Prostate cancer cell proliferation is influenced by LDL-cholesterol availability and cholesteryl ester turnover.

Background: Prostate cancer growth is driven by androgen receptor signaling, and advanced disease is initially treatable by depleting circulating androgens. However, prostate cancer cells inevitably adapt, resulting in disease relapse with incurable castrate-resistant prostate cancer. Androgen deprivation therapy has many side effects, including hypercholesterolemia, and more aggressive and castrate-resistant prostate cancers typically feature cellular accumulation of cholesterol stored in the form of cholesteryl esters.

Epidemiology of acute pancreatitis in Australia from 2007-2019.

Backgrounds: There is a paucity of information on the epidemiology of acute pancreatitis (AP) in Australia.

Methods: Data on hospital admissions for a principal diagnosis of AP were obtained from the Australian Institute of Health and Welfare; population data were extracted from the Australian Bureau of Statistics. Age-adjusted, and age and sex-specific rates for all subtypes of AP were compared.

Extracellular Fatty Acids Are the Major Contributor to Lipid Synthesis in Prostate Cancer.

Prostate cancer cells exhibit altered cellular metabolism but, notably, not the hallmarks of Warburg metabolism. Prostate cancer cells exhibit increased synthesis of fatty acids (FA); however, little is known about how extracellular FAs, such as those in the circulation, may support prostate cancer progression. Here, we show that increasing FA availability increased intracellular triacylglycerol content in cultured patient-derived tumor explants, LNCaP and C4-2B spheroids, a range of prostate cancer cells (LNCaP, C4-2B, 22Rv1, PC-3), and prostate epithelial cells (PNT1).