crossing96/oncoscreening huggingface dataset:
Post-endoscopy esophageal squamous cell carcinoma with invasion of the muscularis mucosa or deeper detected in surveillance endoscopy after esophageal endoscopic resection.	BACKGROUND: Surveillance endoscopy is recommended after endoscopic resection of esophageal squamous cell carcinomas (ESCCs). However, surveillance endoscopy sometimes detects advanced subsequent ESCCs with invasion of the muscularis mucosa (MM) or deeper. We aimed to clarify the clinicopathological features of these advanced subsequent ESCCs. METHODS: This single-center retrospective study identified subsequent ESCCs detected during surveillance endoscopy. ESCCs that invaded the MM or deeper and were detected within 24 months after the previous endoscopy were defined as post-endoscopy esophageal advanced lesions (PEEALs), while the first ESCC detected in the patient was defined as the primary lesion. Study 1 compared the clinicopathological characteristics of PEEALs versus non-advanced lesions. Study 2 compared the endoscopic features of pT1a-MM PEEALs versus pT1a-MM primary lesions. RESULTS: A total of 307 subsequent ESCCs were analyzed in Study 1. Of these, 20 were PEEALs and 287 were non-advanced lesions (pT1a-EP/LPM). The median intervals from the previous endoscopy for PEEALs and non-advanced lesions were 6.1 months and 6.7 months, respectively (P = 0.283). The morphological feature of marginal elevation was seen in 60% of PEEALs. In Study 2, 15 pT1a-MM PEEALs were compared with 149 pT1a-MM primary lesions. Compared with primary lesions, pT1a-MM PEEALs were smaller (median 10 mm vs. 30 mm, P < 0.001) and had a higher prevalence of marginal elevation morphology (53.3% vs. 10.1%, P < 0.001). CONCLUSIONS: The specific feature of PEEALs was marginal elevation. Surveillance endoscopy with careful observation for these lesions is recommended after endoscopic resection of ESCCs.	esophagus
IFI30 Knockdown Inhibits ESCC Progression by Promoting Apoptosis and Senescence via Activation of JNK and P21/P16 Pathways.	BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a prevalent and deadly cancer, making it essential to understand the molecular mechanisms influencing its development and prognosis. The role of interferon-gamma-inducible protein 30 (IFI30) in antigen processing is well-established, but its impact on the progression of ESCC remains unclear. This study aimed to investigate the biological function and potential mechanisms of IFI30 in ESCC progression. METHODS: Public databases, proteomics, and immunohistochemistry (IHC) were employed to analyze IFI30 expression. Cell proliferation, migration, and invasion were evaluated using MTS, colony formation, wound healing, and transwell assays. Nude mouse xenograft models were established to assess the effects of IFI30 knockdown in vivo. Quantitative proteomics was utilized to identify differentially expressed proteins (DEPs) and pathways altered by IFI30 knockdown. Cell apoptosis and senescence were evaluated by flow cytometry, SA-β-gal staining, and reactive oxygen species (ROS) analysis. RESULTS: IFI30 was highly expressed in ESCC and was correlated with advanced stage and poor prognosis. IFI30 knockdown inhibited ESCC cell proliferation, migration, and invasion in vitro and suppressed tumor growth in vivo. DEPs were mainly enriched in biological pathways related to apoptosis, mitophagy, cellular senescence, and lysosome. Furthermore, IFI30 knockdown in ESCC cells upregulated HRAS expression, increased ROS production, activated the JNK signaling pathway, and elevated the expression of P16 and P21, thereby promoting apoptosis and senescence. CONCLUSIONS: This study suggests that IFI30 may regulate the JNK and P21/P16 pathways, exerting pro-tumorigenic effects in ESCC. IFI30 could serve as a potential novel target for ESCC treatment.	esophagus
Neoadjuvant camrelizumab plus trastuzumab and chemotherapy for HER2-positive gastric or gastroesophageal junction adenocarcinoma: a single-arm, phase 2 trial.	BACKGROUND: The impact of neoadjuvant combined chemotherapy, immunotherapy, and targeted therapy on pathologic responses and survival outcomes in HER2-positive locally advanced gastric cancer remains unclear. PATIENTS AND METHODS: In this single-arm, phase 2 trial, patients with HER2-positive resectable cT4 and/or N + M0 gastric or gastroesophageal junction (G/GEJ) adenocarcinoma received four cycles of neoadjuvant camrelizumab plus trastuzumab and CapOx, followed by D2 gastrectomy and four cycles of CapOx. The primary endpoint was pathological complete response (pCR, ypT0N0) rate. RESULTS: Twenty-five patients were enrolled and received neoadjuvant combination treatment. Of these patients, 11 (44%) were in cT3 and 14 (56%) in cT4a; all had positive nodal status. Of the 23 patients who underwent surgery, 5 (21.7%, 95% CI: 7.5-43.7) achieved pCR (ypT0N0), and 7 (30.4%, 95% CI: 13.2-52.9) achieved near pCR (ypT0). The R0 resection rate was 100%. During a median follow-up of 41.0 months, no patients with pCR had recurrence or death. In contrast, five of 18 patients with non-pCR had recurrence, and four of them died. The three-year disease-free survival rate was 78.3%. During neoadjuvant treatment, grade 3 adverse events were observed in 36% of patients, with no grade 4 or 5 adverse events reported. No treatment-related surgical delay or reoperation occurred. CONCLUSION: Neoadjuvant camrelizumab plus trastuzumab and chemotherapy demonstrated favorable response and tolerable safety in HER2-positive G/GEJ adenocarcinoma.	esophagus
Ligation-assisted endoscopic submucosal resection following the unroofing technique for esophageal lesions.	For the treatment method of esophageal subepithelial lesions originating from the muscularis propria, conventional endoscopic resection techniques are time-consuming and lack efficacy for small subepithelial lesions originating from the muscularis propria. Lu et al presented an exploration of the effectiveness and safety of ligation-assisted endoscopic submucosal resection, aiming to provide a minimally invasive method for treatment. We discussed and analyzed this study from the aspects of sample screening, clinical pathological characteristics, case-control analysis, and follow-up data.	esophagus
Risk factors and prediction of intensive care unit readmission after oesophagectomy for cancer‡.	OBJECTIVES: Intensive care unit (ICU) readmission has been proposed as a metric for quality of surgical care. The current study investigated potential factors and developed a prediction model for ICU readmission in patients following oesophagectomy for cancer. METHODS: A total of 3028 patients from January 2019 to December 2022 were retrospectively collated as training cohort, with 829 patients from January 2023 to August 2023 enrolled for validation, respectively. Univariable and multivariable analyses were performed to identify potential factors after which a nomogram based on results from multivariable analysis was constructed and validated. RESULTS: In the training cohort, the rate of ICU readmission was 3.6% (110/3028). Readmitted patients were associated with more reoperations, higher 90-day mortality and prolonged postoperative stay (all P < 0.001). Multivariable analysis demonstrated that older age ≥75 years, neoadjuvant therapy, preoperative albuminaemia, diffusing lung capacity for carbon monoxide (DLCO)%, longer operative duration and retention of endotracheal intubation when entering ICU were independently associated with ICU readmission. Based on these results, a nomogram for predicting readmission was constructed and validated. The Hosmer-Lemeshow test showed the model in the training cohort was well calibrated (χ2 = 5.259, P = 0.73) and area under the receiver operating characteristic curve was 0.739 (95% confidence interval 0.691-0.787). Moreover, the application of the nomogram in the validation cohort showed an improved area under the receiver of 0.780 (95% confidence interval 0.703-0.857). CONCLUSIONS: ICU readmission after oesophagectomy although uncommon (3.6%) was associated with prolonged hospitalization and significant mortality. A nomogram based on 6 variables may assist intensivists to early identifying patients at high risk of readmission.	esophagus
Transmanubrial approach for en bloc resection of oligometastatic extranodal extension positive lymph nodes with partial common carotid artery and trachea resection after esophagectomy.	BACKGROUND AND AIMS: The transmanubrial approach (TMA) provides excellent exposure of the cervical-thoracic border area, allowing for the resection of thoracic outlet structures while preserving the clavicle, avoiding muscle sacrifice, and maintaining full shoulder mobility. METHODS: This report presents the first instance of TMA being utilized for oligometastatic, extranodal extension-positive lymph node dissection en bloc with partial resection of the common carotid artery and trachea following esophagectomy. SURGICAL TECHNIQUE: We describe the surgical technique with illustrated explanations.	esophagus
Pedunculated gastric tube with distal partial gastrectomy for esophageal reconstruction in synchronous or metachronous esophagectomy.	While the stomach is commonly used as an esophageal substitute after esophagectomy, it may not be a viable option in some cases. One alternative for esophageal reconstruction is a pedunculated gastric tube with distal partial gastrectomy (PGT-DPG). However, no studies have comprehensively analyzed its efficacy. We retrospectively evaluated the clinical characteristics and surgical outcomes of patients who underwent PGT-DPG between 2011 and 2023, and reviewed previously published studies on the surgical outcomes of PGT-DPG. Among the nine patients in the current study, seven underwent PGT-DPG for gastric cancer; of which, five were performed concurrently with esophagectomy, while two were conducted following prior esophagectomy. Additionally, PGT-DPG was performed in two cases with benign gastric lesions. The major postoperative complications included pneumonia (two cases), anastomotic leakage (two cases), and recurrent laryngeal nerve paralysis (one case). No graft necrosis or mortality was observed. Our review of these cases, along with previously reported cases, indicated that PGT-DPG showed efficacy due to its availability for antral early gastric cancer, avoidance of bowel reconstruction, simplified technique, and improved cervical elevation. PGT-DPG is a valuable rescue option in cases in which gastric tube reconstruction is challenging. Therefore, esophageal surgeons should be well acquainted with this technique.	esophagus
Application of modified neck drainage in the management of cervical anastomotic fistula in esophageal cancer patients.	BACKGROUND: Anastomotic fistula is a rare but life-threatening complication of esophageal cancer, and its treatment remains challenging.We aimed to evaluate the clinical efficacy of modified cervical drainage in the management of cervical anastomotic fistula in patients after esophageal cancer surgery. METHODS: From June 2017 to December 2021, 25 esophageal cancer patients who developed cervical anastomotic fistula were enrolled in the study. Among them, 14 patients were treated with modified cervical drainage, which served as the observation group, while the remaining 11 patients underwent open incision and drainage, which served as the control group. The treatment outcomes of the two groups were compared and analyzed. RESULTS: The observation group had a significantly shorter healing time, fewer dressing changes, shorter hospital stay, and lower hospitalization costs compared to the control group (P < 0.05). The incidence of complications in the neck was not significantly different between the two groups (P > 0.05). All patients resumed a normal diet without experiencing fever, coughing or other discomfort, and were discharged after a smooth recovery. CONCLUSIONS: Modified neck drainage, as a treatment method for cervical anastomotic leakage in esophageal cancer patients, has preliminarily demonstrated potential in promoting patient recovery. However, its efficacy still requires further validation and confirmation through studies with larger sample sizes.	esophagus
Patterns of diagnostic testing for oesophagogastric cancer-related symptoms in Australian primary care: a retrospective cohort study.	BACKGROUND: Oesophagogastric (OG) cancer-associated symptoms are common in primary care, but most research has focused on patients with a confirmed OG cancer diagnosis, rather than those presenting with symptoms for the first time. AIM: To examine diagnostic testing patterns for upper gastrointestinal (GI) symptoms linked to OG cancer. DESIGN AND SETTING: A retrospective cohort study was undertaken, which used a linked primary care database. It included de-identified patients aged >55 years who presented with symptoms suggestive of OG cancer between 2008 and 2022. METHOD: The study analysed the proportion of patients who underwent pathology, imaging, referral, upper GI endoscopy, or a test of treatment. Differences across socioeconomic groups were also examined, along with the proportion of patients diagnosed with OG cancer. RESULTS: The study cohort consisted of 44 402 patients, of whom 126 (0.3%) were diagnosed with OG cancer within 12 months of presentation. Reflux was the most common symptom (57%), followed by nausea (11%). Patients aged ≥75 years were less likely to be investigated or referred than those aged 56-64 years (odds ratio [OR] 0.59, 95% confidence interval [CI] = 0.56 to 0.62, P<0.001). Those from less disadvantaged areas were 1.4 times more likely to be investigated than people from the most disadvantaged areas (OR 1.44, 95% CI = 1.36 to 1.53, P<0.001). Patients on test-of-treatment medications were less likely to receive further investigation (OR 0.66, 95% CI = 0.63 to 0.69, P<0.001). Multiple symptoms and visits increased the likelihood of investigation (OR 2.77, 95% CI = 2.55 to 3.00, P<0.001). CONCLUSION: Significant variations in diagnostic testing could contribute to disparities in OG cancer outcomes.	esophagus
CircPRKCA facilitates esophageal squamous cell carcinoma metastasis via m5C-dependent CSF2 mRNA stabilization.	BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a serious invasive malignancy with an ambiguous etiology. Evidence indicates that circular RNA (circRNA) is significantly involved in the regulatory processes associated with cancer development. Nevertheless, the specific molecular mechanisms through which circRNA facilitates the progression of ESCC are still largely undefined. METHODS: Here, we identified that the expression of hsa_circ_0007580 (designated circPRKCA) was markedly elevated in ESCC. Fluorescence in situ hybridization (FISH) was conducted to verify the expression, intracellular localization, and potential prognostic value of circPRKCA based on the tissue microarray. Gain- and loss-of-function assays were employed to investigate the effects of circPRKCA both in vitro and in vivo. RNA pull-down and mass spectrometry (MS) were performed to identify the proteins bound to circPRKCA. mRNA sequencing was conducted to screen the downstream target genes of circPRKCA. Furthermore, immunoprecipitation and methylated RNA immunoprecipitation (MeRIP) analysis were used to explore the regulatory mechanisms. RESULTS: We found that circPRKCA exhibited significant upregulation in ESCC tissues and correlated with unfavorable prognostic outcomes. Biological function experiments further confirmed that circPRKCA enhances the capabilities of migration, invasion, and angiogenesis in ESCC. Mechanistically, circPRKCA engages in interaction with Y-box binding protein 1 (YBX1) within the cytoplasmic milieu, consequently preventing the ubiquitination-mediated degradation of YBX1. Increased concentrations of YBX1 increase the stability of granulocyte-macrophage colony-stimulating factor (CSF2) mRNA in a 5-methylcytosine (m5C)-dependent manner. This process facilitates metastasis in ESCC. CONCLUSION: In this research, we identified a correlation between circPRKCA and unfavorable prognoses in patients with ESCC. It is instrumental in the metastatic progression of ESCC via the YBX1/CSF2 signaling pathway. Consequently, targeting circPRKCA may represent a promising therapeutic strategy for ESCC.	esophagus
An organoid library of human esophageal squamous cell carcinomas (ESCCs) uncovers the chemotherapy-resistant ESCC features.	Esophageal squamous cell carcinoma (ESCC) is a deadly cancer with a poor prognosis and a high recurrence rate after chemotherapy, posing a significant clinical challenge. To elucidate the molecular basis of chemotherapy (chemo)-resistance and to develop methods to effectively eliminate chemo-resistant tumor clones, we established an ESCC organoid (ESCCO) library from 24 ESCC patients of various stages, ages, and treatments. These ESCCOs faithfully recapitulate the oncogenic mutations observed in the original ESCC tissues and manifest tumorigenic properties when xenografted. The ESCCOs respond differently to cisplatin and 5-fluorouracil, chemotherapeutic agents commonly used to treat ESCC patients, with 7 ESCCOs exhibiting potent chemo-resistance. Notably, the chemo-resistant ESCCOs show higher genes involved in antioxidant stress response pathways and more accessible chromatin at their loci than the sensitive ESCCOs. These genes can serve as valuable biomarkers to stratify chemo-resistant ESCCs in histopathological specimens. Through drug screening using the ESCCO library, we reveal that fedratinib effectively induces cell death in chemo-resistant ESCCOs. Collectively, our human ESCCO model offers novel insights into the mechanism of chemo-resistance in ESCCs, which is critical for developing effective therapeutic approaches to eradicate the recurrence of ESCCs.	esophagus
Non-muscle myosin heavy chain IIA regulates cell morphology, stress fibre structure, and cell migration in FLO-1 oesophageal adenocarcinoma cells.	The incidence of oesophageal adenocarcinoma (OAC) is increasing at a rapid rate in Western countries. Early oesophageal cancer is often asymptomatic and metastatic disease is common at presentation leading to poor prognosis and survival rates. Cell migration is tightly controlled in the healthy cell but can become dysregulated in diseases such as OAC where increased cell motility and migration can contribute to metastasis. We investigated the role of an actin-based molecular motor, non-muscle myosin heavy chain IIA (NMHCIIA) in the migratory capacity of oesophageal adenocarcinoma cells. Immunofluorescence microscopy and ratiometric imaging demonstrated that NMHCIIA co-localises with F-actin at the leading edge and retracting rear of migrating FLO-1 OAC cells. siRNA-mediated depletion of NMHCIIA from FLO-1 cells altered cell morphology, gave rise to an increased number of stress fibre like structures and reduced FLO-1 cell migration. These findings suggest that NMHCIIA influences FLO-1 cell migration by regulating F-actin dynamics and the actin cytoskeleton, providing insight into the mechanisms of migration employed by OAC cells and identifying NMHCIIA as a potential therapeutic target for this disease.	esophagus
Dual-Mode Radiosensitization of Esophageal Squamous Cell Carcinoma via SOCS6-Loaded Virus-Inspired Manganese-Bismuth Bimetallic Oxide Nanoparticles.	Radioresistance poses a significant obstacle to controlling the recurrence of esophageal squamous cell carcinoma (ESCC) during radiotherapy. It is urgent to develop innovative radiosensitization strategies to improve the prognosis of patients with ESCC. Here, a novel dual-mode radiosensitizer: a virus-inspired hollow mesoporous manganese-bismuth bimetallic oxide nanoparticles (vHMMn-Bi) encapsulating the radiosensitizing plasmids (suppressor of cytokine signaling 6, SOCS6) is developed, designed to significantly amplify ESCC radiotherapy under hypoxic conditions. After intravenous injection, the SOCS6@vHMMn-Bi nanoparticles can be efficiently delivered to the tumor site and rapidly invade tumor cells by virus-like surface-assisted adhesion. Under X-ray irradiation, the nanoparticles exhibits a unique dual-mode sensitization effect, encompassing exogenous and endogenous mechanisms, thereby significantly augmenting the ESCC radiotherapeutic effectiveness. First, the Bi(2)O(3) within the shell can enhance the radiosensitivity owing to its robust X-ray attenuation characteristics. Second, the SOCS6 released from the interior can inhibit both HIF-1α and JAK2/STAT3 signaling pathways, triggering ROS upregulation and intensifying radiation-mediated DNA damage inside ESCC cells. Furthermore, the shell employs MnO(2) to catalyze the decomposition of endogenous H(2)O(2) to increase oxygen generation, alleviating hypoxia within the tumor microenvironment. These nanoparticles demonstrates considerable potential as dual-mode radiosensitizers with no systemic toxicity and low immunogenicity for amplifying radiotherapeutic efficacy in ESCC.	esophagus
Interplay and cooperation between GLI2 and master transcription factors promote progression of esophageal squamous cell carcinoma.	The establishment of gene expression programs that drive cell identity is governed by tightly regulated transcription factors (TFs) that engage in auto- and cross-regulation in a feedforward manner, forming core regulatory circuitries (CRCs). Here, we identify and validate an important interconnected CRC formed by three master TFs-GLI2, TP63, and RUNX1-in esophageal squamous cell carcinoma (ESCC). Furthermore, master TFs co-bind to their own and each other's super-enhancers, forming an interconnected auto-regulatory loop. Mechanistically, these master TFs occupy the majority of ESCC super-enhancers and cooperatively orchestrate the ESCC transcription program. Functionally, GLI2, a master TF, is essential for ESCC viability, migration, invasion, and the growth of xenograft tumors. Moreover, the overexpression of GLI2 is significantly associated with shorter overall survival of patients with ESCC. Downstream, this CRC apparatus coordinately regulates gene expression networks in ESCC, controlling important cancer-promoting pathways, including Hedgehog, glycolysis, and epidermal growth factor receptor signaling pathways. Together, these findings offer significant mechanistic insights into the transcriptional dysregulation in ESCC and recognize GLI2 as a potential therapeutic target and prognostic marker for ESCC. More importantly, CRC-downstream genes and signaling pathways may contain potential therapeutic targets for this malignancy.	esophagus