DDR1 Protein Linked to Pancreatic Cancer Progression
Researchers identified a protein that helps pancreatic cancer cells resist iron-based cell death treatments.
Updated on Sept. 23, 2026 in Cancer

Scientists have determined that elevated expression of the DDR1 protein correlates with a poor prognosis in pancreatic ductal adenocarcinoma. The protein allows cancer cells to evade a form of cell death known as ferroptosis.
Why it matters
Understanding how DDR1 suppresses ferroptosis provides a new target for therapy. By blocking this protein, researchers found they could make cancer cells more vulnerable to treatments.
DDR1 recruits SHC1 to activate the MAPK/ERK pathway, which subsequently drives SLC40A1 to lower intracellular labile iron pools. This process actively suppresses lipid peroxidation and prevents cell death in cancer tissue.
The players
DDR1
This is a protein found to be elevated in pancreatic ductal adenocarcinoma tissues.
Dasatinib
This is a pharmaceutical agent used in the study to inhibit DDR1 and sensitize cancer cells to treatment.
SLC40A1
This protein functions as an iron exporter that reduces intracellular labile iron pools within cancer cells.
The details
The research shows that DDR1-driven upregulation of the SLC40A1 iron exporter protects cancer cells from DHA-induced ferroptosis. When DDR1 was inhibited using Dasatinib, the combination treatment led to increased 4-HNE accumulation and reduced tumor cell proliferation.
Timeline
The findings were published on September 23, 2026.
The Big Picture
This study advances the foundational goals of the NCI Pancreatic Cancer Detection Consortium by providing a specific molecular mechanism that explains therapeutic resistance in pancreatic ductal adenocarcinoma.
This development identifies a new pathway for potential drug therapies that could eventually improve treatment outcomes for pancreatic cancer patients. By combining existing drugs like Dasatinib with ferroptosis-inducing treatments, researchers aim to overcome tumor resistance.
The takeaway
Targeting the DDR1 protein appears to be a viable strategy for enhancing the effectiveness of iron-dependent cancer treatments. This approach suggests that future therapies could focus on dual-targeting to bypass the survival mechanisms utilized by aggressive tumor cells.
Further reading
For additional context on current research, visit the Cancer section.
Source note: This article includes information reported by Nature.







