Ontology highlight
ABSTRACT:
PROVIDER: PRJNA979957 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Esophageal cancer, one of the most prevalent cancers worldwide, frequently exhibits distant metastases. The adipokine visfatin has been implicated in cancer progression and metastasis. However, the mechanisms by which visfatin regulates motility in esophageal cancer remain unclear. Here, we found that visfatin levels are higher in metastatic esophageal cancer patients than in primary esophageal cancer patients. Visfatin stimulation enhances migration and invasion in esophageal cancer cells. miRNA sequencing results revealed that miR-3613-5p controls visfatin-induced cell motility. Visfatin promotes esophageal cancer cell migration by reducing miR-3613-5p expression and subsequently increasing VEZF1/VCAN production. The visfatin/miR-3613-5p axis exhibits a promising target for inhibiting esophageal cancer metastasis.
2025-06-09 | GSE298998 | GEO
Project description:The investigators hypothesize that abnormalities in thromboelastography (TEG) parameters in patients with liver, pancreas, biliary, esophageal, colorectal, and lung adenocarcinoma can serve as biomarkers for oncologic disease burden, cancer recurrence and overall survival as well as thrombotic and hemorrhagic post-operative complications. The investigators further hypothesize that there is histologic pathology correlates to pre-operative TEG abnormalities, and that it identifies patients with virulent tumor biology.
| 2746518 | ecrin-mdr-crc
Project description:Background and Purpose: The current standard of care for locally advanced esophageal and gastroesophageal junctional cancer is neoadjuvant chemoradiation (NCRT) followed by surgery. The genomic and proteomic pathways responsible for response to neoadjuvant chemoradiation are sparsely described, and thus response to treatment cannot be reliably predicted. In this study, we performed an in-depth proteomic analysis of esophageal and gastroesophageal tumors, to describe differences in pathway activation between patients with good and poor prognosis following neoadjuvant chemoradiation. Materials and Methods: This study included locally advanced esophageal and gastroesophageal cancer patients treated with NCRT. The study cohort was dichotomized into two groups of patients- good prognosis (GP) and bad prognosis (BP) according to the post-operative disease-free interval. We performed a mass spectrometry analysis of proteins extracted from the malignant regions of surgical specimens and analyzed data from electronic medical records. Clinical data was correlated with differences in protein expression between GP and BP using validated gene expression pathways. Results: The study included thirty-five patients with adenocarcinoma. GP and BP had statistically significant differences in protein expression patterns. GP exhibited differential enrichment of pathways related to cellular respiration, oxidative phosphorylation and proteins of the RAS oncogene family. Conclusion: In this study we identify enrichment of pathways related to oxidative phosphorylation and RAS oncogene pathway in esophageal cancer patients with a favorable response to NCRT. Larger transcriptomic studies are warranted to portray potential surrogate signature of biomarkers based upon these potential pathways.
2022-05-20 | PXD025192 | Pride
Project description:Anastomotic leakage is a major complication after gastrointestinal surgery, yet early detection remains limited by nonspecific clinical signs and narrow biomarker panels. Here, we used longitudinal data-independent acquisition proteomics to profile postoperative drain fluid from two surgical cohorts, comprising 34 pancreatic surgery patients with 222 drain-fluid samples and 34 colorectal surgery patients with 146 drain-fluid samples. We aimed to define procedure-specific leakage signatures, evaluate established biomarkers across postoperative time, and identify additional candidate markers beyond routinely measured proteins. In pancreatic surgery, established enzyme markers, particularly AMY2A and PNLIP, showed strong early discrimination between leak and non-leak patients. In colorectal surgery, the same predefined marker strategy performed inconsistently, indicating that leakage-associated biology may differ between surgical procedures. Discovery analysis revealed divergent temporal patterns. Pancreatic leakage was dominated by early enzyme enrichment followed by inflammatory, antimicrobial, oxidative stress, and matrix-remodelling-associated proteins. Colorectal leakage showed strongest divergence around POD3 and was driven largely by reduced abundance of proteins linked to uncomplicated recovery, including endothelial integrity, extracellular matrix organization, complement regulation, and coagulation balance. From these procedure-specific patterns, PRSS2 and AZU1 were selected for pancreatic surgery, and FBLN1 and CDH5 for colorectal surgery, as novel candidate markers for targeted follow-up. Targeted ELISA measurements confirmed detectability of selected candidates in drain fluid, supporting their further development as markers for novel leakage detection strategies. Overall, these data show that postoperative leakage follows procedure-specific proteomic trajectories and support drain-fluid proteomics as a framework for biologically informed biomarker discovery beyond routinely measured markers.
2026-09-08 | PXD082170 | Pride
Project description:Anastomotic leakage is a major complication after gastrointestinal surgery, yet early detection remains limited by nonspecific clinical signs and narrow biomarker panels. Here, we used longitudinal data-independent acquisition proteomics to profile postoperative drain fluid from two surgical cohorts, comprising 34 pancreatic surgery patients with 222 drain-fluid samples and 34 colorectal surgery patients with 146 drain-fluid samples. We aimed to define procedure-specific leakage signatures, evaluate established biomarkers across postoperative time, and identify additional candidate markers beyond routinely measured proteins. In pancreatic surgery, established enzyme markers, particularly AMY2A and PNLIP, showed strong early discrimination between leak and non-leak patients. In colorectal surgery, the same predefined marker strategy performed inconsistently, indicating that leakage-associated biology may differ between surgical procedures. Discovery analysis revealed divergent temporal patterns. Pancreatic leakage was dominated by early enzyme enrichment followed by inflammatory, antimicrobial, oxidative stress, and matrix-remodelling-associated proteins. Colorectal leakage showed strongest divergence around POD3 and was driven largely by reduced abundance of proteins linked to uncomplicated recovery, including endothelial integrity, extracellular matrix organization, complement regulation, and coagulation balance. From these procedure-specific patterns, PRSS2 and AZU1 were selected for pancreatic surgery, and FBLN1 and CDH5 for colorectal surgery, as novel candidate markers for targeted follow-up. Targeted ELISA measurements confirmed detectability of selected candidates in drain fluid, supporting their further development as markers for novel leakage detection strategies. Overall, these data show that postoperative leakage follows procedure-specific proteomic trajectories and support drain-fluid proteomics as a framework for biologically informed biomarker discovery beyond routinely measured markers.
2026-09-08 | PXD082236 | Pride
Project description:Esophageal cancer, a highly lethal tumor, contributes to 5% of all cancer deaths, with its primary subtypes being esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC). While most studies focus on ESCC, this study investigates EAC using single-cell RNA sequencing (scRNA-seq) to analyze CD45+ immune cells from tumors and matched non-tumor tissues in therapy-naïve patients. By examining the transcriptional profiles of these immune cells and the entire transcriptome in a cohort of 23 patients, the study identifies distinct transcriptional signatures. These signatures were used to stratify a large cohort of TCGA EAC patients, revealing strong associations with prognosis and clinical outcomes. The findings suggest that these transcriptional profiles can improve prognosis accuracy post-surgery and potentially guide effective therapies, including immunotherapy, for EAC patients.
2024-08-02 | GSE273848 | GEO
Project description:Esophageal cancer, a highly lethal tumor, contributes to 5% of all cancer deaths, with its primary subtypes being esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC). While most studies focus on ESCC, this study investigates EAC using single-cell RNA sequencing (scRNA-seq) to analyze CD45+ immune cells from tumors and matched non-tumor tissues in therapy-naïve patients. By examining the transcriptional profiles of these immune cells and the entire transcriptome in a cohort of 23 patients, the study identifies distinct transcriptional signatures. These signatures were used to stratify a large cohort of TCGA EAC patients, revealing strong associations with prognosis and clinical outcomes. The findings suggest that these transcriptional profiles can improve prognosis accuracy post-surgery and potentially guide effective therapies, including immunotherapy, for EAC patients.
2024-08-02 | GSE273847 | GEO