Molecular and Cellular Mechanisms of Pancreatic Cancer
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: 15 May 2024 | Viewed by 2056
Special Issue Editor
Special Issue Information
Dear Colleagues,
Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal human cancers, with only a five-year overall survival rate in 11% of patients. This poor survival rate is due to the inability to detect PDAC at an early stage and the lack of effective treatment. Mutations are one of the key drivers of PDAC. KRAS, TP53, CDKN2A, SMAD4, and BRCA mutations are frequently observed in PDAC. Additionally, in more than 85% of cases, PDAC is triggered by KRAS mutations such as G12D, G12V, G12R, and G12C. At present, chemotherapy represents the main strategic treatment for unresectable tumors, and its efficacy is limited compared to novel chemotherapy regimens such as FOLFIRINOX and gemcitabine plus nab-paclitaxel. Resistance towards treatments is common for chemotherapy and radiotherapy, and PDAC remains recalcitrant to numerous immune checkpoint therapy agents, such as anti-PD- 1, anti-PD-L1, and anti-CTLA4. The presence of extensive desmoplasia and immunosuppressive conditions in the PDAC stroma is one of the underlying reasons for treatment resistance and failure. Understanding the molecular and cellular mechanisms of PDAC progression and metastasis, and the interaction of cancer cells with stromal cells, will help to improve our knowledge of the biology of PDAC progression, and will aid in developing therapeutic strategies for PDAC and improving its prognosis.
In this Special Issue of IJMS, we invite authors to contribute original research and review articles focusing on elucidating the fundamental molecular and cellular mechanisms underlying the biology of PDAC.
Dr. Sanith Cheriyamundath
Guest Editor
Manuscript Submission Information
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Keywords
- PDAC
- metastasis
- tumor microenvironment
- cancer-associated fibroblasts
- KRAS
- immune cells
- inhibitors
- resistance
- signaling pathways
- EMT
