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Biology subjects

Prete, A.

Publications and source records attributed to Prete, A..

2 recordsLinked to original sources

Glutamine antagonism suppresses tumor growth in adrenocortical carcinoma through inhibition of de novo nucleotide biosynthesis

Dysregulation of cellular metabolism is a hallmark of cancer, which remains poorly understood in adrenocortical carcinoma (ACC). Here, we dissected ACC metabolism by integrating transcriptional profiling from human and mouse ACC, targeted tissue metabolomics from a mouse ACC model, and untargeted serum metabolomics from a large patient cohort, providing cross-species validation of metabolic rewiring in ACC. This study revealed global metabolic dysregulation, involving glutamine-dependent pathways such as non-essential amino-acid and hexosamine biosynthesis, nucleotide metabolism, and glutathione biosynthesis, suggesting glutamine catabolism is a critical metabolic vulnerability in ACC. Treatment with glutamine antagonists 6-Diazo-5-Oxo-L-Norleucine (DON) and JHU-083 elicited robust anti-tumor responses. Mechanistic studies revealed DONs anti-tumor effect was primarily driven by selective inhibition of glutamine-fueled de novo nucleotide biosynthesis. Additionally, DON led to DNA damage, which yielded potent synergism with inhibition of the DNA damage response pathway. Collectively, this work highlights glutamine metabolism as a central metabolic dependency and therapeutic target in ACC. HighlightsO_LIMouse and human ACC share conserved transcriptional-metabolic programs, revealing Gln metabolism as a central, targetable vulnerability. C_LIO_LITargeted tissue metabolomic analysis in a mouse model of ACC validates dysregulation in Gln-dependent metabolic pathways. C_LIO_LITargeting of Gln metabolism with JHU-083 (6-diazo-5-oxo-L-norleucine (DON) pro-drug) achieves marked inhibition of tumor growth in vivo. C_LIO_LIHigh expression of Gln-metabolizing genes mediating de novo nucleotide biosynthesis is associated with poor prognosis in ACC. C_LIO_LIDON drives nucleotide depletion and DNA damage, leading to potent synergy with inhibition of the DNA damage response. C_LIO_LIUntargeted serum metabolomic analysis in a large cohort of patients with adrenal tumors demonstrates dysregulation of Gln and nucleotide metabolism in ACC. C_LI

cancer biology↗

Increased risk of infections in Addison’s disease and congenital adrenal hyperplasia: a primary care database cohort study

ContextMortality and infection-related hospital admissions are increased in patients with primary adrenal insufficiency (PAI). However, the risk of primary care-managed infections in patients with PAI is unknown.\n\nObjectiveTo estimate infection risk in PAI due to Addisons disease (AD) and congenital adrenal hyperplasia (CAH) in a primary care setting.\n\nDesignRetrospective cohort study using UK data collected from 1995 to 2018.\n\nMain outcome measuresIncidence of lower respiratory tract infections (LRTIs), urinary tract infections (UTIs), gastrointestinal infections (GIIs), and prescription counts of antimicrobials in adult PAI patients compared to unexposed controls.\n\nResultsA diagnosis of PAI was established in 1580 AD patients (mean age 51.7 years) and 602 CAH patients (mean age 35.4 years). All AD patients and 42% of CAH patients were prescribed glucocorticoids, most frequently hydrocortisone in AD (82%) and prednisolone in CAH (50%). AD and CAH patients exposed to glucocorticoids, but not CAH patients without glucocorticoid treatment, had a significantly increased risk of LRTIs (adjusted incidence rate ratio AD 2.11 [95% confidence interval 1.64-2.69], CAH 3.23 [1.21-8.61]), UTIs (AD 1.51 [1.29-1.77], CAH 2.20 [1.43-3.34]), and GIIs (AD 3.80 [2.99-4.84], CAH 1.93 [1.06-3.52]). This was mirrored by increased prescription of antibiotics (AD 1.73 [1.69-1.77], CAH 1.77 [1.66-1.89]) and antifungals (AD 1.89 [1.74-2.05], CAH 1.91 [1.50-2.43]).\n\nConclusionsThere is an increased risk of infections and antimicrobial use in PAI in the primary care setting at least partially linked to glucocorticoid treatment. Future studies will need to address whether more physiological glucocorticoid replacement modes could reduce this risk.\n\nPrecisUsing data from 1580 AD patients and 602 CAH patients collected in a UK primary care database from 1995 to 2018, we identified increased risk of infections and antimicrobial prescription counts.

epidemiology↗