Pancreatic ductal adenocarcinoma (PDAC) is a high fatality cancer with one of the worst prognoses in solid tumors. Most patients present with late stage, metastatic disease and are not eligible for potentially curative surgery. Despite complete resection, the majority of surgical patients will recur within the first two years following surgery. Postoperative immunosuppression has been described in different digestive cancers. While the underlying mechanism is not fully understood, there is compelling evidence to link surgery with disease progression and cancer metastasis in the postoperative period. However, the idea of surgery-induced immunosuppression as a facilitator of recurrence and metastatic spread has not been explored in the context of pancreatic cancer. By surveying the existing literature on surgical stress in mostly digestive cancers, we propose a novel practice-changing paradigm: alleviate surgery-induced immunosuppression and improve oncological outcome in PDAC surgical patients by administering oncolytic virotherapy in the perioperative period.
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http://dx.doi.org/10.3389/fonc.2023.1071751 | DOI Listing |
J Control Release
January 2025
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea. Electronic address:
Post-surgical tumor recurrence poses a major challenge in cancer treatment due to residual tumor cells and surgery-induced immunosuppression. Here, we developed hybrid nanoparticles, termed T-DCNPs, designed to promote antigen-specific activation of cytotoxic CD8+ T cells while concurrently inhibiting immunosuppressive pathways within the tumor microenvironment. T-DCNPs were formulated by co-extruding lipid nanoparticles containing a transforming growth factor β inhibitor with dendritic cells that were pre-treated with autologous neoantigens derived from surgically excised tumors.
View Article and Find Full Text PDFCancer Causes Control
October 2024
Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Purpose: Surgery, an established short-term immunosuppressive event, may spur dissemination of circulating tumor cells and promote the growth of micrometastases. Whether surgical treatment for prostate cancer (i.e.
View Article and Find Full Text PDFInt J Surg
November 2024
Neuro-Immunology Research Unit, School of Psychological Sciences, Tel Aviv University.
Background: The perioperative period often involves stress responses and surgery-induced hypothermia, which were suggested to hinder antimetastatic immunity and promote cancer metastasis. During this critical period, immunotherapies are rarely used, given contraindications to surgery. However, recent preclinical studies support the feasibility of perioperative TLR-9 activation using CpG-C.
View Article and Find Full Text PDFCancer Res Commun
April 2024
TIMM Laboratory, Sahlgrenska Center for Cancer Research, Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Unlabelled: Preclinical studies imply that surgery triggers inflammation that may entail tumor outgrowth and metastasis. The potential impact of surgery-induced inflammation in human pancreatic cancer is insufficiently explored. This study included 17 patients with periampullary cancer [pancreatic ductal adenocarcinoma (PDAC) n = 14, ampullary carcinoma n = 2, cholangiocarcinoma n = 1] undergoing major pancreatic cancer surgery with curative intent.
View Article and Find Full Text PDFCell Death Dis
January 2024
Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Regulatory T cells (Tregs) are a key determinant for the immunosuppressive and premetastatic niche for cancer progression after surgery resection. However, the precise mechanisms regulating Tregs function during surgical stress-facilitated cancer metastasis remain unknown. This study aims to unravel the mechanisms and explore potential strategies for preventing surgical stress-induced metastasis by targeting NEDD8.
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