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Published on: November 19, 2019
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CXCL12 in Pancreatic Cancer: Its Function and Potential as a Therapeutic Drug Target
Shivani Malik1, Jill M Westcott2, Rolf A Brekken2
1Kura Oncology, Inc., San Diego, CA 92130, USA.
Cancers
|January 11, 2022
Summary
Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer. Targeting the CXCL12 chemokine, produced by cancer-associated fibroblasts, may offer new therapeutic strategies for PDAC treatment.
Area of Science:
- Oncology
- Cancer Biology
- Immunology
Background:
- Pancreatic ductal adenocarcinoma (PDAC) presents significant therapeutic challenges due to its complex tumor microenvironment.
- Activated fibroblasts within the PDAC stroma promote tumor progression, therapeutic resistance, and immune evasion.
Purpose of the Study:
- This review focuses on the role of the chemokine CXCL12, secreted by cancer-associated fibroblasts, in PDAC.
- It aims to discuss therapeutic strategies targeting CXCL12 signaling in PDAC.
Main Methods:
- Review of existing literature on CXCL12, cancer-associated fibroblasts, and PDAC.
- Analysis of therapeutic approaches targeting CXCL12 signaling.
Main Results:
- CXCL12 secreted by cancer-associated fibroblasts contributes to key hallmarks of PDAC, including growth, metastasis, chemoresistance, and immune evasion.
- Several therapeutic strategies targeting CXCL12 signaling are under development.
Conclusions:
- Targeting CXCL12 signaling represents a promising avenue for PDAC therapy.
- Tipifarnib, a farnesyl transferase inhibitor, is proposed as an unconventional agent to inhibit CXCL12 production in PDAC.
