No Association of the 5′Promoter Region Polymorphism of CYP17 with Breast Cancer Risk in Japan

Hamajima, Nobuyuki; Iwata, Hiroji; Obata, Yuichi; Matsuo, Keitaro; Mizutani, Mitsuhiro; Iwase, Takuji; Miura, Shigeto; Okuma, Katashi; Ohashi, Kazuhiko; Tajima, Kazuo

doi:10.1111/j.1349-7006.2000.tb01029.x

Cited by 33 publications

(23 citation statements)

References 18 publications

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“…Several studies have found a positive association between A2/A2 genotype and the risk of breast cancer in the subgroups such as younger (22-36 years old) Sweden (Bergman-Jungestrom et al, 1999), younger ( 40) Australian (Spurdle et al, 2000) and older ( 55) Japanese (Miyoshi et al, 2000). However, most other studies could not reproduce the positive association between A2/A2 genotype and breast cancer risk; e.g., no association was found in studies conducted for Caucasians in UK (Dunning et al, 1998), US (Weston et al, 1998;Haiman et al, 1999;Ambrosone et al, 2003), Finland (Mitrunen et al, 2000), hispanics and African-Americans in US (Weston et al, 1998), Japanese (Hamajima et al, 2000), Chinese in Singapore (Wu et al, 2003) and Taiwanese (Huang et al, 1999).…”

Section: Genetic Polymorphism Of Cyp17 and Breast Cancer Risk In Korementioning

confidence: 99%

“…A number of epidemiological studies have evaluated the potential role of CYP17 polymorphism in breast cancer development (Feigelson et al, 1997;Dunning et al, 1998;Helzlsouer et al, 1998;Weston et al, 1998;Bergman-Jungestrom et al, 1999;Huang et al, 1999;Hamajima et al, 2000;Kuligina et al, 2000;Mitrunen et al, 2000;Miyoshi et al, 2000;Spurdle et al, 2000;Ambrosone et al, 2003;Cui et al, 2003;Wu et al, 2003;Hefler et al, 2004) since the first association study (Feigelson et al, 1997) reported that A2 carriers had 2.5-fold higher risk of advanced breast cancer in a nested case-control study of multiethnic cohort. However, the results for the association between CYP17 polymorphism and breast cancer risk have been inconsistent.…”

Section: Genetic Polymorphism Of Cyp17 and Breast Cancer Risk In Korementioning

confidence: 99%

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Genetic polymorphism of CYP17 and breast cancer risk in Korean women

Shin

Lee²,

Yang³

et al. 2005

Exp Mol Med

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Section: Genetic Polymorphism Of Cyp17 and Breast Cancer Risk In Korementioning

confidence: 99%

Section: Genetic Polymorphism Of Cyp17 and Breast Cancer Risk In Korementioning

confidence: 99%

Genetic polymorphism of CYP17 and breast cancer risk in Korean women

Shin

Lee²,

Yang³

et al. 2005

Exp Mol Med

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“…14 In contrast, CYP17 genotype was not associated with breast cancer risk in other studies conducted in the US, 14 -16 United Kingdom, 17 Norway, 18 Finland, 19 Russia 20 and Japan. 21 High endogenous estrogen levels in association with the A2 allele have been reported, 16,22 although more recent data suggest that the association may be relatively weak. 23 The inconsistent findings in relation to this CYP17 polymorphism and, more importantly, the inadequacy of studying single genes one at a time 24 led to the investigations of other genes in conjunction with CYP17 that are involved in the biosynthesis and metabolism of estrogens.…”

mentioning

confidence: 99%

HSD17B1 and CYP17 polymorphisms and breast cancer risk among Chinese women in Singapore

Seow

Arakawa

et al. 2003

Intl Journal of Cancer

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Reasons for the recent trend of increasing breast cancer incidence among Chinese and other Asian women are not well understood. Endogenous estrogen levels are strongly associated with breast cancer risk and its determinants include both genetic and lifestyle factors. We conducted a nested case-control study to investigate, within the Singapore Chinese Health Study Cohort, the relationships between polymorphisms in 2 genes involved in estrogen metabolism, CYP17 and HSD17B1, and the risk of breast cancer. For this analysis, 188 incident breast cancer cases and 671 female cohort control subjects were compared. When the HSD17B1 A allele was considered as the "putative high-risk" allele, there was a modest increased risk (adjusted relative risk, RR‫,73.1؍‬ 95% CI‫09.0؍‬ -2.07 for HSD17B1 AA vs. other); this association was statistically significant in analysis restricted to postmenopausal women (RR‫,68.1؍‬ 95% CI‫41.1؍‬ -3.03). There was no significant association between the CYP17 MspAI polymorphism and risk in all subjects (RR‫,60.1؍‬ 95% CI‫47.1-56.0؍‬ for CYP17 A2A2 vs. CYP17 A1A1) or in postmenopausal women only. When we evaluated breast cancer risk in relation to the joint stratification of CYP17 and HSD17B1 genotypes and according to the combined number of putative high-risk alleles (range, 0 -4), we observed an elevated joint effect of the CYP17 and HSD17B1 genes on risk. Women who possessed all 4 putative high-risk alleles of both genes (CYP17 A2A2 and HSD17B1 AA) vs. less displayed a nearly 2-fold increased risk (RR‫,38.1؍‬ 95% CI‫;)44.3-79.0؍‬ this finding was statistically significant in postmenopausal women (RR‫,13.2؍‬ 95% CI‫-70.1؍‬ 4.98). Risk of breast cancer was similar among women possessing the other genotypes (i.e., less than 4 putative high-risk alleles in the joint CYP17/HSD17B1 genotypes). In addition, the significant increased risk of breast cancer associated with nulliparity or late age at first live birth (age 31 years or older) was largely limited to women with the high-risk CYP17 A1A2/ A2A2 or HSD17B1 AA genotypes (RR‫,14.2؍‬ 95% CI‫65.1؍‬ -3.72; RR‫93.4؍‬ , 95% CI‫-17.1؍‬ 11.30 , respectively). The latter gene-parity effects were especially pronounced in postmenopausal women. © 2003 Wiley-Liss, Inc. A large and compelling body of epidemiological and experimental evidence exists that implicates estrogens in the etiology of human breast cancer. Menstrual and reproductive factors as well as other lifestyle factors (e.g., physical activity and various dietary components including fat, fiber and soy) may directly or indirectly influence the endogenous hormonal milieu and thus the risk of breast cancer. 1-4 More recently, attention has turned to the study of polymorphisms in genes that are involved in estrogen biosynthesis and intracellular binding. 5,6 Of the many cytochrome-dependent monooxygenases (CYP) that are involved in the biosynthesis of sex-steroid hormones, CYP17, a gene encoding cytochrome p450c17␣ enzyme, has stimulated considerable interest in studies of breast and other hormon...

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“…While some authors suggested that the CYP17 A2 allele was associated with an increased risk of the disease 24 others reported no difference in the distribution of the different alleles among healthy and breast cancer patients. 16,25 The strong experimental evidence that the T to C substitution does not create a binding site for Sp-1 16 refutes the hypothesis that the CYP17 A2 would be the risk allele and suggest that these genotypes alone are of little value for breast cancer risk estimation. 25 …”

Section: Discussionmentioning

confidence: 93%

“…16,25 The strong experimental evidence that the T to C substitution does not create a binding site for Sp-1 16 refutes the hypothesis that the CYP17 A2 would be the risk allele and suggest that these genotypes alone are of little value for breast cancer risk estimation. 25 …”

Section: Discussionmentioning

confidence: 93%

No association of the 5′ promoter region polymorphism of CYP17 gene with prostate cancer risk

Santos

Ribeiro

Mesquita

et al. 2002

Prostate Cancer P D

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4Hemocentro de São José do Rio Preto, Sáo Paulo, Brazil CYP17 gene encodes the enzyme cytochrome p450c17a, which mediates two steps in the steroid biosynthesis pathway. Steroid hormones are believed to play a key role in the etiology of prostate cancer. A polymorphic T?C transition in the 5 0 promoter region of CYP17 creates an additional Sp1-type (CCACC box) promoter site (allele A2). We have evaluated the genotypic and allelic distribution of this polymorphism among 92 prostate cancer patients in order to assess risk by comparison with a population-based series of 200 healthy individuals from Brazil. Our results provide no evidence for an association between prostate cancer risk and CYP17 T/C polymorphism. Prostate Cancer and Prostatic Diseases (2002) 5, 28-31. DOI: 10.1038/sj/pcan/4500550Keywords: CYP17 gene; T/C polymorphism; prostate cancer risk IntroductionProstate cancer is the most common malignancy and the third most common cause of cancer mortality in Brazilian men. 1 Studies of risk factors such as occupation, diet, smoking, alcohol and sexual activity are still inconclusive, however, age, ethnicity and family history clearly affect the risk of prostate cancer. 2 -7 There is evidence to support the hypothesis of hormonal etiology of prostate cancer involving androgen action. 8 -10 Androgen is required for differentiation and growth of the prostate in utero and at puberty. 8 Testosterone, the most abundant circulating androgen is synthesized from cholesterol by a series of enzymatic reactions involving the cytochrome p450c17a. The enzyme has a bifunctional active site: the catalytic center performs the 17a-hydroxylation of pregnenolone and progesterone while the 17,20-lyase activity is responsible for the conversions of 17a-hydroxypregnenolone to dehydroepiandrosterone and 17a-hydroxyprogesterone to androstenedione, precursors of testosterone and estrogen. 11 Testosterone is converted to 5a-dihydrotestosterone (DHT) in the prostate by the enzyme 5a-reductase. DHT binds to AR (androgen receptor gene), and the DHT -AR complex transactivates a number of genes with ARresponsive elements. These events ultimately result in cell division in the prostate. 12 The CYP17 gene codes for cytochrome p450c17a enzyme, is located on chromosome 10, spans 6569 bp, and is divided into eight exons. 13 A polymorphic T?C transition in the 5 0 promoter region of CYP17 creates an additional Sp1-type (CCACC box) promoter site. 14 This base pair change also creates a recognition site for the MspA I restriction enzyme, which allows the identification of the CYP17 A2 allele. Since the number of 5 0 promoter elements correlates with promoter activity, it has been proposed that the A2 allele may lead to an increased rate of transcription, thus increasing the prostate cancer risk. 15 Recent in vitro evidence suggests that the 5 0 Sp1 type site resulting from the T to C substitution does not actually bind transcription factor Sp1, but there is still some functional evidence to indicate that this polymorphism may act as a risk facto...

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No Association of the 5′Promoter Region Polymorphism of CYP17 with Breast Cancer Risk in Japan

Cited by 33 publications

References 18 publications

Genetic polymorphism of CYP17 and breast cancer risk in Korean women

Genetic polymorphism of CYP17 and breast cancer risk in Korean women

HSD17B1 and CYP17 polymorphisms and breast cancer risk among Chinese women in Singapore

No association of the 5′ promoter region polymorphism of CYP17 gene with prostate cancer risk

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