USP18. ISG15 conjugation is only detected after USP18 depletion with siRNA. Silencing USP18 significantly increased sensitivity to 5-FU and oxaliplatin, inducing extensive apoptosis in both cell lines previously regarded as apoptosis incompetent. USP18 depletion also elevated LC3 II expression and autophagosome formation induced by IFN-α ( ± chemotherapeutic agents), indicative of autophagy. These findings demonstrate that strategies to inhibit USP18 could re-engage cell death signalling and restore sensitivity to chemo-resistant oesophageal cancer cells.	esophagus
Mathematical modelling of magnetic field and nanoparticle effects on calcium signalling in malignant esophageal cells.	Purpose.This study aimed to develop a mathematical model investigating how low-frequency magnetic fields and magnetic nanoparticles theoretically affect calcium signalling in esophageal squamous cell carcinoma (ESCC) cells through mechanosensitive channel activation.Methods.We modified the Chang model to incorporate magnetic field-induced membrane shear stress mechanisms, simulating intracellular calcium dynamics using ordinary differential equations in Python and Julia. The model examined rotating magnetic fields at 25 mT across frequencies from 0 to 1.7πmHz, analyzing calcium oscillation patterns and their potential effects on mitogen-activated protein kinase (MAPK) signalling pathways.Results.Simulations demonstrated that low-frequency rotating magnetic fields at 1.7πmHz and lower frequencies disrupted normal calcium oscillations, creating inter-burst periods of at least 588.2 seconds. This minimum period exceeds the sensitivity threshold of MAPK signalling (1.7-17 mHz), suggesting potential inhibition of proliferation pathways dependent on calcium oscillation frequency. The model predicted reduced oscillation magnitude and altered temporal dynamics compared to control conditions.Conclusions.The mathematical framework provides theoretical foundation for magnetic field interactions with cellular calcium dynamics through mechanosensitive channels, offering conceptual basis for potential therapeutic applications. All findings require comprehensive experimental validation before any clinical implications can be considered.	esophagus
Exosomal miR-145-5p impairs neoadjuvant chemotherapy by suppressing TFRC-mediated macrophage iron uptake and driving M2 polarization in esophageal cancer.	Esophageal cancer (EC) remains a highly aggressive malignancy with limited therapeutic success, partly due to heterogeneous responses to neoadjuvant chemotherapy (NAC). Tumor-derived exosomes and tumor-associated macrophages play critical roles in shaping the immunosuppressive tumor microenvironment, but their crosstalk in EC chemoresistance remains unclear. In this study, we identified tumor-derived exosomal miR-145-5p as a potential predictor of poor NAC response. Elevated exosomal miR-145-5p levels were associated with increased M2 macrophage infiltration and enhanced expression of M2 markers in EC tissues. Mechanistically, miR-145-5p promoted M2 macrophage polarization through the suppression of transferrin receptor (TFRC) and subsequent disruption of iron uptake. Consequently, these tumor-promoting M2-polarized macrophages enhanced EC cell proliferation, migration, invasion, and cisplatin resistance. In vivo, macrophages overexpressing miR-145-5p facilitated tumor growth and markedly weakened the therapeutic effects of cisplatin. Overall, our findings reveal that EC cells utilize exosomal miR-145-5p to remodel macrophages into a pro-tumorigenic phenotype through TFRC-dependent iron metabolic reprogramming, contributing to malignant progression and chemoresistance. Exosomal miR-145-5p may represent a promising biomarker for NAC response and a therapeutic target to improve treatment outcomes in EC.	esophagus