CYP1A1, GSTM1, and GSTT1 polymorphisms and breast cancer risk in Brazilian women

Amorim, Lı́dia Maria da Fonte de; Rossini, Ana; Mendonça, Gulnar Azevedo Silva; Lotsch, Priscila Falagan; Simão, Tatiana de Almeida; Gallo, C.; Pinto, Luís Felipe Ribeiro

doi:10.1016/s0304-3835(02)00058-7

Cited by 57 publications

(34 citation statements)

References 19 publications

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“…10-5.90). An effect of GSTT1 null genotype on breast cancer risk is in agreement with three previous studies [24][25][26] but such risk was not observed in eight other studies [27][28][29][30][31][32][33][34]. Our observation may be a chance finding, also in view of the absence of an association for current smokers, even for those who smoke more than 20 cigarettes per day.…”

Section: Discussionsupporting

confidence: 92%

Cumulative genetic defects in carcinogen metabolism may increase breast cancer risk (The Netherlands)

Hel

Bueno-de-Mesquita

Gils

et al. 2005

Cancer Causes Control

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Variants in the metabolic genes NAT1, NAT2, GSTM1 or GSTT1, may cause differences in individual detoxifying capacity of possible carcinogens. We examined the cumulative effect of putative at risk genotypes on breast cancer risk and we examined the extent to which these polymorphisms modify the association between smoking and breast cancer. A case cohort study was conducted in the DOM cohort with 676 breast cancer cases and a random sample of 669 individuals. No effect of the NAT1, NAT2 or GSTM1 genotypes on breast cancer risk was observed. However, women with GSTT1 null genotype had a 30% increased breast cancer risk compared to women with GSTT1 present (RR = 1.30 (95% confidence interval (CI) 1.04-1.64)). Smoking did not influence breast cancer risk nor did genetic variations in NAT1, NAT2 or GSTM1 in combination with smoking. Compared to women who never smoked with GSTT1 present, women with GSTT1 null genotype and who formerly smoked showed an increased breast cancer risk (RR = 2.55 (95% CI 1.10-5.90)), but current smokers who smoked 20 cigarettes or more per day did not (RR = 1.06 (95% CI 0.51-2.18)). Increasing numbers of putative at risk genotypes increased breast cancer risk in a dose dependent manner (p for trend 0.01). The risk was more than doubled in women with all four risk genotypes, RR = 2.45 (95% CI 1.24-4.86), compared to women with zero putative at risk genotypes. In conclusion, the results of this study suggest that presence of three or more putative at risk genotypes increases breast cancer risk.Abbreviations: BMI -body mass index; CI -confidence interval; DOM -diagnostic study on breast cancer; GSTglutathione S-transferase; IRR -incidence rate ratio; NAT -N-acetyltransferase

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Section: Discussionsupporting

confidence: 92%

Cumulative genetic defects in carcinogen metabolism may increase breast cancer risk (The Netherlands)

Hel

Bueno-de-Mesquita

Gils

et al. 2005

Cancer Causes Control

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“…Numerous studies have detected no overall association between the GSTM1 null genotype and risk of breast cancer (Zhong et al [8];Ambrosone et al [9];Kelsey et al [10];Bailey et al [11];Charrier et al [12];Ambrosone et al [13];GarciaClosas et al [14];Lizard-Nacol et al [15];Curran et al [16];Millikan et al [17];Park et al [18];Krajinovic et al [19];Mitrunen et al [20];Dialyna et al [21];Gudmundsdottir et al [22];da Fonte de Amorim et al [23];Siegelmann-Danieliand Buetow [24];Zheng et al [25];Zheng et al [26];Khedhaier et al [27];Park et al [28];Vogl et al [29];Egan et al [30];Linhares et al [31];van der Hel et al [32];Cheng et al [33];Wu et al [34]), although a few have suggested the association might differ by menopausal status (Helzlsouer et al [35];Charrier et al [12];Park et al [18];Mitrunen et al [20];Park et al [28]), smoking (Terry and Goodman [36]), alcohol use (Park et al [18];Zheng et al [37]), consumption of well-done meat (Zheng et al [25]), and a combination of parity and age at first full-term pregnancy (Park et al [38]). The majority of studies examining the GSTP1 Ile105Val polymorphism and breast cancer risk have also yielded null results (Harries et al [39];Helzlsouer et al [35];Curran et al …”

Section: Introductionmentioning

confidence: 99%

Glutathione S-transferase M1 and P1 polymorphisms and risk of breast cancer and fibrocystic breast conditions in Chinese women

Sakoda

Blackston

Xue

et al. 2007

Breast Cancer Res Treat

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Enzymes encoded by the glutathione S-tranferase mu 1 (GSTM1) and pi 1 (GSTP1) genes, which are expressed in breast tissue, catalyze the detoxification of endogenous and exogenous electrophiles. Reduced enzyme activity, due to carriage of the GSTM1 deletion or the GSTP1 Ile105Val Val allele, may therefore affect susceptibility to breast cancer and related conditions. In a case-control study of Chinese women, we examined whether these polymorphisms were associated with risk of breast cancer and fibrocystic breast conditions. Women diagnosed with breast cancer (n=615) or fibrocystic breast conditions (n=467) were compared to women without clinical breast disease (n=878). We also examined whether these associations differed by menopausal status or by presence of proliferation in the extra-tumoral epithelium among women with breast cancer and in lesions among women with fibrocystic conditions. No overall association of either GST polymorphism with risk of breast cancer or fibrocystic breast conditions was observed. There was some evidence of slightly elevated cancer risk associated with carriage of the GSTM1 null genotype and at least one GSTP1 105-Val allele (OR=1.33, 95% CI, 0.99-1.80), compared to carriage of the GSTM1 non-null and GSTP1 Ile/Ile genotypes. This relationship was stronger in women who have breast cancer with extra-tumoral tissue proliferation (OR=1.77, 95% CI, 1.03-3.04). Our results suggest that GSTM1 and GSTP1 genotypes do not individually influence susceptibility to breast cancer or fibrocystic breast conditions. The observed increased risk of breast cancer associated with joint carriage of the GSTM1 null genotype and GSTP1 105-Val allele needs confirmation in other studies.

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“…[7][8][9][10] Overall, the clinical relevance of these single-nucleotide polymorphisms (SNPs) in the evaluation of breast carcinoma risk is controversial. Most published studies focused on a small number of SNPs in candidate genes but did not calculate interactions or adequately correct for multiple comparisons.…”

mentioning

confidence: 99%

Estrogen‐metabolizing gene polymorphisms in the assessment of breast carcinoma risk and fibroadenoma risk in Caucasian women

Hefler

Tempfer

Grimm

et al. 2004

Cancer

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BACKGROUNDGenes encoding enzymes involved in estrogen metabolism are held to be candidate genes for associations with breast disease. In these candidate genes, no critical combination of single‐nucleotide polymorphisms (SNPs) for assessing breast carcinoma risk has been reported to date.METHODSIn a large case–control study, the authors investigated 10 estrogen‐metabolizing SNPs in 396 patients with breast carcinoma, 154 patients with fibroadenoma, and 1936 healthy control patients without breast carcinoma in their personal history. The following 10 SNPs were analyzed using sequencing‐on‐chip technology via a solid‐phase polymerase chain reaction assay performed on oligonucleotide microarrays: catechol‐O‐methyltransferase Val158Met G→A, 17‐beta‐hydroxysteroid dehydrogenase type 1 vIV A→C, cytochrome P‐450 (CYP) family 17 A2 allele T→C, CYP1A1‐1 MspI restriction fragment length polymorphism (RFLP) T→C, CYP1A1‐2 Ile462Val A→G, CYP19‐1 Trp39Arg T→C, CYP19‐2 Arg264Cys C→T, CYP19‐3 Cys1558Thr C→T, steroid‐5‐alpha reductase type 2 Val89Leu G→C, and vitamin D receptor BsmI RFLP. A total of 21,350 genotypes were evaluated. Associations and two‐way interaction models were calculated using stepwise logistic regression.RESULTSIn a multiple model, CYP1A1‐1 (P = 0.004) and CYP1A1‐2 (P = 0.03) were found to be associated with significantly decreased and increased risks of breast carcinoma, respectively. When two‐way interactions involving investigated SNPs were ascertained, no significant interactions among polymorphisms were noted. Comparison of patients with fibroadenoma with control patients revealed significantly increased and decreased risks of fibroadenoma when the mutant alleles of CYP17 (P = 0.02) and CYP1A1‐1 (P = 0.04), respectively, were present.CONCLUSIONSThe authors obtained the first SNP data indicating that CYP17 and CYP1A1‐1 play a role in the pathogenesis of fibroadenoma. Although the authors were not able to develop interaction models involving SNPs, they did provide evidence that CYP1A1 is a low‐penetrance susceptibility gene with respect to breast carcinoma in a large series of Caucasian women. Cancer 2004. © 2004 American Cancer Society.

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CYP1A1, GSTM1, and GSTT1 polymorphisms and breast cancer risk in Brazilian women

Cited by 57 publications

References 19 publications

Cumulative genetic defects in carcinogen metabolism may increase breast cancer risk (The Netherlands)

Cumulative genetic defects in carcinogen metabolism may increase breast cancer risk (The Netherlands)

Glutathione S-transferase M1 and P1 polymorphisms and risk of breast cancer and fibrocystic breast conditions in Chinese women

Estrogen‐metabolizing gene polymorphisms in the assessment of breast carcinoma risk and fibroadenoma risk in Caucasian women

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