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CYP17 and breast cancer risk: the polymorphism in the 5' flanking area of the gene does not influence binding to Sp-1.

TLDR
Genotyping of 510 breast cancer patients and 201 controls revealed no difference in genotype frequencies and age at onset, tumor grade, lymph node status and distant metastases, stage, and estrogen and progesterone receptor status were not associated with the CYP17 genotype.
Abstract
The ability of a motif of the CYP17 5' untranslated region, created by a polymorphic T to C substitution, to bind to the human transcription factor Sp-1 was investigated. No binding of any of the polymorphic alleles was observed in electromobility shift assay. No other sequence within +1 to +100 of each of the CYP17 alleles formed complex with the Sp-1 or enhanced binding to the polymorphic CACC box. Genotyping of 510 breast cancer patients and 201 controls revealed no difference in genotype frequencies. Age at onset, tumor grade, lymph node status and distant metastases, stage, and estrogen and progesterone receptor status were not associated with the CYP17 genotype.

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Molecular epidemiology of sporadic breast cancer: The role of polymorphic genes involved in oestrogen biosynthesis and metabolism

TL;DR: In this paper, the potential role of polymorphic genes encoding for enzymes involved in oestrogen biosynthesis and conversion of the oestrogens metabolites and their by-products in modulating individual susceptibility to breast cancer are reviewed.
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Genes other than BRCA1 and BRCA2 involved in breast cancer susceptibility.

TL;DR: Data from this review will help focus on the further analysis of genetic polymorphisms in populations of appropriate size, and especially on the combinations of such polymorphisms, to facilitate determination of population attributable risks, understanding of gene-gene interactions, and improving estimates of genetic cancer risks.
Journal Article

The relationship between a polymorphism in CYP17 with plasma hormone levels and breast cancer.

TL;DR: It is suggested that the A2 allele of CYP17 modifies endogenous hormone levels, but is not a strong independent risk factor for breast cancer.
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SNP-SNP interactions in breast cancer susceptibility

TL;DR: Evidence for gene-gene (SNP-SNP) interaction among these SNPs, which were associated with increased breast cancer risk are demonstrated, which has the potential to identify complex biological links among breast cancer genes and processes.
Journal Article

Increased Risk of Prostate Cancer and Benign Prostatic Hyperplasia Associated with a CYP17 Gene Polymorphism with a Gene Dosage Effect

TL;DR: The results suggest that the A1 allele of the CYP17 polymorphism is associated with an increased risk of prostate cancer and BPH, with a gene dosage effect, however, the CyP17 genotype does not seem to influence the disease status in prostate cancer.
References
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Journal ArticleDOI

Isolation of cDNA encoding transcription factor Sp1 and functional analysis of the DNA binding domain.

TL;DR: It is found that purified Sp1 requires Zn(II) for sequence-specific binding to DNA, and it is likely that Sp1 interacts with DNA by binding of the Zn (II) fingers.
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Plasma sex steroid hormone levels and risk of breast cancer in postmenopausal women.

TL;DR: The data, in conjunction with past epidemiologic and animal studies, provide strong evidence for a causal relationship between postmenopausal estrogen levels and the risk of breast cancer.
Journal ArticleDOI

Multiple specific contacts between a mammalian transcription factor and its cognate promoters

TL;DR: The human transcription factor Sp1 binds upstream of certain viral and cellular promoters and activates initiation of RNA synthesis from these promoters by RNA polymerase II.
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Cloning and sequence of the human gene for P450c17 (steroid 17 alpha-hydroxylase/17,20 lyase): similarity with the gene for P450c21.

TL;DR: The human P450XVIIA1 gene lying on chromosome 10 is cloned and sequenced, which encodes P450c17, a single cytochrome P450 enzyme mediating both 17 alpha-hydroxylase and 17,20 lyase activities in the biosynthesis of steroid hormones.
Journal ArticleDOI

P450 enzymes of estrogen metabolism

TL;DR: Endogenous and exogenous estrogens undergo extensive oxidative metabolism by specific cytochrome P450 enzymes, resulting in reactive estrogens that are capable of damaging cellular proteins and DNA and may be carcinogenic in specific cells.
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