Abstract
Pancreatic ductal adenocarcinoma (PDAC) remains an aggressive malignancy with a 5-year survival rate below 10%. Its unique genetic makeup and tumor microenvironment produce a lack of response to current treatments, including chemotherapy, radiotherapy, and immunotherapy. Recent preclinical studies have revealed that ferroptosis, an iron-dependent form of nonapoptotic cell death driven by unrestricted lipid peroxidation, may be an attractive therapeutic goal in PDAC. Understanding the dual role of ferroptotic cell death in both promoting and suppressing tumor immunity, as well as its integrated regulatory mechanisms and signaling pathways, may lead to more effective treatment designs for clinical trials of PDAC and may minimize or delay the emergence of drug resistance or side effects.
Original language | English (US) |
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Pages (from-to) | 891-901 |
Number of pages | 11 |
Journal | Trends in Cancer |
Volume | 7 |
Issue number | 10 |
DOIs | |
State | Published - Oct 2021 |
Keywords
- cell death
- ferroptosis
- pancreatic cancer
- redox signaling
- therapy resistance
- tumor microenvironment
ASJC Scopus subject areas
- Oncology
- Cancer Research