Girdin functions as an Akt phosphorylation enhancer (APE), which expedites the proliferation and survival of many types of tumours. However, the influence of Girdin on pancreatic cancer and the underlying molecular mechanisms have yet to be uncovered. Hence, in the present study, we sought to elucidate the function of Girdin in pancreatic cancer malignancy, particularly its role in pancreatic cancer cell proliferation, migration and apoptosis. Immunohistochemistry (IHC) was used to evaluate Girdin expression in pancreatic cancer tissues and to analyse its correlation with pathological grade. Girdin expression was further validated in pancreatic cancer cell lines (AsPC‑1, BxPC‑3 and PANC‑1), and human pancreatic ductal epithelial (HPNE) cells were used as a control. Recombinant adenovirus vectors containing Girdin‑siRNA were constructed to inhibit Girdin expression and were used in subsequent experiments to determine the effects of Girdin silencing on pancreatic cancer cells. Girdin silencing suppressed pancreatic cancer cell proliferation and induced pancreatic cancer cell apoptosis in vitro and in vivo. According to the results of further mechanistic investigations, Girdin may regulate cell processes through the phosphatidylinositol‑3‑kinase/protein kinase B (PI3K/Akt) signalling pathway to exert additive effects on pancreatic cancer.
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http://dx.doi.org/10.3892/or.2018.6469 | DOI Listing |
Ann Surg Oncol
January 2025
Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Background: Hematologic changes after splenectomy and hyperthermic intraperitoneal chemotherapy (HIPEC) can complicate postoperative assessment of infection. This study aimed to develop a machine-learning model to predict postoperative infection after cytoreductive surgery (CRS) and HIPEC with splenectomy.
Methods: The study enrolled patients in the national TriNetX database and at the Johns Hopkins Hospital (JHH) who underwent splenectomy during CRS/HIPEC from 2010 to 2024.
Cancer Res
January 2025
University of Cambridge, Cambridge, United Kingdom.
Pancreatic ductal adenocarcinoma (PDAC) contains an extensive stroma that modulates response to therapy, contributing to the dismal prognosis associated with this cancer. Evidence suggests that PDAC stromal composition is shaped by mutations within malignant cells, but most previous work has focused on pre-clinical models driven by KrasG12D and mutant Trp53. Elucidation of the contribution of additional known oncogenic drivers, including KrasG12V mutation and Smad4 loss, is needed to increase understanding of malignant cell-stroma crosstalk in PDAC.
View Article and Find Full Text PDFObjective: Sodium-glucose cotransporter (SGLT) 2 inhibitors are expected to demonstrate secondary effects against malignancy. However, long-term and large-scale data are required to evaluate the effects of SGLT2 inhibitors on malignancy, which has not been sufficiently studied in clinical practice. This study aimed to evaluate the association between SGLT2 inhibitors and malignancy using the spontaneous adverse reaction database.
View Article and Find Full Text PDFCancer
February 2025
Division of Hematology/Oncology, University of Illinois Chicago, Chicago, Illinois, USA.
J Am Coll Surg
January 2025
Division of Immunotherapy, The Hiram C. Polk Jr., MD Department of Surgery, Immuno-Oncology Program, Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Introduction: Irreversible electroporation(IRE) has augmented the effects of certain immunotherapies in pancreatic cancer(PDA). Yeast-derived particulate beta-glucan induces trained innate immunity and has successfully reduces murine PC tumor burden. This is a Phase II study to test the hypothesis that IRE may augment beta-glucan induced trained immunity in patients with PDA.
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