Advanced pancreatic cancer is one of the prominent contributors to cancer-related mortality globally. Chemotherapy, especially gemcitabine, is generally used for the treatment of advanced pancreatic cancer. Despite the treatment, the fatality rate for advanced pancreatic cancer is alarmingly high. Thus, the dire need for better treatment alternatives has drawn focus to cancer vaccinations. The Wilms tumor gene (WT1), typically associated with Wilms tumor, is found to be excessively expressed in some cancers, such as pancreatic cancer. This characteristic feature is harvested to develop cancer vaccines against WT1. This review aims to systematically summarize the clinical trials investigating the efficacy and safety of WT1 vaccines in patients with advanced pancreatic cancer. An extensive literature search was conducted on databases Medline, Web of Science, ScienceDirect, and Google Scholar using the keywords "Advanced pancreatic cancer," "Cancer vaccines," "WT1 vaccines," and "Pulsed DC vaccines," and the results were exclusively studied to construct this review. WT1 vaccines work by introducing peptides from the WT1 protein to trigger an immune response involving cytotoxic T lymphocytes via antigen-presenting cells. Upon activation, these lymphocytes induce apoptosis in cancer cells by specifically targeting those with increased WT1 levels. WT1 vaccinations, which are usually given in addition to chemotherapy, have demonstrated clinically positive results and minimal side effects. However, there are several challenges to their widespread use, such as the immunosuppressive nature of tumors and heterogeneity in expression. Despite these limitations, the risk-benefit profile of cancer vaccines is encouraging, especially for the WT1 vaccine in the treatment of advanced pancreatic cancer. Considering the fledgling status of their development, large multicentric, variables-matched, extensive analysis across diverse demographics is considered essential.
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http://dx.doi.org/10.7759/cureus.56934 | DOI Listing |
Fam Cancer
January 2025
Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Multiple endocrine neoplasia type 1 (MEN1) syndrome is an autosomal dominant disorder caused by a germline pathogenic variant in the MEN1 tumor suppressor gene. Patients with MEN1 have a high risk for primary hyperparathyroidism (PHPT) with a penetrance of nearly 100%, pituitary adenomas (PitAd) in 40% of patients, and neuroendocrine neoplasms (NEN) of the pancreas (40% of patients), duodenum, lung, and thymus. Increased MEN1-related mortality is mainly related to duodenal-pancreatic and thymic NEN.
View Article and Find Full Text PDFRev Gastroenterol Peru
January 2025
Department of Pathology, Santa Casa Hospital, Porto Alegre, Brazil.
Pancreatic ductal adenocarcinoma during pregnancy is extremely rare. Overall, including our case, only 19 cases confirmed antepartum have been reported to date. We report the case of a 37 year-old woman at 24 weeks of pregnancy in whom a pancreatic adenocarcinoma was identified during investigation of a suspected acute pancreatitis.
View Article and Find Full Text PDFInt J Cancer
January 2025
Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Early Drug Development Center, Peking University Cancer Hospital and Institute, Beijing, China.
Pancreatic cancer is a particularly aggressive tumor, distinguished by the presence of a prominent collagenous stroma and desmoplasia that envelops the tumor cells. Pancreatic stellate cell (PSC) contributes to the formation of a dense fibrotic stroma and has been demonstrated to facilitate tumor progression. As the significance of PSCs is increasingly revealed, more explorations are focused on the complex molecular mechanisms and tumor-stromal crosstalk in order to guide potential therapeutic approaches through deactivating or reprogramming PSCs.
View Article and Find Full Text PDFCell Physiol Biochem
January 2025
UR-UPJV 4667, UFR Sciences, Université de Picardie Jules Verne, Amiens, France,
Quiescent pancreatic stellate cells (PSCs) represent only a very low proportion of the pancreatic tissue, but their activation leads to stroma remodeling and fibrosis associated with pathologies such as chronic pancreatitis and pancreatic ductal adenocarcinoma (PDAC). PSC activation can be induced by various stresses, including acidosis, growth factors (PDGF, TGFβ), hypoxia, high pressure, or intercellular communication with pancreatic cancer cells. Activated PSC targeting represents a promising therapeutic strategy, but little is known regarding the molecular mechanisms underlying the activation of PSCs.
View Article and Find Full Text PDFChem Biol Drug Des
January 2025
Department of Hepato-Biliary-Pancreatic Surgery, Shaoxing People's Hospital, Shaoxing, People's Republic of China.
Gallbladder cancer is the most prevalent malignancy of the biliary tract and has a dismal overall survival even in the present day. The development of new drugs holds promise for improving the prognosis of this lethal disease. The possible anti-neoplastic role of morusin was investigated both in vitro and in vivo.
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