Association between the CYP1B1 polymorphisms and risk of cancer: a meta-analysis

Liu, Jie-Ying; Yang, Yuanzheng; Liu, Zhizhong; Xie, Jian‐Jun; Du, Ya-Ping; Wang, Wei

doi:10.1007/s00438-014-0946-x

Cited by 22 publications

(23 citation statements)

References 130 publications

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“…However, the all cases odds ratio of 0.92 (95% CI 0.86, 0.99) in the current study is consistent with the odds ratio of 0.93 (95% CI 0.81, 1.08) reported for carriers of one Gly allele in the meta-analysis by Economopoulos and Sergentanis [84]. Another meta-analysis reported an odds ratio of 0.93 (95% CI 0.79, 1.10) for the 48Gly variant based on a recessive model [81]. While these modest associations were not significant in either meta-analysis, these studies did not conduct analyses by ER subtype, whereby we discovered a stronger ER+ association.…”

Section: Discussionsupporting

confidence: 91%

“…This gene contains two common missense SNPs that were gene-wide significant for ER+ breast cancer: rs10012 (Arg48Gly) and rs1056827 (Ala119Ser). These two SNPs have previously been associated with other cancers (prostate [79–81], lung [82], endometrial [81, 83]) in mostly European samples. Modest associations have also been reported for rs1056827 with breast cancer in recent meta-analyses [80, 81], although another meta-analysis reported no association [84].…”

Section: Discussionmentioning

confidence: 99%

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Hormone-related pathways and risk of breast cancer subtypes in African American women

Haddad

Lunetta

Ruiz-Narváez

et al. 2015

Breast Cancer Res Treat

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Purpose We sought to investigate genetic variation in hormone pathways in relation to risk of overall and subtype-specific breast cancer in women of African ancestry (AA). Methods Genotyping and imputation yielded data on 143,934 SNPs in 308 hormone-related genes for 3663 breast cancer cases (1098 ER-, 1983 ER+, 582 ER unknown) and 4687 controls from the African American Breast Cancer Epidemiology and Risk (AMBER) Consortium. AMBER includes data from four large studies of AA women: the Carolina Breast Cancer Study, the Women's Circle of Health Study, the Black Women's Health Study, and the Multiethnic Cohort Study. Pathway- and gene-based analyses were conducted, and single SNP tests were run for the top genes. Results There were no strong associations at the pathway level. The most significantly associated genes were GHRH, CALM2, CETP, and AKR1C1 for overall breast cancer (gene-based nominal p ≤0.01); NR0B1, IGF2R, CALM2, CYP1B1, and GRB2 for ER+ breast cancer (p ≤0.02); and PGR, MAPK3, MAP3K1, and LHCGR for ER- disease (p ≤0.02). Single-SNP tests for SNPs with pairwise linkage disequilibrium r2 <0.8 in the top genes identified 12 common SNPs (in CALM2, CETP, NR0B1, IGF2R, CYP1B1, PGR, MAPK3, and MAP3K1) associated with overall or subtype-specific breast cancer after gene-level correction for multiple testing. Rs11571215 in PGR (progesterone receptor) was the SNP most strongly associated with ER- disease. Conclusion We identified eight genes in hormone pathways that contain common variants associated with breast cancer in AA women after gene-level correction for multiple testing.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Hormone-related pathways and risk of breast cancer subtypes in African American women

Haddad

Lunetta

Ruiz-Narváez

et al. 2015

Breast Cancer Res Treat

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“…For example, the allelic variant CYP1B1*3 (leu432val), results in reduced expression and altered metabolism of PAHs and has been positively correlated to susceptibility to lung cancer. 49 The CYP1B1*3 allelic variant is found in 37% of Caucasians and 23% of Japanese individuals. 50 Volunteers were required to be non-smokers with no gut motility issues, but there was no control for diets high in PAHs or other potential CYP inducing exposures.…”

Section: Discussionmentioning

confidence: 99%

Human Microdosing with Carcinogenic Polycyclic Aromatic Hydrocarbons: In Vivo Pharmacokinetics of Dibenzo[def,p]chrysene and Metabolites by UPLC Accelerator Mass Spectrometry

Madeen

Ognibene

Corley

et al. 2016

Chem. Res. Toxicol.

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Metabolism is a key health risk factor for exposures to pro-carcinogenic polycyclic aromatic hydrocarbons (PAHs) such as dibenzo[def,p]chrysene (DBC), an IARC classified 2A probable human carcinogen. Human exposure to PAHs occurs primarily from the diet in non-smokers. However, little data is available on the metabolism and pharmacokinetics in humans of high molecular weight PAHs (≥4 aromatic rings), including DBC. We previously determined the pharmacokinetics of DBC in human volunteers orally administered a micro-dose (29 ng; 5 nCi) of [14C]-DBC by accelerator mass spectrometry (AMS) analysis of total [14C] in plasma and urine. In the current study, we utilized a novel “moving wire” interface between ultra-performance liquid chromatography (UPLC) and the AMS to detect and quantify parent DBC and its major metabolites. The major [14C] product identified in plasma was unmetabolized [14C]-DBC itself, (Cmax= 18.5 ± 15.9 fg/mL, Tmax= 2.1 ± 1.0 h), whereas the major metabolite was identified as [14C]-(+/−)-DBC-11,12-diol (Cmax= 2.5 ± 1.3 fg/mL, Tmax= 1.8 h). Several minor species of [14C]-DBC metabolites were also detected for which no reference standards were available. Deconjugated and conjugated metabolites were detected in urine with [14C]-(+/−)-DBC-tetraol identified as the major metabolite, 88.7% of which was detected upon enzymatic deconjugation (Cmax= 35.8 ± 23.0 pg/pool, Tmax= 6–12 h pool). [14C]-DBC-11,12-diol, of which 94.4% was conjugated and identified in urine (Cmax= 29.4 ± 11.6 pg/pool, Tmax= 6–12 h pool). Parent [14C]-DBC was not detected in the urine. This is the first dataset to assess metabolite profiles and associated pharmacokinetics of a carcinogenic PAH in human volunteers at an environmentally relevant dose, providing the data necessary for translation of high dose laboratory animal models to human translation for environmental health risk assessment.

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“…Figure S2, orange) are 376 and 2591 bp in length compared to 390 and 3032 bp, respectively for h CYP1B1 . Both mRNAs are 5.2 kb and both proteins are 543 amino acids (AA) in length . The six substrate responsive sites (SRS) of the enzyme have a similar AA sequence and alignment as follows: SRS1, AA 116–139, 81%; SRS2, AA 224–236, 100%; SRS3, AA 259–263, 80%; SRS4, AA 330–343, 100%; SRS5, AA 392–401, 90%; SRS6, AA 503–513, 90% (Suppl.…”

Section: Methodsmentioning

confidence: 99%

“…Among endogenous substrates, hCYP1B1 is active in the 4‐hydroxylation of 17β‐estradiol , a metabolite linked to estrogen‐dependent carcinogenesis . hCYP1B1 and polymorphisms of hCYP1B1 have been linked to several hormone‐induced cancers, including prostate, breast, endometrial, and ovarian .…”

Section: Introductionmentioning

confidence: 99%

Dibenzo[def,p]chrysene transplacental carcinogenesis in wild-type,Cyp1b1knockout, andCYP1B1humanized mice

et al. 2016

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The cytochrome P450 (CYP) 1 family is active toward numerous environmental pollutants, including polycyclic aromatic hydrocarbons (PAHs). Utilizing a mouse model, null for Cyp1b1 and expressing human CYP1B1, we tested the hypothesis that hCYP1B1 is important for dibenzo[def,p]chrysene (DBC) transplacental carcinogenesis. Wild-type mCyp1b1, transgenic hCYP1B1 (mCyp1b1 null background), and mCyp1b1 null mice were assessed. Each litter had an equal number of siblings with Ahrb-1/d and Ahrd/d alleles. Pregnant mice were dosed (gavage) on gestation day 17 with 6.5 or 12 mg/kg of DBC or corn oil. At 10 months of age, mortality, general health, lymphoid disease, and lung tumor incidence and multiplicity were assessed. hCYP1B1 genotype did not impact lung tumor multiplicity, but tended to enhance incidence compared to Cyp1b1 wild-type mice (p = 0.07). As with Cyp1b1 in wild-type mice, constitutive hCYP1B1 protein is non-detectable in liver but was induced with 2,3,7,8-tetrachlorodibenzo-p-dioxin. Wild type mice were 59% more likely to succumb to T-cell Acute Lymphoblastic Leukemia (T-ALL). Unlike an earlier examination of the Ahr genotype in this model (Yu et al., Cancer Res., 2006), but in agreement with a more recent study (Shorey et al., Toxicol. Appl. Pharmacol., 2013), this genotype was not associated with lung tumor incidence, multiplicity, or mortality. Sex was not significant with respect to lung tumor incidence or mortality but males exhibited significantly greater multiplicity. Lung tumor incidence was greater in mCyp1b1 nulls compared to wild-type mice. To our knowledge this is the first application of a humanized mouse model in transplacental carcinogenesis.

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Association between the CYP1B1 polymorphisms and risk of cancer: a meta-analysis

Cited by 22 publications

References 130 publications

Hormone-related pathways and risk of breast cancer subtypes in African American women

Hormone-related pathways and risk of breast cancer subtypes in African American women

Human Microdosing with Carcinogenic Polycyclic Aromatic Hydrocarbons: In Vivo Pharmacokinetics of Dibenzo[def,p]chrysene and Metabolites by UPLC Accelerator Mass Spectrometry

Dibenzo[def,p]chrysene transplacental carcinogenesis in wild-type,Cyp1b1knockout, andCYP1B1humanized mice

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