Dietary consumption of tea and the risk of prostate cancer in the prostate, lung, colorectal, and ovarian cancer screening trial.

e13559 Background: The popular beverage tea, brewed from infused leaves of camellia sinesis, contains non-phytoestrogenic polyphenols such as flavonoids, anthocyanidins, flavanols (epigallocatechin gallate); phenolic acids (ellagic acid) and stimulants (caffeine, theophylline). Laboratory studies report tea promotes antioxidant enzyme formation, slows cancer cell proliferation and unblocks apoptosis. Clinically, the Pomi-T randomised study reported tea extract (along with three other foods) reduced PSA progression in men with prostate cancer1. Evidence of prostate cancer prevention, however, from prospective cohort data is conflicting with one recent study even implying an increased risk2. Methods: We analysed 25,097 men within the intervention arm of the 155,000 participant PLCO screening trial. Histological confirmed cases of prostate cancer were reported in 3,088 men (12.3%) during the 11.5 year follow up. Tea consumption was assessed with a food frequency questionnaire (FFQ). Baseline characteristics were compared between groups using Chi-square and Kruskal-Wallis tests. Cox regression models were used to assess the association between tea intake and prostate cancer incidence. Results: Overall tea consumption was associated with a significantly lower risk of prostate cancer (p = 0.009). More precisely, the participants in the highest third of consumption group had a significantly lower risk compared to those in the lowest third (HR 1.16 (CI 1.05-1.29, p = 0.004). This pattern persisted with adjustments for age, sex, race and education level (p = 0.034), family history of cancer (p = 0.037). Those who never drank tea, however, had no statistical lower risk of prostate cancer compared to other groups (p = 0.501). Conclusions: Among tea drinkers, this data revealed a positive association between drinking tea and a reduced risk of prostate cancer. This data supports the consideration of future prospective intervention studies investigating the role of tea as part of a prostate cancer prevention programme. 1. Thomas et al. The NCRN Pomi-T RCT. Prostate cancer & prostatic diseases (2014), 2,180. 2. Reger et al. Dietary isoflavones and prostate cancer risk. Int J. Cancer (2017), 142; 4, 719.

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Dietary consumption of tea and the risk of prostate cancer in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial

British Journal Of Nutrition ◽

10.1017/s0007114521003664 ◽

2021 ◽

pp. 1-16

Author(s):

Robert Thomas ◽

Basma Greef ◽

Alex McConnachie ◽

Bethany Stanley ◽

Madeleine Williams

Keyword(s):

Prostate Cancer ◽

Ovarian Cancer ◽

Cancer Screening ◽

Cox Regression ◽

Positive Association ◽

Epidemiological Studies ◽

Tea Consumption ◽

Ovarian Cancer Screening ◽

Cancer Screening Trial ◽

Screening Trial

Abstract Tea contains polyphenols such as flavonoids, anthocyanidins, flavanols and phenolic acids which in laboratory studies have reported to promote antioxidant enzyme formation, reduces excess inflammation, slow cancer cell proliferation and promote apoptosis. Evidence from epidemiological studies, on the effect of tea consumption on CaP incidence has been conflicting. We analysed data from 25 097 men within the intervention arm of the 155000 participant Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial screening trial. Histologically confirmed cases of prostate cancer were reported in 3,088 men (12.3%) during the median 11.5 year follow up. Tea consumption was assessed with a food frequency questionnaire. Baseline characteristics were compared between groups using Chi-square and Kruskal-Wallis tests. Cox regression models were used to assess associations between tea intake and CaP incidence. There was no statistical difference between the risk of CaP between men who never drank tea to those who drank tea at any quantity. Amongst tea drinkers, those in the highest third of consumption group had a small but significantly lower risk compared to those in the lowest third (11.2% v 13.2% HR 1.16; 95% CI 1.05-1.29, p=0.004). This pattern persisted with adjustments for demographics and lifestyle. In conclusion, among tea drinkers, there was a small positive association between drinking tea and a reduced risk of prostate cancer. It does not support starting to drink tea, if men previously did not, to reduce the risk. Further research is needed to establish whether tea is justified for future prospective nutritional intervention studies investigating CaP prevention.

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Serum androgens and prostate cancer risk: results from the placebo arm of the Prostate Cancer Prevention Trial

Cancer Causes & Control ◽

10.1007/s10552-015-0695-0 ◽

2015 ◽

Vol 27 (2) ◽

pp. 175-182 ◽

Cited By ~ 18

Author(s):

Jeannette M. Schenk ◽

Cathee Till ◽

Ann W. Hsing ◽

Frank Z. Stanczyk ◽

Zhihong Gong ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Cancer Prevention ◽

Prostate Cancer Risk ◽

Prevention Trial ◽

Prostate Cancer Prevention ◽

Prostate Cancer Prevention Trial ◽

Serum Androgens

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Development of the Prostate Cancer Prevention Trial Prostate Cancer Risk Calculator

Prostate Cancer Screening ◽

10.1007/978-1-60327-281-0_12 ◽

2009 ◽

pp. 195-203

Author(s):

Donna P. Ankerst ◽

Ian M. Thompson

Keyword(s):

Prostate Cancer ◽

Cancer Risk ◽

Cancer Prevention ◽

Prostate Cancer Risk ◽

Prevention Trial ◽

Risk Calculator ◽

Prostate Cancer Prevention ◽

Prostate Cancer Prevention Trial

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Associations Between Polymorphisms in Genes Related to Oxidative Stress and DNA Repair, Interactions With Serum Antioxidants, and Prostate Cancer Risk: Results From the Prostate Cancer Prevention Trial

Frontiers in Oncology ◽

10.3389/fonc.2021.808715 ◽

2022 ◽

Vol 11 ◽

Author(s):

Zhihong Gong ◽

Mary E. Platek ◽

Cathee Till ◽

Phyllis J. Goodman ◽

Catherine M. Tangen ◽

...

Keyword(s):

Oxidative Stress ◽

Prostate Cancer ◽

Dna Repair ◽

Cancer Prevention ◽

Prostate Cancer Risk ◽

Minor Allele ◽

Cancer Etiology ◽

Lower Serum ◽

Prostate Cancer Prevention

Study of polymorphisms in genes related to the generation and removal of oxidative stress and repair of oxidative DNA damage will lead to new insights into the genetic basis of prostate cancer. In the Prostate Cancer Prevention Trial (PCPT), a double-blind, randomized controlled trial testing finasteride versus placebo for prostate cancer prevention, we intend to investigate the role of oxidative stress/DNA repair mechanisms in prostate cancer etiology and whether these polymorphisms modify prostate cancer risk by interacting with antioxidant status in both placebo and finasteride arms. We evaluated associations of selected candidate polymorphisms in genes in these pathways, and interactions with pre-diagnostic serum antioxidants, and the risk of prostate cancer among 1,598 cases and 1,706 frequency-matched controls enrolled in the PCPT. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multivariable-adjusted logistic regression models. While there were no statistically significant associations observed in the placebo arm, several SNPs were associated with prostate cancer in the finasteride arm. Specifically, APEX1-rs1760944 was associated with increased risk of total prostate cancer (per minor allele: p-trend=0.04). OGG1-rs1052133 was positively (CG/GG vs. CC: OR=1.32, 95% CI: 1.01-1.73) and NOS3-rs1799983 was inversely (per minor allele: p-trend=0.04) associated with risk of low-grade prostate cancer. LIG3-rs1052536 and XRCC1-rs25489 were suggestively associated with reduced risk of high-grade prostate cancer (per minor allele: both p-trend=0.04). In the placebo arm, significant associations were observed among men with higher serum lycopene for APEX1-rs1760944 and NQO1-rs1800566, or higher serum β-cryptoxanthin for ERCC4-rs1800067. In the finasteride arm, stronger associations were observed among men with lower serum lycopene for NOS3-rs1799983, higher serum α-carotene, β-carotene, and β-cryptoxanthin for LIG3-rs1052536, or lower serum retinol for SOD2-rs1799725. These results suggest that germline variations in oxidative stress and DNA repair pathways may contribute to prostate carcinogenesis and that these associations may differ by intraprostatic sex steroid hormone status and be further modified by antioxidant status. Findings provide insights into the complex role of gene, gene-antioxidant and -finasteride interactions in prostate cancer etiology, and thus may lead to the development of preventative strategies.

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