crossing96/oncoscreening huggingface dataset:
Post-endoscopy esophageal squamous cell carcinoma invading into muscularis mucosa or submucosal layer: a case series.	This study aimed to identify the clinicopathological features of esophageal squamous cell carcinoma (ESCC), detected at the stage of T1a-MM or deeper despite undergoing annual endoscopic surveillance. This retrospective study included cases of early ESCC treated with endoscopic resection at this hospital from January 2015 to October 2024. Inclusion criteria were: (i) A case identified as a high-risk patient for ESCC due to the presence of multiple Lugol-voiding lesions . (ii) Screening endoscopy performed at intervals of 12 months or less. (iii) The depth of lesions detected under appropriate screening and treated with endoscopic resection was pT1a-MM or deeper. Five cases met the criteria, with a median age of 68 years (range: 48-81); all patients were male. The prior endoscopic examination before the detection was performed 6 months earlier in two cases and 12 months earlier in three cases. Among the cases, three lesions were located in the cervical esophagus (Ce), one in the middle thoracic esophagus (Mt), and one in the lower thoracic esophagus (Lt); the Mt and Lt lesions were on the anterior wall. The three Ce lesions measured 5-10 mm, while the Mt and Lt lesions measured 6 mm and 10 mm, respectively. Four lesions were diagnosed as pT1a-MM, and the Ce lesion as pT1b-SM2 with positive vascular invasion. The patient diagnosed with submucosa lesion received additional chemoradiotherapy. None of the patients have experienced cancer recurrence. This case series suggests that the Ce and the anterior wall of the Mt and Lt may be areas that require particular attention during routine ESCC surveillance. These findings may help improve quality of surveillance endoscopy for ESCC high-risk patients.	esophagus
Treatment outcomes of esophageal squamous cell carcinoma with cM1 lymph node without organ metastasis.	Stage IVB esophageal cancer typically has a poor prognosis; patients with non-regional lymph-node metastasis (cM1 LYM) but no organ metastasis generally fare better. However, comprehensive reports on treatment outcomes are limited. We included 158 patients with esophageal squamous cell carcinoma (ESCC) and cM1 LYM without organ metastasis treated at our institute between October 2006 and November 2022; their treatment outcomes were assessed, and prognostic factors were evaluated. The 3-year overall survival (OS) rates for all patients and those treated with surgery, chemoradiotherapy, chemotherapy, or palliative radiotherapy were 43.7%, 60.7%, 38.5%, 22.4%, and 20.0%, respectively. Surgery or chemoradiotherapy significantly improved OS compared to chemotherapy. Univariate and multivariate analyses identified significant OS prognostic factors: Eastern Cooperative Oncology Group performance status (ECOG PS) (1/2 vs. 0), type of cM1 LYM areas (two areas vs. thoracic area), and clinical response (stable/progressive disease vs. complete/partial response). In the subgroup receiving surgery or chemoradiotherapy, both analyses identified ECOG PS (1/2 vs. 0) and clinical response (stable/progressive disease vs. complete/partial response) as prognostic factors for OS. ESCC patients with cM1 LYM without organ metastasis had relatively good survival; those with good PS and a favorable clinical response especially achieved long-term survival. Because patients who underwent surgery or chemoradiotherapy had significantly better OS than those treated with chemotherapy, appropriate localized treatment might be necessary even in these cases.	esophagus
Outcomes of additional chemotherapy for esophageal squamous cell carcinoma following non-curative endoscopic submucosal dissection.	BACKGROUND: Pathological T1a-muscularis mucosa with lymphovascular invasion and T1b-submucosa are high-risk factors for lymph node metastasis in esophageal squamous cell carcinoma (ESCC). Esophagectomy and chemoradiotherapy are recommended following endoscopic submucosal dissection (ESD) but can lead to complications. Here, we evaluated the efficacy and safety of chemotherapy following ESD. METHODS: This prospective and retrospective study included patients with pathological T1a-muscularis mucosa with lymphovascular invasion or T1b-submucosa who underwent esophageal ESD between June 2006 and August 2023, followed by chemotherapy or chemoradiotherapy. The overall survival, cause-specific survival, recurrence-free survival, hospitalization period, and the occurrence of grade ≥ 3 adverse events were compared between the chemotherapy and chemoradiotherapy groups. RESULTS: The patient and tumor characteristics and pathological findings did not significantly differ between the chemotherapy (n = 16) and chemoradiotherapy (n = 15) groups. The 5-year overall and recurrence-free survival rates were significantly higher in the chemotherapy group than in the chemoradiotherapy group (100.0% vs. 77.8%, P < 0.001 and 92.3% vs. 84.9%, P = 0.007, respectively; log-rank test). The 5-year cause-specific survival rate did not significantly differ between groups (100.0% vs. 83.3%, P = 0.14, log-rank test). The hospitalization period was significantly shorter in the chemotherapy group than in the chemoradiotherapy group (34 vs. 48 days, P < 0.001). Grade ≥ 3 adverse events occurred in 4 (25.0%) and 11 (73.3%) patients in the chemotherapy and chemoradiotherapy groups, respectively. CONCLUSIONS: Chemotherapy is a safe and effective additional treatment for ESCC (pathological T1a-muscularis mucosa with lymphovascular invasion or T1b-submucosa) after ESD.	esophagus
[Research progress on radiotherapy and chemotherapy combined with immunotherapy for locally advanced esophageal squamous cell carcinoma].	The standard treatment for locally advanced esophageal squamous cell carcinoma (ESCC) is neoadjuvant chemoradiotherapy, followed by surgery or definitive radiotherapy, but clinical results are unsatisfactory. In recent years, relevant studies have shown that immunotherapy combined with chemoradiotherapy has become a new treatment option for locally advanced ESCC. This article summarizes the current progress of chemoradiotherapy combined with immunotherapy in the treatment of locally advanced ESCC, and provides necessary theoretical basis for the comprehensive understanding and optimization of chemoradiotherapy combined with immunotherapy regimens for ESCC.	esophagus
Comparing outcomes following open, hybrid, minimally invasive, and robotic-assisted esophagectomy: A systematic review.	BACKGROUND: Esophagectomy remains the standard of care for patients with resectable locally advanced malignancies of the esophagus. AIM: To compare perioperative and long-term outcomes across open (OE), hybrid (HE), minimally invasive (LMIE), and robotic-assisted esophagectomy (RAMIE) for esophageal pathologies using randomised controlled trial (RCT) data. METHODS: A systematic search of the EMBASE, SCOPUS and PUBMED databases was performed to identify RCTs comparing OE, HE, LMIE and RAMIE. Descriptive statistics were performed using SPSS v26.0. RESULTS: Sixteen RCTs with 2729 total patients were included. Overall, 50.6 % of patients underwent OE (1381/2729), 5.4 % underwent HE (148/2729), 31.4 % underwent LMIE (856/2729) and 12.6 % underwent RAMIE (344/2729). LMIE and RAMIE demonstrated reduced pulmonary complications and hospital stay compared with OE. RAMIE achieved superior lymph node dissection rates, compared to LMIE. HE demonstrated lower complication rates than OE, with comparable lymph node yields. In-hospital mortality remained low across all groups, with no significant differences, though LMIE and RAMIE had demonstrated better short-term recovery. Meta-analysis of 9 RCTs showed higher 30-day mortality with OE compared to MI (RR 1.84, 95 % CI 1.02-3.34; I(2) = 0 %). Long-term survival and disease-free survival rates were largely comparable across all techniques. Quality of life (QOL) metrics one year post-surgery indicated that LMIE and RAMIE provided better physical functioning, pain reduction, and social functioning than OE. CONCLUSION: LMIE and RAMIE were superior in terms of blood loss, pulmonary complications, hospital stays, improved QOL, and lymph node yield compared to OE. Notwithstanding these concerted benefits, equipoise was demonstrated in terms of rates of surgical site infection, chyle leak, mortality, survival and oncological outcomes. Thus, minimally invasive techniques should be considered where surgeon and institution expertise allow.	esophagus
[LINC00261 suppresses esophageal squamous cell carcinoma proliferation, invasion, and metastasis by targeting the miR-23a-3p/ZNF292 axis].	OBJECTIVES: To evaluate the regulatory effects of lncRNA LINC00261 on proliferation, invasion, and metastasis of esophageal squamous cell carcinoma (ESCC) cells. METHODS: The differentially expressed RNAs in ESCC were identified using the GSE149612 dataset from the GEO database. PCR was used to detect LINC00261 expression levels in clinical ESCC and normal esophageal tissue samples and in multiple ESCC cell lines and normal esophageal epithelial cells (HEEC). In ESCC cells, the effects of overexpression of LINC00261 on cell proliferation, invasion, metastasis and apoptosis were analyzed using CCK-8 assay, clone formation assay, Transwell assay and flow cytometry. The potential targets of LINC00261 were predicted using bioinformatics tools including ENCORI and verified using dual-luciferase reporter assay and Western blotting. The effects of LINC00261 overexpression on ESCC were confirmed in a nude mouse model bearing ESCC xenograft. RESULTS: Analysis of the GSE149612 dataset revealed significantly lower LINC00261 expression in ESCC tissues and cell lines. In cultured ESCC cells, LINC00261 overexpression markedly suppressed cell proliferation, invasion, and metastasis and promoted cell apoptosis. Dual-luciferase reporter assays confirmed that LINC00261 targets the miR-23a-3p/ZNF292 axis. In the tumor-bearing mouse model, LINC00261 overexpression significantly inhibited ESCC xenograft proliferation and metastasis. CONCLUSIONS: LINC00261 suppresses ESCC progression by targeting the miR-23a-3p/ZNF292 axis, suggesting a potential therapeutic strategy for ESCC treatment.	esophagus
Long-term outcome of neoadjuvant tislelizumab plus chemotherapy in locally advanced esophageal squamous cell carcinoma.	BACKGROUND: Current understanding of neoadjuvant immunochemotherapy for locally advanced esophageal squamous cell carcinoma (ESCC) lacks high-level evidence. This study provides additional efficacy data for this treatment regimen. METHODS: Clinical trials investigating neoadjuvant tislelizumab plus chemotherapy in locally advanced ESCC were identified through literature search. Raw data from investigators were pooled for analysis. Primary endpoint was pCR; secondary endpoints included MPR, R0 resection rate, EFS, DFS, and OS. RESULTS: Six studies involving 306 patients were analyzed; 275 (89.9%) underwent surgery. Among surgical patients, pCR rate was 25.5% and MPR rate was 49.5%. Most patients (98.5%) achieved R0 resection. At median follow-up of 31.3 months, median EFS, DFS, and OS were not reached. The 1-/2-/3-year rates were: EFS 81.8%/66.9%/59.1%; DFS 79.0%/68.7%/62.3%; and OS 91.7%/77.5%/73.4%. Tislelizumab dose intensity correlated with MPR. MPR and R0 resection were independent prognostic factors for EFS and OS, while pathological staging was associated with DFS and OS. CONCLUSIONS: Neoadjuvant tislelizumab combined with chemotherapy demonstrated promising efficacy with encouraging pathological responses and survival outcomes in locally advanced ESCC, supporting clinical application.	esophagus
Epigenetically inhibiting CYP3A5 modulates the migration and invasion of esophageal squamous cell carcinoma.	Esophageal squamous cell carcinoma (ESCC) is a major global health threat characterized by high incidence and mortality rates. The aberrant suppression of CYP3A5 is frequently observed in ESCC. However, its precise function and the epigenetic mechanism mediating its transcriptional repression remain poorly elucidated. Herein, we found that CYP3A5 expression is significantly reduced in ESCC tumor tissues compared to normal tissues. Crucially, high CYP3A5 expression was associated with a favorable prognosis and reduced tumor metastasis in ESCC. Intriguingly, administration of the histone deacetylase inhibitor trichostatin A resulted in the upregulation of CYP3A5 expression. Further mechanistic experiments revealed that histone deacetylase 4 is the key deacetylase responsible for reducing H3K18/K27 acetylation levels at the CYP3A5 promoter, mediated by P300/CREB binding protein. Functionally, CYP3A5 overexpression effectively inhibited ESCC cell migration and invasion both in vitro and in vivo. In conclusion, CYP3A5 was crucial in ESCC and may serve as a promising therapeutic target for the prevention of tumor metastasis in ESCC. SIGNIFICANCE STATEMENT: CYP3A5 expression was downregulated in esophageal squamous cell carcinoma (ESCC) due to histone hypoacetylation at CYP3A5 promoter region. Because ESCC develops, CYP3A5 suppression promotes tumor metastasis and invasion. CYP3A5 is a potential biomarker and therapeutic target for ESCC.	esophagus
Relationship Between Angiogenesis and Hypoxia-inducible Factor-1α and Erythropoietin in Superficial Esophageal Carcinoma.	BACKGROUND/AIM: Hypoxia-inducible factor 1α (HIF-1α) plays a significant role in angiogenesis; however, few studies have examined its expression in superficial esophageal carcinoma. This study examined the timing at which the hypoxia-induced angiogenesis switch is turned on by investigating the expression of HIF-1α and its downstream target, erythropoietin (Epo), in superficial esophageal carcinoma. MATERIALS AND METHODS: We used 53 lesions of superficial esophageal carcinoma and conducted immunohistochemistry for HIF-1α and Epo. Cases were divided into three groups: T1a-EP/LPM group (22 lesions), T1a-MM/T1b-SM1 group (15 lesions), and T1b-SM2,3 group (16 lesions). HIF-1α and Epo expression levels were compared across groups using H scores. Additionally, in 24 cases with intraepithelial spread, expression was compared between intraepithelial and invasive components. RESULTS: Both HIF-1α and Epo were most strongly expressed in T1a-EP/LPM, with significantly reduced expression observed in tumors that invaded the muscularis mucosae or deeper layers. A strong positive correlation was found between HIF-1α and Epo expression scores. HIF-1α and Epo values were significantly higher in the intraepithelial area than in the invaded area. CONCLUSION: In esophageal carcinoma, HIF-1α and Epo were strongly expressed at the earliest stages of carcinogenesis. As the carcinoma progressed beyond the muscularis mucosae, the expression of these markers significantly declined, suggesting a resolution of hypoxia likely associated with active angiogenesis.	esophagus
Environmental nanoplastics exert dual effects: promoting tumor progression in cancer cells while inducing pyroptosis in normal esophageal epithelium.	Esophageal squamous cell carcinoma (ESCC) is a prevalent malignant tumor in the human digestive tract. The occurrence and development of esophageal cancer are closely related to environmental factors. As a new type of pollutant, microplastics have been intensively studied regarding their impact on health. The link between microplastics, an emerging environmental pollutant, and esophageal cancer remains uncertain, presenting a scientific question that requires investigation. This study utilized KYSE-30 and TE-1 esophageal squamous cell carcinoma cell lines in an in vitro model. Various biochemical experiments were conducted, such as MTT, flow cytometry, laser confocal microscopy, and Western-blot. Confocal microscopy observations showed that nanoplastics (NPs) were internalized into esophageal squamous cell carcinoma cells. Cell proliferation experiments indicated that NPs promoted the proliferation of esophageal cancer cell lines. Additional experiments demonstrated that NPs stimulation enhances glycolysis in esophageal cancer cells, leading to increased tumor cell proliferation. Mechanistic studies indicated that microplastics altered mitochondrial membrane potential, triggering mPTP opening and mt-DNA release into the cytoplasm, which activated the cGAS-STING-NF-κB signaling pathway. NF-κB enhances HIF-1α expression, leading to increased glycolysis and proliferation in esophageal cancer cells. In a normal esophageal epithelial cell model, we assessed the toxicological impact of nanoplastics, revealing that microplastics induced damage via NLRP3-mediated inflammation and pyroptosis. The study reveals that microplastics, as emerging pollutants, can enhance tumor cell proliferation and harm normal esophageal epithelium. These results suggest that NPs exhibit dual toxicological effects on tumor cells and normal esophageal epithelial cell models.	esophagus
A case report of primary amelanotic malignant melanoma of esophagus.	Primary malignant melanoma of the esophagus (PMME) is an extremely rare malignant tumor. Primary amelanotic malignant melanoma is a subtype of PMME which shows no pigmentation under esophagogastroduodenoscopy (EGD). A lack of understanding of this disease makes it susceptible to misdiagnosis and limits its treatment options. Here, we reported a case which misdiagnosed as esophageal polyps with malignant transformation or esophageal cancer when observed on gastroscopy examination, while proved as primary amelanotic malignant melanoma by immunohistochemistry in our department. The aim of this study is to draw the attention of physicians by describing a case of primary amelanotic malignant melanoma and to aid in the diagnosis of this disease in the future.	esophagus
Renji endoscopic submucosal dissection video data set for Esophagus.	Progress in artificial intelligence has markedly improved computer-supported interventions, professional education for surgeons, and post-procedural analysis of operative recordings, considerably enhancing surgical proficiency and clinical outcomes. Phase recognition frameworks for endoscopic procedures utilizing deep learning methodologies depend critically on well-annotated comprehensive datasets. Our study introduces the Renji database containing endoscopic submucosal dissection (ESD) videos for esophageal lesions, comprising 25 procedural recordings with 141,909 phase-specific classifications jointly annotated by a specialized endoscopy team. To the best of our knowledge, this constitutes the inaugural publicly available collection of esophageal ESD videos with comprehensive phase annotations, and we believe this contribution will assist in establishing benchmarks for future esophageal ESD databases. The complete video repository and associated annotations have been made freely accessible to researchers through the Figshare repository.	esophagus
miR‑100‑5p and miR‑203a‑3p suppress esophageal squamous cell carcinoma progression by targeting FKBP5.	Poorly differentiated cancers, including esophageal squamous cell carcinoma (ESCC), exhibit higher malignant potential and worse prognoses than well‑differentiated types. The present study aimed to identify microRNAs (miRNAs or miRs) involved in ESCC progression and their target mRNAs, focusing on tumor differentiation. miRNA candidates were selected using a miRNA array‑based approach and GEO datasets, comparing expression levels between poorly and non‑poorly differentiated ESCC. Clinical samples (n=61) and cell lines were analyzed to determine the significance and function of the selected miRNAs and their target mRNA. miR‑100‑5p and miR‑203a‑3p were significantly downregulated in poorly differentiated ESCC, with lower expression strongly associated with poorer overall survival (OS) (miR‑100‑5p: P=0.02; miR‑203a‑3p: P=0.05) and relapse‑free survival (RFS) (miR‑100‑5p: P=0.04; miR‑203a‑3p: P=0.12). Overexpression of these miRNAs suppressed cell migration and invasion. FKBP5 was identified as a common target, with its expression significantly reduced upon double‑transfection with miR‑100‑5p and miR‑203a‑3p. FKBP5 downregulation reduced tumor aggressiveness in KYSE70 cells, and clinical samples showed significantly worse survival rates in patients with high FKBP5 expression (OS: P=0.02; RFS: P=0.04). These findings suggest that miR‑100‑5p and miR‑203a‑3p act as tumor suppressors by targeting FKBP5, highlighting FKBP5 as a potential therapeutic target in ESCC.	esophagus
The Knockdown of ACTL6A Enhances the Radiosensitivity of Esophageal Squamous Cell Carcinoma by Modulating the Wnt/β-Catenin Signaling Pathway.	Actin-like protein 6A (ACTL6A) is thought to be associated with the survival and prognosis of patients with a variety of human cancers. This study investigates the effect of ACTL6A knockdown on ESCC radiosensitivity and explores molecular mechanisms that may enhance radiotherapy efficacy. The ACTL6A expression level was increased in esophageal squamous carcinoma cells after radiation irradiation. The protein expression level of ACTL6A in tumor tissue samples of clinical esophageal squamous cell carcinoma patients was analyzed by immunohistochemistry, and it was found that the prognosis of the high expression group was worse than that of the low expression group. Further knocking down the ACTL6A gene in esophageal squamous cell carcinoma cells, it was found that ACTL6A could regulate the proliferation, migration, invasion, DNA damage repair, cell cycle, and apoptosis of esophageal squamous cell carcinoma cells, which further affected the radiosensitivity of esophageal squamous cell carcinoma cells. Through functional enrichment analysis of gene set enrichment and validation of the mechanism using the Wnt pathway inhibitor XAV939, it was shown that ACTL6A is involved in the regulation of the Wnt/β-catenin signaling pathway. Knockdown of ACTL6A can inhibit the activity of this pathway, thereby increasing the radiosensitivity of esophageal squamous cell carcinoma. ACTL6A may become an important therapeutic target for esophageal squamous cell carcinoma, providing a necessary theoretical basis for future treatment strategies.	esophagus
MarvelD3 regulates the radiosensitivity of Esophageal squamous cell carcinoma via the MYB/IFI6 axis.	Tight junction proteins have been implicated in the progression of various diseases. MarvelD3, a member of the MARVEL domain protein family involved in tight junction formation, exhibits diverse expression patterns and functions across different tissues. However, its specific role in esophageal squamous cell carcinoma (ESCC) remains to be elucidated. This study demonstrated that MarvelD3 is significantly overexpressed in ESCC tissues. Furthermore, the knockdown of MarvelD3 enhances the radiosensitivity of ESCC in both in vitro and in vivo models. RNA-sequencing analysis identified Interferon alpha inducible protein 6 (IFI6) as a target of MarvelD3. Co-immunoprecipitation assays revealed an interactive regulatory relationship between MarvelD3 and MYB. Additionally, dual-luciferase reporter gene assays and chromatin immunoprecipitation assays confirmed that MYB directly binds to the promoter of the IFI6 gene, thereby regulating IFI6 transcription. Collectively, these findings suggest that MarvelD3 plays a critical role in modulating the radiosensitivity of ESCC via the MYB/IFI6 axis, uncovering a promising mechanism underlying the pathogenesis and progression of ESCC.	esophagus