Toenail selenium and risk of hepatocellular carcinoma mortality in Haimen City, China

Sakoda, Lori C.; Graubard, Barry I.; Evans, Alison A.; London, William T.; Wang, Lin; Shen, Fumin; McGlynn, Katherine A.

doi:10.1002/ijc.20937

Cited by 33 publications

(18 citation statements)

References 36 publications

(36 reference statements)

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“…It has been demonstrated that various forms of selenium inhibit the initiation phase of carcinogenesis. 17 Recent observations have indicated that the selenium level may interact with alcohol drinking 43 and may be associated with the extent of DNA damage. 44 Based on those observations, we have tested hypotheses that dietary selenium intake may interact with ALDH2, an alcohol metabolic gene, and XRCC1, a DNA repair gene, on the risk of ESCC, although the biologic mechanisms remain largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Dietary selenium intake, aldehyde dehydrogenase‐2 and X‐ray repair cross‐complementing 1 genetic polymorphisms, and the risk of esophageal squamous cell carcinoma

Cai

You

et al. 2006

Cancer

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BACKGROUND.To the authors' knowledge, few studies have been conducted to date regarding dietary selenium and the potential gene-nutrient interactions with single-nucleotide polymorphisms (SNPs) in different pathways on the risk of esophageal cancer. METHODS. The authors investigated the role of dietary selenium intake and itsinterplay with SNPs of the ALDH2 (glutamic acid [Glu] 487 lysine [Lys]) and the X-ray repair cross-complementing 1 (XRCC1) (arginine [Arg] 399 glutamine [Gln]) genes on the risk of esophageal squamous cell carcinoma (ESCC) in a populationbased, case-control study in China. In total, 218 patients with ESCC and 415 healthy population control participants were interviewed. Dietary selenium intake was estimated from a food frequency questionnaire with 97 food items. ALDH2 and XRCC1 polymorphisms were detected with a polymerase chain reaction-restriction fragment length polymorphism assay. RESULTS.The adjusted odds ratio (OR) for the highest quintile of dietary selenium intake, compared with the lowest quintile of intake, was 0.48 (95% confidence interval [95% CI], 0.25-0.89), with a strong dose-response relation (P for trend, Ͻ.01). The ALDH2 Lys and XRCC1 Gln variant alleles were associated with an increased risk of ESCC with adjusted ORs of 1.91 (95% CI, 0.96-3.80) and 1.67 (95% CI, 1.08-2.59), respectively. An elevation of the risk for ESCC was pronounced most among carriers of ALDH2 Lys/Lys and XRCC1 399Gln/Gln or Gln/Arg who consumed a low level of dietary selenium (adjusted OR, 4.16; 95% CI, 1.14-15.12). CONCLUSIONS.To the authors' knowledge, this is the first in-depth study to suggest that genetic susceptibility may modify the association between selenium intake and the risk of ESCC. The findings indicated that individuals with low dietary selenium intake and ALDH2 Lys/Lys and XRCC1 399Gln/Gln or Gln/Arg genotypes were associated with an increased ESCC risk, especially in the presence of exposure to tobacco and alcohol carcinogens. A ccumulating evidence from prior epidemiologic studies suggests an association between esophageal cancer and the use of alcohol and tobacco. [1][2][3] The combined use of alcohol and tobacco leads to synergistically increased risk of esophageal cancers. 4,5 In Europe and North America, it is believed that 90% of esophageal cancers are related to tobacco smoking and alcohol drinking. Simultaneous exposure to similarly moderate amounts of smoking and alcohol drinking increased the risk 12-fold and 19-fold in men and women, respectively. 6 Engel et al., in a multicenter, population-based, case-control study, observed that ever-smoking and alcohol consumption accounted for 56.9% and 72.4% of esophageal squamous cell carcinoma (ESCC) in men and women, respectively. 7 Diet has been implicated in many pathways involved in carcinogenesis, including DNA repair and carcinogen metabolism. In addition to myriad phytochemicals, diet provides numerous trace minerals that are essential for normal metabolism, including selenium, which is suggested as a potential chemopreven...

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Section: Discussionmentioning

confidence: 99%

Dietary selenium intake, aldehyde dehydrogenase‐2 and X‐ray repair cross‐complementing 1 genetic polymorphisms, and the risk of esophageal squamous cell carcinoma

Cai

You

et al. 2006

Cancer

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“…These epidemiology studies have generated both positive and negative results, but do provide substantial support for the hypothesis that Se compounds have cancer preventive activity (Combs, 2005). In recent years, numerous investigators have reported inverse associations between Se biomarkers (toenail Se or serum Se levels) and the risk of neoplasia in several sites, including the prostate (van den Brandt et al, 2003, Vogt et al, 2003, Li et al, 2004, esophagus and gastric cardia (Wei et al, 2004), liver (Sakoda et al, 2005), colon (Ghadirian et al, 2000;Jacobs et al, 2004;Peters et al, 2006), lung (van den Brandt et al, 1993, Zhuo et al, 2004, skin (Burke et al, 1992), and urinary bladder (Zeegers et al, 2002). It should be noted, however, other studies have found no association between Se status and the risk of cancer of the breast (Dorgan et al, 1998;Ghadirian et al, 2000;Männistö et al, 2000), prostate (Ghadirian et al, 2000;Allen et al, 2004), ovary (Pan et al, 2004), non-cardiac stomach (Wei et al, 2004), urinary bladder (Michaud et al, 2002), or lung (Mahabir et al, 2006).…”

Section: Introductionmentioning

confidence: 98%

Subchronic oral toxicity studies of Se-methylselenocysteine, an organoselenium compound for breast cancer prevention

Johnson

Morrissey

Kapetanović

et al. 2008

Food and Chemical Toxicology

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Se-methylselenocysteine (MSC) is an organoselenium compound being developed for breast cancer chemoprevention. To characterize MSC toxicity, CD rats received daily gavage doses of 0, 0.5, 1.0, or 2.0 mg/kg/day (0, 3, 6, or 12 mg/m 2 /day), and beagle dogs received daily gavage doses of 0, 0.15, 0.3, or 0.6 mg/kg/day (0, 3, 6, or 12 mg/m 2 /day) for 28 days. In rats, MSC induced dose-related hepatomegaly in both sexes; mild anemia, thrombocytopenia, and elevated liver enzymes were observed in high dose females only. Microscopic pathology included hepatocellular degeneration (high dose males, all doses in females); arrested spermatogenesis (high dose males); and atrophy of corpora lutea (middle and high dose females). In dogs, MSC induced mild anemia in middle and high dose males, and in high dose females. Toxicologically significant microscopic lesions in dogs were seen only in the liver (peliosis and vacuolar degeneration in high dose males, midzonal necrosis in males in all dose groups). Based on liver pathology seen in female rats in all dose groups, the No Observed Adverse Effect Level [NOAEL] for MSC in rats is < 0.5 mg/kg/day. Based on alterations in hematology parameters and liver morphology in male dogs in all dose groups, the NOAEL for MSC in dogs is <0.15 mg/kg/day.

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“…In addition to chronic HBV infection (2), several other environmental and nutritional cofactors may modify or contribute to risk of liver disease and hepatocarcinogenesis (3,4). One such factor may be folate, a water-soluble B vitamin naturally occurring in several foods.…”

Section: Introductionmentioning

confidence: 99%

Blood Folate Levels and Risk of Liver Damage and Hepatocellular Carcinoma in a Prospective High-Risk Cohort

Welzel

Katki

Sakoda

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Studies in experimental animals suggest that low folate levels may play a role in liver damage and hepatocarcinogenesis. To examine this association in humans, folate levels in blood and risk for subsequent liver damage and hepatocellular carcinoma (HCC) were assessed in a population at high risk of liver cancer in China. Methods: Four hundred fifteen hepatitis B surface antigenpositive participants of the Haimen City Cohort were prospectively followed between 1998 and 2002. Serum and RBC folate levels were determined at baseline. Alanine aminotransferase (ALT) and hepatitis B virus DNA levels were measured semiannually. Logistic regression modeling was used to examine the presence of hepatitis B virus DNA and HCC, whereas linear regression with a log-link function was used to examine ALT levels. Results: There was a statistically significant inverse association between serum folate level and ALT level. ALT levels

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Toenail selenium and risk of hepatocellular carcinoma mortality in Haimen City, China

Cited by 33 publications

References 36 publications

Dietary selenium intake, aldehyde dehydrogenase‐2 and X‐ray repair cross‐complementing 1 genetic polymorphisms, and the risk of esophageal squamous cell carcinoma

Dietary selenium intake, aldehyde dehydrogenase‐2 and X‐ray repair cross‐complementing 1 genetic polymorphisms, and the risk of esophageal squamous cell carcinoma

Subchronic oral toxicity studies of Se-methylselenocysteine, an organoselenium compound for breast cancer prevention

Blood Folate Levels and Risk of Liver Damage and Hepatocellular Carcinoma in a Prospective High-Risk Cohort

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