scholarly journals SNPs near the gene encoding estrogen receptor-α for predicting breast cancer risk in Latina women

2014 ◽  
Vol 7 (45) ◽  
pp. 1336-1336
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Estrogen Receptor Α ◽  
Latina Women ◽  
Gene Encoding

The Estrogen Receptor α Gene and Breast Cancer Risk (The Netherlands)

2005 ◽  
Vol 16 (10) ◽  
pp. 1195-1202 ◽  
Author(s):  
N. Charlotte Onland-Moret ◽  
Carla H. van Gils ◽  
Mark Roest ◽  
Diederick E. Grobbee ◽  
Petra H. M. Peeters
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
The Netherlands ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Α Gene

scholarly journals Estrogen receptor α polymorphisms and postmenopausal breast cancer risk

2007 ◽  
Vol 107 (3) ◽  
pp. 415-419 ◽  
Author(s):  
A. M. González-Zuloeta Ladd ◽  
A. Arias Vásquez ◽  
F. Rivadeneira ◽  
C. Siemes ◽  
A. Hofman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Postmenopausal Breast Cancer ◽  
Estrogen Receptor Α ◽  
Postmenopausal Breast Cancer Risk

scholarly journals Association of estrogen receptor α polymorphisms with breast cancer risk in older Caucasian women

2005 ◽  
Vol 116 (6) ◽  
pp. 984-991 ◽  
Author(s):  
Francesmary Modugno ◽  
Joseph M. Zmuda ◽  
Douglas Potter ◽  
Chao Cai ◽  
Elad Ziv ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Estrogen Receptor Α ◽  
Caucasian Women

scholarly journals Breast Cancer Risk in Usual Ductal Hyperplasia Is Defined by Estrogen Receptor-α and Ki-67 Expression

2002 ◽  
Vol 160 (2) ◽  
pp. 597-604 ◽  
Author(s):  
Abeer M. Shaaban ◽  
John P. Sloane ◽  
Christopher R. West ◽  
Christopher S. Foster
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Estrogen Receptor Α ◽  
Ki 67 ◽  
Usual Ductal Hyperplasia ◽  
Ductal Hyperplasia

scholarly journals Aromatase and breast cancer susceptibility.

1999 ◽  
pp. 165-173 ◽  
Author(s):  
N M Probst-Hensch ◽  
S A Ingles ◽  
A T Diep ◽  
R W Haile ◽  
F Z Stanczyk ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Cancer Incidence ◽  
Breast Cancer Incidence ◽  
Latina Women ◽  
Repeat Polymorphism ◽  
Cyp19 Gene ◽  
Functional Relevance

Based on experimental and epidemiological evidence it is hypothesized that estrogen increases breast cancer risk by increasing mitotic activity in breast epithelial cells. Aromatase is crucial to the biosynthesis of estrogens and may therefore play a role in breast cancer development. Supporting data for an etiological role of aromatase in breast tumor biology are several-fold. First, the association between weight and postmenopausal breast cancer risk may be mediated by aromatase. Secondly, a pilot study found a higher aromatase expression in normal breast adipose tissue from breast cancer cases as opposed to healthy women. Thirdly, experimental data in animals suggest that aromatase activity predisposes mammary tissue to preneoplastic and neoplastic changes. In a multiethnic cohort study conducted in Los Angeles and on Hawaii we investigated (i) whether the plasma estrone to androstenedione (E1/A) ratio in different ethnic groups was associated with ethnic differences in breast cancer incidence, and (ii) whether genetic variation in the CYP19 gene encoding the P450 aromatase protein was associated with breast cancer risk. The age- and weight-adjusted ethnic specific E1/A ratios x 100 among women without oophorectomy were 7.92 in African-Americans, 8.22 in Japanese, 10.73 in Latinas and 9.29 in non-Latina Whites (P=0.09). The high E1/A ratio in Latina women was not associated with a high breast cancer incidence; in fact Latina women had the lowest breast cancer incidence in the cohort observed so far. We found no consistent association of an intronic (TTTA)n repeat polymorphism with breast cancer risk in different ethnic groups. This polymorphism was not associated with differences in the plasma E1/A ratio in a way that would predict its functional relevance. We describe a newly identified TTC deletion in intron 5 of the CYP19 gene that is associated with the (TTTA)n repeat polymorphism. Neither this polymorphism, nor a polymorphism at codon 264 in exon VII of the CYP19 gene, was associated with breast cancer. We did not identify any genetic variation in exon VIII in 54 African-American subjects. We identified rare genetic variants of unknown functional relevance in the promoter 1.4 of the CYP19 gene in 3 out of 24 Latina women. Further investigation into the role of aromatase in breast cancer etiology is important, given that the potential use of aromatase inhibitors as breast cancer chemopreventives depends on these results.

scholarly journals Associations of obesity and circulating insulin and glucose with breast cancer risk: a Mendelian randomization analysis

2018 ◽  
Vol 48 (3) ◽  
pp. 795-806 ◽  
Author(s):  
Xiang Shu ◽  
Lang Wu ◽  
Nikhil K Khankari ◽  
Xiao-Ou Shu ◽  
Thomas J Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Type 2 Diabetes ◽  
Estrogen Receptor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Mendelian Randomization ◽  
Menopausal Status ◽  
Inverse Association ◽  
Fasting Insulin

Abstract Background In addition to the established association between general obesity and breast cancer risk, central obesity and circulating fasting insulin and glucose have been linked to the development of this common malignancy. Findings from previous studies, however, have been inconsistent, and the nature of the associations is unclear. Methods We conducted Mendelian randomization analyses to evaluate the association of breast cancer risk, using genetic instruments, with fasting insulin, fasting glucose, 2-h glucose, body mass index (BMI) and BMI-adjusted waist-hip-ratio (WHRadj BMI). We first confirmed the association of these instruments with type 2 diabetes risk in a large diabetes genome-wide association study consortium. We then investigated their associations with breast cancer risk using individual-level data obtained from 98 842 cases and 83 464 controls of European descent in the Breast Cancer Association Consortium. Results All sets of instruments were associated with risk of type 2 diabetes. Associations with breast cancer risk were found for genetically predicted fasting insulin [odds ratio (OR) = 1.71 per standard deviation (SD) increase, 95% confidence interval (CI) = 1.26-2.31, p  =  5.09  ×  10–4], 2-h glucose (OR = 1.80 per SD increase, 95% CI = 1.3 0-2.49, p  =  4.02  ×  10–4), BMI (OR = 0.70 per 5-unit increase, 95% CI = 0.65-0.76, p  =  5.05  ×  10–19) and WHRadj BMI (OR = 0.85, 95% CI = 0.79-0.91, p  =  9.22  ×  10–6). Stratified analyses showed that genetically predicted fasting insulin was more closely related to risk of estrogen-receptor [ER]-positive cancer, whereas the associations with instruments of 2-h glucose, BMI and WHRadj BMI were consistent regardless of age, menopausal status, estrogen receptor status and family history of breast cancer. Conclusions We confirmed the previously reported inverse association of genetically predicted BMI with breast cancer risk, and showed a positive association of genetically predicted fasting insulin and 2-h glucose and an inverse association of WHRadj BMI with breast cancer risk. Our study suggests that genetically determined obesity and glucose/insulin-related traits have an important role in the aetiology of breast cancer.

scholarly journals Body mass index, mammographic density, and breast cancer risk by estrogen receptor subtype

2019 ◽  
Vol 21 (1) ◽  
Author(s):  
Yiwey Shieh ◽  
Christopher G. Scott ◽  
Matthew R. Jensen ◽  
Aaron D. Norman ◽  
Kimberly A. Bertrand ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Body Mass Index ◽  
Estrogen Receptor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Body Mass ◽  
Mammographic Density ◽  
Receptor Subtype
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