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Molecular Mechanisms and Therapies of Pancreatic Cancer: 3rd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 587

Special Issue Editor

Special Issue Information

Dear Colleagues,

Pancreatic cancer (PC) is one of the most aggressive solid malignancies, with an overall 5-year survival rate of ~8%, and it is predicted to become the second leading cause of cancer-related death by 2030. PC progression and metastasis are strongly influenced by metabolic stress imposed by the tumor microenvironment (TME) due to limited oxygen and nutrient supply and unfavorable pH. In this context, deregulation and reprogramming of energy metabolism are hallmarks of PC, which leads tumor cells to rewire their glucose, amino acid, and lipid metabolism on the basis of the bioenergetic and biosynthetic demands needed to survive and escape immunosurveillance. For this reason, exploiting cellular plasticity through targeted reprogramming of metabolic features in PC could lead to the generation of promising and novel selective therapeutic approaches for patients’ treatment.

This Special Issue was set up to encourage researchers to carry out studies on the following:

  • Reprogramming of the intracellular metabolism of nutrients (including glucose, amino acids and lipids) to impact PC progression;
  • Identification of novel pathways underlying metabolic reprogramming as therapeutic targets for PC;
  • Exploitation of cancer cell plasticity to modulate chemoresistance;
  • Shaping of the tumor microenvironment to sensitize cancer cells to chemotherapy.

Articles consisting exclusively of bioinformatics or computational analyses of public databases or pure clinical studies will not be accepted. Basic studies or translational studies including molecular characterizations of patients from real practice are welcome. Reviews are also appreciated.

Dr. Donatella Delle Cave
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • pancreatic cancer
  • metabolism
  • cellular plasticity
  • tumor microenvironment
  • target therapy

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Published Papers (1 paper)

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Research

16 pages, 349 KB  
Communication
High Intratumoral PROS1 Expression Correlates with Improved Survival and Is Associated with Suppressed Oncogenic Signaling in Pancreatic Ductal Adenocarcinoma
by Teagan Prouse, Rinku Majumder and Samarpan Majumder
Int. J. Mol. Sci. 2026, 27(7), 2964; https://doi.org/10.3390/ijms27072964 - 25 Mar 2026
Viewed by 361
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a five-year survival rate of approximately 13%. Patients with PDAC also have an elevated incidence of venous thromboembolism (VTE), despite prophylactic anticoagulation. Thus, there is an urgent need for therapeutic strategies that target [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a five-year survival rate of approximately 13%. Patients with PDAC also have an elevated incidence of venous thromboembolism (VTE), despite prophylactic anticoagulation. Thus, there is an urgent need for therapeutic strategies that target tumor progression and hypercoagulability. Protein S (PS), a physiological anticoagulant encoded by the PROS1 gene, has recently been shown to inhibit PDAC growth in preclinical models. To further examine the physiological relevance of intratumoral PS in PDAC, we performed a meta-analysis of four independent PDAC patient cohorts obtained from cBioPortal. Patients were stratified based on low versus high intratumoral PROS1 expression based on below- and above-average mean expression, overall survival, and gene expression of select pro-growth genes, implementing a fixed-effects model. High intratumoral PROS1 expression was associated with a 41.8% reduction in the risk of death compared with low PROS1 expression (pooled hazard ratio = 0.581) within 30 months of diagnosis from survival data in three cohorts. Elevated PROS1 expression correlated with marked downregulation of key genes implicated in PDAC invasion and metastasis, including MMP2 and SNAI2, in all four cohorts. Collectively, these findings suggest that PROS1 is a potential prognostic biomarker and molecular regulator in PDAC and thus support further investigation into the dual role of PS in tumor progression. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapies of Pancreatic Cancer: 3rd Edition)
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