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Patients exposed to a surgical safety checklist experience better postoperative outcomes, but this could simply reflect wider quality of care in hospitals where checklist use is routine.

The androgen receptor (AR) is the key oncogenic driver of prostate cancer and despite implementation of novel AR targeting therapies, patient outcomes for metastatic disease remain dismal. There is an urgent need to better understand androgen regulated cellular processes, in order to more effectively target the AR-dependence of prostate cancer cells through new therapeutic vulnerabilities. Transcriptomic studies have consistently identified lipid metabolism as a hallmark of enhanced AR signaling in prostate cancer, however the relationship between AR and the lipidome remain undefined. Using mass spectrometrybased lipidomics, this study revealed increased fatty acyl chain length in phospholipids from prostate cancer cells and patient-derived explants as one of the most striking androgenregulated changes to lipid metabolism. Potent and direct AR-mediated induction of ELOVL Fatty Acid Elongase 5 (ELOVL5), an enzyme that catalyzes fatty acid elongation, was demonstrated in prostate cancer cells, xenografts and clinical tumors. Assessment of mRNA and protein in large-scale datasets revealed ELOVL5 as the predominant ELOVL expressed in both primary and metastatic prostate cancer, and upregulated compared to non-malignant prostate. ELOVL5 depletion by siRNA markedly altered mitochondrial function to induce oxidative stress, resulting in significant inhibition of prostate cancer cell viability, 3D growth, and in vivo tumor growth and metastasis. Supplementation with the monounsaturated fatty acid cis-vaccenic acid, a direct product of ELOVL5 elongation, reversed the oxidative stress and associated cell viability caused by ELOVL5 knockdown. We have identified lipid elongation as a pro-survival metabolic pathway in prostate cancer that is androgenregulated, critical for metastasis and targetable via ELOVL5.