Why the study?
Although androgen deprivation therapy is linked to obesity and inflammation, an understanding of the molecular-level changes in adipose tissue induced by castration therapies is missing.
Does profound androgen deprivation therapy induce transcriptional changes in periprostatic fat tissue in patients with high-risk prostate tumours?
Does profound androgen deprivation therapy induce transcriptional changes in periprostatic fat tissue in patients with high-risk prostate tumours?
Androgen deprivation therapy in high-risk prostate cancer patients induces a pro-inflammatory, obesity-like microenvironment in periprostatic fat, which may partially counteract its therapeutic benefits.
May partially counteract ADT benefits in high-risk prostate cancer; hypothesis-generating for periprostatic fat modulation.
Prostate cancer is a leading cause of morbidity and cancer-related death worldwide. Androgen deprivation therapy (ADT) is the cornerstone of management for advanced disease. The use of these therapies is associated with multiple side effects, including metabolic syndrome and truncal obesity. At the same time, obesity has been associated with both prostate cancer development and disease progression, linked to its effects on chronic inflammation at a tissue level. The connection between ADT, obesity, inflammation and prostate cancer progression is well established in clinical settings; however, an understanding of the changes in adipose tissue at the molecular level induced by castration therapies is missing. Here, we investigated the transcriptional changes in periprostatic fat tissue induced by profound ADT in a group of patients with high-risk tumours compared to a matching untreated cohort. We find that the deprivation of androgen is associated with a pro-inflammatory and obesity-like adipose tissue microenvironment. This study suggests that the beneficial effect of therapies based on androgen deprivation may be partially counteracted by metabolic and inflammatory side effects in the adipose tissue surrounding the prostate.
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Mangiola et al. (2019) studied this question.
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