Targeted Therapies in Pancreatic Cancer—Current Landscape and Future Directions

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 1121

Special Issue Editor


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Guest Editor
Division of Surgical Oncology, Department of Surgery, Medical College of Wisconsin, Milwaukee, WI 53226, USA
Interests: pancreatic neoplasms

Special Issue Information

Dear Colleagues,

Pancreatic cancer remains one of the most challenging malignancies to treat, with a notoriously low survival rate and often late-stage diagnosis. Recent advancements in targeted therapies offer new hope and opportunities for improved outcomes in this aggressive cancer. By honing in on specific molecular and genetic abnormalities, targeted therapies aim to disrupt cancer progression while minimizing the impact on healthy tissues. This Special Issue, titled "Targeted Therapies in Pancreatic Cancer—Current Landscape and Future Directions", seeks to explore the latest breakthroughs and ongoing research in this dynamic field. We will focus on novel therapeutic targets, including advancements in the inhibitors of KRAS and other oncogenic pathways; the role of immunotherapy; artificial intelligence and its ability to predict sensitivity to targeted agents; and personalized medicine approaches that promise to transform the landscape of pancreatic cancer treatment. Our aim is to bring together insights from leading researchers and clinicians to propel our understanding and treatment of pancreatic cancer in this rapidly evolving landscape of targeted therapies. We invite contributions that discuss innovative therapeutic strategies, novel translational research, breaking clinical trial results, and thoughtful perspectives on the future of pancreatic cancer care.

Dr. Yongwoo Dave Seo
Guest Editor

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Keywords

  • pancreatic cancer
  • precision oncology
  • targeted therapies
  • immunotherapy
  • KRAS inhibitors
  • novel clinical trial design

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Published Papers (1 paper)

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Review

34 pages, 2332 KiB  
Review
Treatment of KRAS-Mutated Pancreatic Cancer: New Hope for the Patients?
by Kamila Krupa, Marta Fudalej, Emilia Włoszek, Hanna Miski, Anna M. Badowska-Kozakiewicz, Dominika Mękal, Michał P. Budzik, Aleksandra Czerw and Andrzej Deptała
Cancers 2025, 17(15), 2453; https://doi.org/10.3390/cancers17152453 - 24 Jul 2025
Viewed by 821
Abstract
Pancreatic cancer, specifically pancreatic ductal adenocarcinoma (PDAC), ranks among the most lethal malignancies, with a 5-year survival rate of under 10%. The most prevalent KRAS mutations occur in three hotspot residues: glycine-12 (G12), glycine-13 (G13), and glutamine-61 (Q61), leading to the constant activation [...] Read more.
Pancreatic cancer, specifically pancreatic ductal adenocarcinoma (PDAC), ranks among the most lethal malignancies, with a 5-year survival rate of under 10%. The most prevalent KRAS mutations occur in three hotspot residues: glycine-12 (G12), glycine-13 (G13), and glutamine-61 (Q61), leading to the constant activation of the Ras pathway, making them the primary focus in oncologic drug development. Selective KRAS G12C inhibitors (e.g., sotorasib, adagrasib) have demonstrated moderate efficacy in clinical trials; however, this mutation is infrequent in PDAC. Emerging therapies targeting KRAS G12D and G12V mutations, such as MRTX1133, PROTACs, and active-state inhibitors, show promise in preclinical studies. Pan-RAS inhibitors like ADT-007, RMC-9805, and RMC-6236 compounds provide broader coverage of mutations. Their efficacy and safety are currently being investigated in several clinical trials. A major challenge is the development of resistance mechanisms, including secondary mutations and pathway reactivation. Combination therapies targeting the RAS/MAPK axis, SHP2, mTOR, or SOS1 are under clinical investigation. Immunotherapy alone has demonstrated limited effectiveness, attributed to an immunosuppressive tumor microenvironment, although synergistic effects are noted when paired with KRAS-targeted agents. Furthermore, KRAS mutations reprogram cancer metabolism, enhancing glycolysis, macropinocytosis, and autophagy, which are being explored therapeutically. RNA interference technologies have also shown potential in silencing mutant KRAS and reducing tumorigenicity. Future strategies should emphasize the combination of targeted therapies with metabolic or immunomodulatory agents to overcome resistance and enhance survival in KRAS-mutated PDAC. Full article
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