Plasma Antioxidants, Genetic Variation in SOD2, CAT, GPX1, GPX4, and Prostate Cancer Survival

Blarigan, Erin L. Van; Ma, Jing; Kenfield, Stacey A.; Stampfer, Meir J.; Sesso, Howard D.; Giovannucci, Edward; Witte, John S.; Erdman, John W.; Chan, June M.; Penney, Kathryn L.

doi:10.1158/1055-9965.epi-13-0670

Cited by 28 publications

(25 citation statements)

References 30 publications

(38 reference statements)

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“…We previously reported on potential interaction effects between GPX4 , gamma-tocopherol, and risk of lethal prostate cancer. (60) Our observation of potential interaction between a variant in SEC14L2 (rs5753106), vitamin E assignment, and high-grade prostate cancer was somewhat consistent with the prior report from the ATBC trial, as rs2299825 is in strong linkage disequilibrium with rs5753106. Additionally, rs5753106 in SEC14L2 is strong LD with the 3’- and 5’-UTR regions for several other genes, including: SF3A1, CCDC157, and RNF215 .…”

Section: Discussionsupporting

confidence: 90%

Selenium- or Vitamin E–Related Gene Variants, Interaction with Supplementation, and Risk of High-Grade Prostate Cancer in SELECT

Chan

Darke

Penney

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background Epidemiological studies and secondary analyses of randomized trials supported the hypothesis that selenium and vitamin E lower prostate cancer risk. However, the Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed no benefit of either supplement. Genetic variants involved in selenium or vitamin E metabolism or transport may underlie the complex associations of selenium and vitamin E. Methods We undertook a case-cohort study of SELECT participants randomized to placebo, selenium or vitamin E. The subcohort included 1,434 men; our primary outcome was high-grade prostate cancer (N=278 cases, Gleason 7 or higher cancer). We used weighted Cox regression to examine the association between SNPs and high-grade prostate cancer risk. To assess effect modification, we created interaction terms between randomization arm and genotype and calculated log likelihood statistics. Results We noted statistically significant (p<0.05) interactions between selenium assignment, SNPs in CAT, SOD2, PRDX6, SOD3, and TXNRD2 and high-grade prostate cancer risk. Statistically significant SNPs that modified the association of vitamin E assignment and high-grade prostate cancer included SEC14L2, SOD1, and TTPA. In the placebo arm, several SNPs, hypothesized to interact with supplement assignment and risk of high-grade prostate cancer, were also directly associated with outcome. Conclusion Variants in selenium and vitamin E metabolism/transport genes may influence risk of overall and high-grade prostate cancer, and may modify an individual man’s response to vitamin E or selenium supplementation with regards to these risks. Impact The effect of selenium or vitamin E supplementation on high-grade prostate cancer risk may vary by genotype.

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Section: Discussionsupporting

confidence: 90%

Selenium- or Vitamin E–Related Gene Variants, Interaction with Supplementation, and Risk of High-Grade Prostate Cancer in SELECT

Chan

Darke

Penney

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Although there are few reports of GPX4 in tumor tissue, GPX4 was found to be increased in colon carcinomas [15] and in hepatocellular carcinomas [16], and decreased GPX4 level has been reported in pancreatic cancer [17], breast cancer cells [18], clear cell renal cell carcinomas [19], and gastric cancer [21]. A variant of the gene encoding GPX4 has been reported to influence prostate cancer risk [20]. Despite these reports, there is yet no consensus on the expression and role of GPX4 in tumors.…”

Section: Discussionmentioning

confidence: 99%

“…The GPX family member GPX4, also known as phospholipid-hydroperoxide glutathione peroxidase, is considered one of the most important antioxidant enzymes in mammals [12][13][14]. Recently, there have been reports suggesting that overexpression or depletion of GPX4 is responsible for tumorigenesis and tumor progression [15][16][17][18][19][20][21]. However, the frequency of GPX4 expression in malignant lymphoma including DLBCL, its histological relevance, and its relevance prognosis are not currently known.…”

Section: Introductionmentioning

confidence: 99%

Glutathione peroxidase 4 overexpression inhibits ROS-induced cell death in diffuse large B-cell lymphoma

Kinowaki

Kurata

Ishibashi

et al. 2018

Laboratory Investigation

123

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Regulation of oxidative stress and redox systems has important roles in carcinogenesis and cancer progression, and for this reason has attracted much attention as a new area of cancer therapeutic targets. Glutathione peroxidase 4 (GPX4), an antioxidant enzyme, has biological important functions such as signaling cell death by suppressing peroxidation of membrane phospholipids. However, few studies exist on the expression and clinical relevance of GPX4 in malignant lymphomas such as diffuse large B-cell lymphoma. In this study, we assessed the expression of GPX4 immunohistochemically. GPX4 was expressed in 35.5% (33/93) cases of diffuse large B-cell lymphoma. The GPX4-positive group had poor overall survival (P = 0.0032) and progression-free survival (P = 0.0004) compared with those of the GPX4-negative group. In a combined analysis of GPX4 and 8-hydroxydeoxyguanosine (8-OHdG), an oxidative stress marker, there was a negative correlation between GPX4 and 8-hydroxydeoxyguanosine (P = 0.0009). The GPX4-positive and 8-hydroxydeoxyguanosine-negative groups had a significantly worse prognosis than the other groups in both overall survival (P = 0.0170) and progression-free survival (P = 0.0005). These results suggest that the overexpression of GPX4 is an independent prognostic predictor in diffuse large B-cell lymphoma. Furthermore, in vitro analysis demonstrated that GPX4-overexpressing cells were resistant to reactive oxygen species-induced cell death (P = 0.0360). Conversely, GPX4-knockdown cells were sensitive to reactive oxygen species-induced cell death (P = 0.0111). From these data, we conclude that GPX4 regulates reactive oxygen species-induced cell death. Our results suggest a novel therapeutic strategy using the mechanism of ferroptosis, as well as a novel prognostic predictor of diffuse large B-cell lymphoma.

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“…49 articles were excluded: 3 were reviews; 9 were conference abstracts; 4 were related to other SNPs of the CAT gene; 11 did not report extractable data; 22 were irrelevant papers. Finally, a total of 33 articles678111215161718192021222324252627282930313233343536373839404142 published from 2005 to 2015met the inclusion criteria and were included in our meta-analysis. There were 27 publications678111215161718192123242526272829303133343537383940 regarding susceptibility analysis, which involved 35 case-control or cohort studies with 15531 cancer patients and 41816 controls, while 8 publications620222932364142 contained the survival data.…”

Section: Resultsmentioning

confidence: 99%

The Role of Catalase C262T Gene Polymorphism in the Susceptibility and Survival of Cancers

Wang

Sun

Chen

et al. 2016

Sci Rep

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Catalase (CAT), one antioxidant enzyme, may provide resistance against many diseases. Many previous studies reported predictive and prognostic values of CAT C262T polymorphism in cancers, with divergent results. This study aimed to summarize the overall relationships between CAT C262T polymorphism and cancer risk or survival. A total of 27 eligible publications were included in susceptibility analysis, while 8 publications contained survival outcomes. The results revealed significant relationship between CAT C262T polymorphism and cancer risk(TT + CT vs CC: OR = 1.05, 95%CI = 1.00–1.10, P = 0.036), subgroup analyses indicated the CAT C262T polymorphism was significantly correlated with an increased risk for prostate cancer (TT vs CC + CT: OR = 1.43, 95%CI = 1.20–1.70, P < 0.001) and increased risk among Caucasians (TT vs CC + CT: OR = 1.19, 95%CI = 1.09–1.31, P < 0.001), while no associations between the polymorphism and Asian or mixed population were established. In the survival analysis, no interactions were identified between this polymorphism and cancer survival (TT + CT vs CC: HR = 1.37, 95%CI = 0.70–2.70, P = 0.36). In conclusion, the CAT C262T polymorphismmay be a candidate markerfor cancer risk with type-specific and population-specific effects but not a fine prognostic factor for cancer survival.

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Plasma Antioxidants, Genetic Variation in SOD2, CAT, GPX1, GPX4, and Prostate Cancer Survival

Cited by 28 publications

References 30 publications

Selenium- or Vitamin E–Related Gene Variants, Interaction with Supplementation, and Risk of High-Grade Prostate Cancer in SELECT

Selenium- or Vitamin E–Related Gene Variants, Interaction with Supplementation, and Risk of High-Grade Prostate Cancer in SELECT

Glutathione peroxidase 4 overexpression inhibits ROS-induced cell death in diffuse large B-cell lymphoma

The Role of Catalase C262T Gene Polymorphism in the Susceptibility and Survival of Cancers

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