Comparisons of prostate cancer mortality rates with dietary practices in the United States

Colli, Janet; Colli, Albert

doi:10.1016/j.urolonc.2005.03.020

Cited by 17 publications

(2 citation statements)

References 36 publications

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“…In contrast to omega-3 PUFAs, which are reported to inhibit PCa progression ( Wang et al, 2012 ), omega-6 PUFAs ( Khankari et al, 2016 ; Brown et al, 2010 ), and higher omega-6/omega-3 PUFA ratio, increase PCa risk ( Williams et al, 2011 ; Apte et al, 2013 ). Dietary intervention by decreasing total fat intake and increasing omega-3 PUFAs was found to improve PCa survivorship ( Epstein et al, 2012 ; Colli and Colli, 2005 ; Davies et al, 2011 ; Ornish et al, 2005 ). It is unclear whether there is a preference for n-6 or n-3 PUFA β-oxidation in PCa cells, however both require DECR1 for complete β-oxidation.…”

Section: Discussionmentioning

confidence: 99%

Human DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis

Nassar

Mah

Dehairs

et al. 2020

eLife

117

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Fatty acid β-oxidation (FAO) is the main bioenergetic pathway in human prostate cancer (PCa) and a promising novel therapeutic vulnerability. Here we demonstrate therapeutic efficacy of targeting FAO in clinical prostate tumors cultured ex vivo, and identify DECR1, encoding the rate-limiting enzyme for oxidation of polyunsaturated fatty acids (PUFAs), as robustly overexpressed in PCa tissues and associated with shorter relapse-free survival. DECR1 is a negatively-regulated androgen receptor (AR) target gene and, therefore, may promote PCa cell survival and resistance to AR targeting therapeutics. DECR1 knockdown selectively inhibited β-oxidation of PUFAs, inhibited proliferation and migration of PCa cells, including treatment resistant lines, and suppressed tumor cell proliferation and metastasis in mouse xenograft models. Mechanistically, targeting of DECR1 caused cellular accumulation of PUFAs, enhanced mitochondrial oxidative stress and lipid peroxidation, and induced ferroptosis. These findings implicate PUFA oxidation via DECR1 as an unexplored facet of FAO that promotes survival of PCa cells.

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Section: Discussionmentioning

confidence: 99%

Human DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis

Nassar

Mah

Dehairs

et al. 2020

eLife

117

View full text Add to dashboard Cite

show abstract

“…Stott-Miller and colleagues’ ( 2013 ) study on fried chicken demonstrated that fried chicken would place individuals at heightened risk of PCa. Also statistics of the United States revealed strong positive correlation between PCa mortality and per capita consumption of chicken ( Colli & Colli, 2005 ). There was also study claiming decreased risk when high amount of poultry intake compared with low intake ( Hu et al, 2008 ).…”

Section: Introductionmentioning

confidence: 99%

Poultry consumption and prostate cancer risk: a meta-analysis

Wan

et al. 2016

PeerJ

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Background. Several kinds of foods are hypothesized to be potential factors contributing to the variation of prostate cancer (PCa) incidence. But the effect of poultry on PCa is still inconsistent and no quantitative assessment has been published up to date. So we conducted this meta-analysis to clarify the association between them.Materials and Methods. We conducted a literature search of PubMed and Embase for studies examining the association between poultry consumption and PCa up to June, 2015. Pooled risk ratio (RR) and corresponding 95% confidence interval (CI) of the highest versus lowest poultry consumption categories were calculated by fixed-effect model or random-effect model.Results. A total of 27 (12 cohort and 15 case-control) studies comprising 23,703 cases and 469,986 noncases were eligible for inclusion. The summary RR of total PCa incidence was 1.03 (95% CI [0.95–1.11]) for the highest versus lowest categories of poultry intake. The heterogeneity between studies was not statistically significant (P = 0.768, I2 = 28.5%). Synthesized analysis of 11 studies on high stage PCa and 8 studies on chicken exposure also demonstrated null association. We also did not obtain significant association in the subgroup of cohort study (RR = 1.04, 95% CI [0.98–1.10]), as well as in the subgroups of population-based case-control study and hospital-based case-control study. Then the studies were divided into three geographic groups: Western countries, Asia and South America. The pooled RRs in these areas did not reveal statistically significant association between poultry and PCa.Conclusions. This meta-analysis suggests no association between poultry consumption and PCa risk. Further well-designed studies are warranted to confirm the result.

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Saturated fat intake predicts biochemical failure after prostatectomy

Strom

Yamamura

Forman

et al. 2008

Intl Journal of Cancer

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Previous reports show that obesity predicts biochemical failure after treatment for localized prostate cancer. Since obesity is associated with increased fat consumption, we investigated the role that dietary fat intake plays in modulating obesity-related risk of biochemical failure. We evaluated the association between saturated fat intake and biochemical failure among 390 men from a previously described prostatectomy cohort. Participants completed a food frequency questionnaire collecting nutrient information for the year prior to diagnosis. Because fat and energy intake are highly correlated, the residual method was used to adjust fat (total and saturated) intakes for energy. Biochemical-failure-free-survival rates were calculated using the Kaplan-Meier method. Crude and adjusted effects were estimated using Cox proportional hazards models. During a mean follow-up of 70.6 months, 78 men experienced biochemical failure. Men who consumed highsaturated fat (HSF) diets were more likely to experience biochemical failure (p 5 0.006) and had significantly shorter biochemicalfailure-free-survival than men with low saturated fat (LSF) diets (26.6 vs. 44.7 months, respectively, p 5 0.002). After adjusting for obesity and clinical variables, HSF-diet patients were almost twice as likely to experience biochemical failure (hazard ratio 5 1.95, p 5 0.008) compared to LSF diet patients. Men who were both obese and consumed HSF diets had the shortest biochemicalfailure-free-survival (19 months), and nonobese men who consumed LSF diets had the longest biochemical-failure-free-survival (46 months, p < 0.001). Understanding the interplay between modifiable factors, such as diet and obesity, and disease characteristics may lead to the development of behavioral and/or targeted interventions for patients at increased risk of progression.

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Comparisons of prostate cancer mortality rates with dietary practices in the United States

Cited by 17 publications

References 36 publications

Human DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis

Human DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis

Poultry consumption and prostate cancer risk: a meta-analysis

Saturated fat intake predicts biochemical failure after prostatectomy

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