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"Pancreatic ductal adenocarcinoma is highly resistant to current treatments and is expected to become the second most common cause of cancer-related death in the United States during this decade,
" said senior author caus Radu, MD, Calif.
Investigator at the UCLA Jonsson Comprehensive Cancer Center and professor in the Department of Molecular and Pharmacology at UCLA
The preclinical study, which used tumor cells from patients and xenograft tumors from cell lines, was published online Jan.
11 in Cell Reports
.
It studies sting-driven type I interferons, immune system signaling molecules that disrupt cancer cell proliferation in laboratory studies but often have the opposite effect in clinical practice, where tumor cells adapt to them, And often develop resistance to treatments such as radiotherapy, chemotherapy and immune checkpoint blockade
"We determined that a subset of PDAC tumors exhibited an inherent interferon response that was not modeled under standard cell culture conditions
.
Using some advanced techniques, we discovered that interferon signaling causes tumor cells to become dependent on a specific signaling pathway to survive
The results suggest that novel small-molecule drugs that inhibit ATR are being investigated for the treatment of several cancers, including PDAC, and could be used in combination with interferon "amplification" to block the escape ability of tumor cells
.
The researchers defined a series of molecular interactions that lead to a cascade of reactions within cells
.
Through its effects on several genes, interferons alter the metabolic processes that underpin the DNA base of cancer cells, reducing the supply of biochemical modules that DNA needs to survive
Dr.
Donahue said that based on the results of this study, a potential intervention worth further exploration is a therapy that activates another signaling pathway called STING
.
"STING activation induces interferon signaling in PDAC cells and triggers ATR activation," he said
.
"This strategy would enhance the onslaught of interferon signaling while shutting down collateral pathways through ATR-inhibiting drugs, preventing their escape
Journal Reference :
Evan R.
