Context.—: Pancreatic ductal adenocarcinoma has some of the worst prognostic outcomes among various cancer types. Detection of histologic patterns of pancreatic tumors is essential to predict prognosis and decide the treatment for patients. This histologic classification can have a large degree of variability even among expert pathologists.
Objective.—: To detect aggressive adenocarcinoma and less aggressive pancreatic tumors from nonneoplasm cases using a graph convolutional network-based deep learning model.
Design.—: Our model uses a convolutional neural network to extract detailed information from every small region in a whole slide image. Then, we use a graph architecture to aggregate the extracted features from these regions and their positional information to capture the whole slide-level structure and make the final prediction.
Results.—: We evaluated our model on an independent test set and achieved an F1 score of 0.85 for detecting neoplastic cells and ductal adenocarcinoma, significantly outperforming other baseline methods.
Conclusions.—: If validated in prospective studies, this approach has a great potential to assist pathologists in identifying adenocarcinoma and other types of pancreatic tumors in clinical settings.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10356903 | PMC |
http://dx.doi.org/10.5858/arpa.2022-0035-OA | DOI Listing |
Cancer Sci
January 2025
Department of Traumatic Orthopedics, Shenzhen Longhua District Central Hospital, Shenzhen, Guangdong, China.
The development of mesothelin (MSLN) epitope reactive T cells is observed in mice that are immunized with the MSLN vaccine. Engineered T cells expressing MSLN-reactive high-affinity TCR exhibit extraordinary therapeutic effects for invasive pancreatic ductal adenocarcinoma in a mouse model. However, the generation of MSLN-reactive T cells through the introduction of MSLN-deficient thymus and the transplantation of the latter as a cure for cancer treatment have not been tested to date.
View Article and Find Full Text PDFJ Cell Mol Med
January 2025
Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, China.
Hepatocellular carcinoma (HCC) poses a continual therapeutic challenge owing to its elevated incidence and unfavourable prognosis, underscoring the critical need for the discovery of new molecular targets for detection and therapy. This work included the analysis of three publically accessible HCC datasets from TCGA and GEO. Instrumental variables (IVs) were derived via expression quantitative trait loci (eQTL) analysis, then followed by two-sample Mendelian randomisation (MR) analysis utilising publically available summary statistics.
View Article and Find Full Text PDFCurr Oncol
January 2025
Radiobiology Unit, Research and Development Department, CNAO National Center for Oncological Hadrontherapy, 27100 Pavia, Italy.
Pancreatic cancer (PC) is one of the most aggressive and lethal malignancies, calling for enhanced research. Pancreatic ductal adenocarcinoma (PDAC) represents 70-80% of all cases and is known for its resistance to conventional therapies. Carbon-ion radiotherapy (CIRT) has emerged as a promising approach due to its ability to deliver highly localized doses and unique radiobiological properties compared to X-rays.
View Article and Find Full Text PDFCells
January 2025
Department of Hepatology and Gastroenterology, Charité University Medicine Berlin, 13353 Berlin, Germany.
Neuroendocrine neoplasms (NENs) are a diverse group originating from endocrine cells/their precursors in pancreas, small intestine, or lung. The key serum marker is chromogranin A (CgA). While commonly elevated in patients with NEN, its prognostic value is still under discussion.
View Article and Find Full Text PDFCells
January 2025
Department of Biomedical & Molecular Sciences, Queen's University, Kingston, ON K7L 3N6, Canada.
Metastasizing cancer cells surreptitiously can adapt to metabolic activity during their invasion. By initiating their communications for invasion, cancer cells can reprogram their cellular activities to initiate their proliferation and migration and uniquely counteract metabolic stress during their progression. During this reprogramming process, cancer cells' metabolism and other cellular activities are integrated and mutually regulated by tunneling nanotube communications to alter their specific metabolic functional drivers of tumor growth and progression.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!