Nut and peanut butter consumption and risk of prostate cancer in the NIH‐AARP diet and health study

Purpose Gleason grading is an important predictor of prostate cancer (PCa) outcomes. Studies using surrogate PCa end points suggest outcomes for Gleason score (GS) 7 cancers vary according to the predominance of pattern 4. These studies have influenced clinical practice, but it is unclear if rates of PCa mortality differ for 3 + 4 and 4 + 3 tumors. Using PCa mortality as the primary end point, we compared outcomes in Gleason 3 + 4 and 4 + 3 cancers, and the predictive ability of GS from a standardized review versus original scoring. Patients and Methods Three study pathologists conducted a blinded standardized review of 693 prostatectomy and 119 biopsy specimens to assign primary and secondary Gleason patterns. Tumor specimens were from PCa patients diagnosed between 1984 and 2004 from the Physicians' Health Study and Health Professionals Follow-Up Study. Lethal PCa (n = 53) was defined as development of bony metastases or PCa death. Hazard ratios (HR) were estimated according to original GS and standardized GS. We compared the discrimination of standardized and original grading with C-statistics from models of 10-year survival. Results For prostatectomy specimens, 4 + 3 cancers were associated with a three-fold increase in lethal PCa compared with 3 + 4 cancers (95% CI, 1.1 to 8.6). The discrimination of models of standardized scores from prostatectomy (C-statistic, 0.86) and biopsy (C-statistic, 0.85) were improved compared to models of original scores (prostatectomy C-statistic, 0.82; biopsy C-statistic, 0.72). Conclusion Ignoring the predominance of Gleason pattern 4 in GS 7 cancers may conceal important prognostic information. A standardized review of GS can improve prediction of PCa survival.

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Associations of low-dose aspirin or other NSAID use with prostate cancer risk in the Danish Diet, Cancer and Health Study

Cancer Causes & Control ◽

10.1007/s10552-019-01252-5 ◽

2019 ◽

Vol 31 (2) ◽

pp. 139-151 ◽

Cited By ~ 1

Author(s):

Charlotte Skriver ◽

Christian Dehlendorff ◽

Michael Borre ◽

Klaus Brasso ◽

Signe Benzon Larsen ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Low Dose ◽

Prostate Cancer Risk ◽

Health Study ◽

Dose Aspirin ◽

Low Dose Aspirin

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Risk of Total and Aggressive Prostate Cancer and Pesticide Use in the Agricultural Health Study

American Journal of Epidemiology ◽

10.1093/aje/kws225 ◽

2012 ◽

Vol 177 (1) ◽

pp. 59-74 ◽

Cited By ~ 92

Author(s):

Stella Koutros ◽

Laura E. Beane Freeman ◽

Jay H. Lubin ◽

Sonya L. Heltshe ◽

Gabriella Andreotti ◽

...

Keyword(s):

Prostate Cancer ◽

Health Study ◽

Pesticide Use ◽

Aggressive Prostate Cancer ◽

Agricultural Health ◽

Agricultural Health Study

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Nut and Peanut Butter Consumption and Mortality in the NIH-AARP Diet and Health Study (P18-001-19)

Current Developments in Nutrition ◽

10.1093/cdn/nzz039.p18-001-19 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

Author(s):

Vineeth Amba ◽

Gwen Murphy ◽

Arash Etemadi ◽

Shao Ming Wang ◽

Christian Abnet ◽

...

Keyword(s):

Peanut Butter ◽

The United States ◽

Health Study ◽

Differential Mortality ◽

Inverse Association ◽

Funding Sources ◽

Hazard Ratios ◽

Disease Mortality ◽

Specific Mortality ◽

Risk Of Cancer

Abstract Objectives Although previous studies have shown inverse associations between nut consumption and mortality, the associations between nut consumption and less common causes of mortality have not been studied. Additionally, approximately 50% of peanut consumption in the United States is through peanut butter, but the association between peanut butter consumption and mortality has not been thoroughly investigated. The objective of this study was to examine the associations between nut and peanut butter consumption and the risk of all-cause and cause-specific mortality. Methods The NIH-AARP Diet and Health Study recruited 566,398 individuals aged 50–71 at baseline in 1995–1996. A food-frequency questionnaire was used to evaluate nut and peanut butter consumption. Cox proportional hazard models were used to estimate hazard ratios and 95% confidence intervals for mortality using the non-consumers as reference groups. Results After excluding subjects with chronic diseases at baseline, there were 64,464 deaths with a median follow-up time of 15.5 years. We observed a significant inverse association between nut consumption and overall mortality (HR C4 vs C1 = 0.78, 95% CI = 0.76, 0.81). Nut consumption was significantly associated with reduced risk of cancer, cardiovascular, respiratory, infectious, renal and liver disease mortality, but not with diabetes, and Alzheimer's disease mortality. We observed no significant associations between peanut butter consumption and all-cause (HR C4 vs C1 = 1.00, 95% CI = 0.98, 1.04) and cause-specific mortality. Conclusions In a middle-aged US population, nut intake was inversely associated with all-cause mortality and certain types of cause-specific mortality. However, peanut butter consumption was not associated with differential mortality. Funding Sources This study was supported by the Intramural Research Program of the National Cancer Institute, NIH.

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Discovery and validation of a 30-gene expression signature to identify prostate cancer patients who are candidates for active surveillance.

Journal of Clinical Oncology ◽

10.1200/jco.2015.33.7_suppl.10 ◽

2015 ◽

Vol 33 (7_suppl) ◽

pp. 10-10

Author(s):

Travis Gerke ◽

Svitlana Tyekucheva ◽

Kathryn Penney ◽

Christopher Sweeney ◽

Rosina Lis ◽

...

Keyword(s):

Gene Expression ◽

Prostate Cancer ◽

Active Surveillance ◽

Control Sample ◽

Gene Expression Signature ◽

Health Study ◽

Validation Data ◽

Expression Signature ◽

Indolent Disease

10 Background: Considerable attention has been devoted to the search for biomarkers of aggressive prostate cancer. While many promising markers have been proposed, it is often unclear whether their ability to risk classify is adequate to reduce overtreatment of indolent cancers. We present and validate a gene expression signature that is highly specific for indolent disease and that, when combined with Gleason, improves upon the prognostic power of Gleason alone. Methods: A 30-gene signature of indolent disease was derived from a case-control sample of men (n=254) from the Health Professionals Follow-Up Study (HPFS) who were followed prospectively from cancer diagnosis for a median of 13.7 years. Cases were defined as men with prostate cancer who experienced a metastatic event or died of cancer during follow-up, while indolent controls survived at least 8 years without metastases. Whole-transcriptome gene expression was quantified from archival formalin-fixed, paraffin-embedded (FFPE) tumor tissue specimens acquired at prostatectomy. Genes were selected by a novel analytic strategy that maximizes a partial area under the curve (pAUC) to accurately identify indolent tumors. We validated the signature in two independent cohorts: the Physicians’ Health Study (PHS; n=150) and a Swedish Watchful Waiting cohort (WW; n=253) with respective median follow-up times of 14.4 and 9.0 years. Results: When compared to a model with Gleason alone, application of the signature to both validation data sets significantly improved prognostic accuracy as measured by pAUC (p=0.003 in PHS and p<0.001 in WW). Performance was particularly strong among men diagnosed with Gleason 7, where unit standard deviation increases in the signature score were associated with odds ratios of indolence of 5.24 (95% CI 2.21-15.75; p<0.001) and 2.37 (95% CI 1.45-4.19; p=0.001) in the PHS and WW cohorts, respectively. Conclusions: We present a signature of indolent prostate cancer that adds prognostic information beyond Gleason and has the potential to guide men to active surveillance and avoid overtreatment. Validation across both treated and untreated cohorts supports the discovery of a robust signature.

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