Circulatory Estrogen Level Protects Against Breast Cancer in Obese Women

Suba, Zsuzsanna

doi:10.2174/1574892811308020004

Cited by 39 publications

(52 citation statements)

References 162 publications

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“…While a high BMI increases the risk of BC, it is believed that clinically significant estrogen levels may protect women from a certain degree of BC risk, so that an increased BC risk may not be detected in premenopausal women (Suba, 2013). Similarly, an increased BC risk in obese women has not been identified in postmenopausal women receiving hormone replacement therapy (Morimoto et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Association of molecular subtypes with breast cancer risk factors

Rauh¹,

Gaß²,

Haeberle³

et al. 2015

European Journal of Cancer Prevention

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As breast cancer (BC) screening identifies many BCs with a good prognosis, which might be overdiagnosed and therefore overtreated, the identification of subgroups with a high risk for aggressive subtypes might be helpful. The aim of this case-case analysis was to investigate the association between epidemiological risk factors and molecular subtypes in a cohort of BC patients. Epidemiological risk factors for 2587 BC patients were obtained using a structured questionnaire and from the patients' charts. The histopathological information (estrogen and progesterone receptor, HER2 and Ki-67) used in the analysis was retrieved from the original pathology reports. Analyses using conditional inference regression trees were carried out on these data. The strongest influence factor on the distribution of the molecular subtypes was age at first diagnosis of BC. An influence of BMI was also identified in patients aged either more than 42 years or 49.6 years or less. Older patients aged more than 49.6 years and perimenopausal women with a BMI of 32.4 kg/m or less were most likely to develop luminal A-like BC. Young patients aged 42 years or less and perimenopausal patients with a BMI more than 32.4 kg/m more often developed triple-negative BC. The study confirmed that age at diagnosis is an important factor influencing the distribution of molecular subtypes. In the perimenopausal group, it may be postulated that BMI plays a critical role in the pathogenesis of BC, defining a subgroup that is more likely to develop triple-negative BC or luminal B-like disease and another group in which there is a more postmenopausal distribution pattern.

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Section: Discussionmentioning

confidence: 99%

Association of molecular subtypes with breast cancer risk factors

Rauh¹,

Gaß²,

Haeberle³

et al. 2015

European Journal of Cancer Prevention

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“…Obesity is associated with dysmetabolism and endangers the healthy equilibrium of sexual hormone production. In reality, among premenopausal women, obesity-associated insulin resistance is moderate, being counteracted by their maintained or increased circulating estrogen levels [15,42]. In conclusion, it is not obesity but rather the still suitable estrogen level that may be protective against breast cancer in young women.…”

Section: Obesity-associated Failure Of Estrogen Signaling Is a Strongmentioning

confidence: 98%

“…Among obese premenopausal women with regular ovulatory cycles, a femaletype gluteofemoral deposition of adipose tissue may be associated with the Crossroad between Obesity and Cancer: A Defective Signaling Function of Heavily Lipid-Laden… DOI: http://dx.doi.org/10.5772/intechopen.85995 maintenance of healthy insulin sensitivity, whereas they have no increased risk for either cardiovascular or neoplastic diseases [15]. Abdominal adipocytes of healthy women exhibit higher insulin sensitivity as compared with those of men [16].…”

Section: Weak Estrogen Signaling In Men and Postmenopausal Women Provmentioning

confidence: 99%

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Crossroad between Obesity and Cancer: A Defective Signaling Function of Heavily Lipid-Laden Adipocytes

Suba¹

2020

Understanding the Molecular Crosstalk in Biological Processes

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Obesity and its comorbidities exhibit a gender-related dimorphism. Obese males tend to accrue more visceral fat leading to abdominal adiposity, which shows a strong correlation with serious obesity-associated comorbidities, cardiovascular diseases and cancers. In contrast, obese females accumulate excessive fatty tissue predominantly subcutaneously enjoying strong protection from the obesity-related diseases. The health advantage of obese women as compared with obese men may be attributed to their higher estrogen production and an increased transactivation of estrogen receptors (ERs). The recently clarified intracrine, paracrine, and endocrine functions of adipose tissue illuminate that concentrations of estrogens and the suitable expression and activity of ERs strongly define all regulatory functions in both men and women. All well-known cancer risk factors are in correlation with defects of estrogen signaling in partnership with glucose intolerance as estrogen regulates all steps of glucose uptake. In central obesity, increased secretions of cytokines and growth factors are not causal factors of developing insulin resistance, and unrestrained cell proliferation, but rather, they are compensatory processes so as to increase estrogen synthesis and ER transactivation. In conclusion, a causal therapy against obesity and obesity-related diseases aims to improve estrogen signaling in both men and women.

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“…(5) Estrogenpossess crucial role in regulation of growth hormone (GH) activity through inhibitory effects on its secretion and on cellular GH receptor functions. These observations suggest a close correlation between estrogen and their antidiabetogenic as well as anticancer capacities by regulating GH-insulin like growth factor (IGF)-I axis [50][51][52] .…”

Section: Effects Of Estrogen On Glucose Metabolismmentioning

confidence: 99%

A Bidirectional Relationship Between Menopause and Diabetes Mellitus

S¹,

Dhivya²,

C³

et al. 2018

IRJPS

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Menopause is described as a transition from the state of reproductivity to infertility. It is clinically diagnosed by estimating cessation of spontaneous menstruation over a period of 12 months. Estrogen governs insulin production capacity of the pancreatic islet cells as well as glucose homeostasis by several possible pathways in animal models. In the liver, estrogen regulates insulin sensitivity by activating glycogen synthetase and glycolytic enzymes; aromatase knockout is an enzyme responsible for estrogen biosynthesis which upon inactivation, mice develops insulin resistance due to estrogen deficiency which was reversed by estrogen therapy. Estrogen receptor possesses roles in cellular glucose uptake by governing glucose transporter (GLUT) and also modulates insulin receptor substrate-1 phosphorylation. In women insulin resistance may contribute to hyper-androgenism and an ovulatory dysfunction through several pathways. The compensated phase of insulin resistance stimulates the testosterone biosynthesis of human ovarian theca cells from women with polycystic ovarian syndrome which induces the earlier or late menopause. Thus this review elucidates a bidirectional relationship between diabetes mellitus and menopause.

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Circulatory Estrogen Level Protects Against Breast Cancer in Obese Women

Cited by 39 publications

References 162 publications

Association of molecular subtypes with breast cancer risk factors

Association of molecular subtypes with breast cancer risk factors

Crossroad between Obesity and Cancer: A Defective Signaling Function of Heavily Lipid-Laden Adipocytes

A Bidirectional Relationship Between Menopause and Diabetes Mellitus

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