Why the study?
Prostate cancer cells rely on lipids for growth, prompting the hypothesis that cardiovascular-targeted hyperlipidemic factors are dysregulated in metastatic disease.
Are levels of PCSK9, ANGPTL3, Apo CIII, leptin, and lipids elevated in metastatic prostate cancer compared to localized prostate cancer and controls?
Population
35 men per group with mPCa, localized Gleason 8/9 PCa, and controls
Comparison
Patients with mPCa vs localized Gleason 8/9 PCa vs controls at risk
Design
Case-control study
Key result
Metastatic prostate cancer was associated with higher levels of triglycerides (2.3 vs 1.7 mmol/L; p=0.0004), Apo CIII, ANGPTL3, and leptin compared to controls.
Authors
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Should not yet change practice; hypothesis-generating for lipid pathway targeting in metastatic prostate cancer and cardiometabolic-oncology cross-talk.
Case-Control (n=105)
Are levels of PCSK9, ANGPTL3, Apo CIII, leptin, and lipids elevated in metastatic prostate cancer compared to localized prostate cancer and controls?
Whole-body lipid metabolic rewiring, characterized by elevated triglycerides, Apo CIII, ANGPTL3, and leptin, is a feature restricted to the metastatic phase of prostate cancer.
Boulay et al. (2026) conducted a case-control in Prostate cancer (n=105). Metastatic prostate cancer vs. Localized prostate cancer and controls was evaluated on Levels of PCSK9, ANGPTL3, Apo CIII, leptin, and the lipid profile. Metastatic prostate cancer was associated with higher levels of triglycerides (2.3 vs 1.7 mmol/L; p=0.0004), Apo CIII, ANGPTL3, and leptin compared to controls.
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