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Updated: Oct 6, 2025
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Fatty acid synthetase expression in triple-negative breast cancer
Jin Hee Park1, Hye Seung Han1, So Dug Lim1
1Department of Pathology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul, Korea.
Background:
Triple-negative breast cancer (TNBC) has a relatively poor prognosis. Research has identified potential metabolic targets, including fatty acid metabolism, in TNBC. The absence of effective target therapies for TNBC led to exploration of the role of fatty acid synthetase (FASN) as a potential target for TNBC therapy. Here, we analyzed the expression of FASN, a representative lipid metabolism-related protein, and investigated the association between FASN expression and Ki-67 and the programmed death ligand 1 (PD-L1) biomarkers in TNBC.
Methods:
Immunohistochemical expression of FASN was analyzed in 166 patients with TNBC. For analytical purposes, patients with 0-1+ FASN staining were grouped as low-grade FASN and patients with 2-3+ FASN staining as high-grade FASN.
Results:
FASN expression was observed in 47.1% of TNBC patients. Low and high expression of FASN was identified in 75.9% and 24.1%, respectively, and no statistically significant difference was found in T category, N category, American Joint Committee on Cancer stage, or recurrence rate between the low and high-FASN expression groups. Ki-67 proliferation level was significantly different between the low and high-FASN expression groups. FASN expression was significantly related to Ki-67 as the level increased. There was no significant difference in PD-L1 positivity between the low- and high-FASN expression groups.
Conclusions:
We identified FASN expression in 166 TNBC patients. The Ki-67 proliferation index was positively correlated with FASN level, indicating higher proliferation activity as FASN increases. However, there was no statistical association with PD-L1 SP142, the currently FDA-approved assay, or FASN expression level.
Insights
Fatty acid synthetase (FASN) is expressed in triple-negative breast cancer (TNBC). Higher FASN levels correlate with increased tumor cell proliferation (Ki-67), but not with PD-L1 expression.
Area of Science:
- Oncology
- Cancer Metabolism
- Biomarker Research
Background:
- Triple-negative breast cancer (TNBC) presents a significant clinical challenge due to its poor prognosis and lack of targeted therapies.
- Fatty acid metabolism, particularly the role of fatty acid synthetase (FASN), is an emerging area of interest for TNBC treatment strategies.
- Investigating FASN expression and its correlation with key biomarkers is crucial for developing novel therapeutic approaches.
Purpose of the Study:
- To analyze the expression of fatty acid synthetase (FASN) in triple-negative breast cancer (TNBC) tissues.
- To explore the association between FASN expression levels and the proliferation marker Ki-67.
- To determine the relationship between FASN expression and programmed death ligand 1 (PD-L1) expression in TNBC.
Main Methods:
- Immunohistochemical analysis of FASN expression in 166 TNBC patient samples.
- Categorization of patients into low-grade (0-1+ staining) and high-grade (2-3+ staining) FASN expression groups.
- Statistical analysis to correlate FASN expression with clinicopathological features, Ki-67, and PD-L1 status.
Main Results:
- FASN expression was detected in 47.1% of TNBC patients, with high expression in 24.1%.
- A significant positive correlation was found between FASN expression levels and Ki-67 proliferation index.
- No significant association was observed between FASN expression and PD-L1 positivity.
Conclusions:
- FASN is expressed in a subset of TNBC patients, and its level is positively correlated with tumor proliferation.
- Increased FASN expression in TNBC suggests a potential role in tumor growth.
- FASN expression is not statistically associated with PD-L1 SP142 status in this cohort, limiting its utility as a predictive biomarker for immunotherapy in conjunction with PD-L1.
