Aromatase, Nuclear Receptors, Adipose Tissue, And Breast Cancer

2002 ◽  
pp. 175-180
Author(s):  
Evan R Simpson ◽  
Colin Clyne ◽  
Caroline Speed ◽  
Gary Rubin
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Nuclear Receptors

scholarly journals Cellular and Molecular Players in the Interplay between Adipose Tissue and Breast Cancer

2021 ◽  
Vol 22 (3) ◽  
pp. 1359
Author(s):  
Francesca Reggiani ◽  
Paolo Falvo ◽  
Francesco Bertolini
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Metabolic Disorders ◽  
Current Knowledge ◽  
Therapeutic Interventions ◽  
Preclinical Research ◽  
The World ◽  
Adipose Cells

The incidence and severity of obesity are rising in most of the world. In addition to metabolic disorders, obesity is associated with an increase in the incidence and severity of a variety of types of cancer, including breast cancer (BC). The bidirectional interaction between BC and adipose cells has been deeply investigated, although the molecular and cellular players involved in these mechanisms are far from being fully elucidated. Here, we review the current knowledge on these interactions and describe how preclinical research might be used to clarify the effects of obesity over BC progression and morbidity, with particular attention paid to promising therapeutic interventions.

scholarly journals The Prognostic Impact of Body Composition for Locally Advanced Breast Cancer Patients Who Received Neoadjuvant Chemotherapy

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 608
Author(s):  
Toshiaki Iwase ◽  
Aaroh Parikh ◽  
Seyedeh S. Dibaj ◽  
Yu Shen ◽  
Tushaar Vishal Shrimanker ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Body Composition ◽  
Adipose Tissue ◽  
Neoadjuvant Chemotherapy ◽  
Advanced Breast Cancer ◽  
Locally Advanced Breast Cancer ◽  
Locally Advanced ◽  
Pathologic Complete Response ◽  
Complete Response ◽  
Advanced Breast

Our previous study indicated that a high amount of visceral adipose tissue was associated with poor survival outcomes in patients with early breast cancer who received neoadjuvant chemotherapy. However, inconsistency was observed in the prognostic role of body composition in breast cancer treatment outcomes. In the present study, we aimed to validate our previous research by performing a comprehensive body composition analysis in patients with a standardized clinical background. We included 198 patients with stage III breast cancer who underwent neoadjuvant chemotherapy between January 2007 and June 2015. The impact of body composition on pathologic complete response and survival outcomes was determined. Body composition measurements had no significant effect on pathologic complete response. Survival analysis showed a low ratio of total visceral adipose tissue to subcutaneous adipose tissue (V/S ratio ≤ 34) was associated with shorter overall survival. A changepoint method determined that a V/S ratio cutoff of 34 maximized the difference in overall survival. Our study indicated the prognostic effect of body composition measurements in patients with locally advanced breast cancer compared to those with early breast cancer. Further investigation will be needed to clarify the biological mechanism underlying the association of V/S ratio with prognosis in locally advanced breast cancer.

scholarly journals Estrogen Receptor (ER)α-regulated Lipocalin 2 Expression in Adipose Tissue Links Obesity with Breast Cancer Progression

2014 ◽  
Vol 290 (9) ◽  
pp. 5566-5581 ◽  
Author(s):  
Brian G. Drew ◽  
Habib Hamidi ◽  
Zhenqi Zhou ◽  
Claudio J. Villanueva ◽  
Susan A. Krum ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Lipocalin 2

scholarly journals Mouse breast cancer model-dependent changes in metabolic syndrome-associated phenotypes caused by maternal dioxin exposure and dietary fat

2009 ◽  
Vol 296 (1) ◽  
pp. E203-E210 ◽  
Author(s):  
Michele La Merrill ◽  
David S. Baston ◽  
Michael S. Denison ◽  
Linda S. Birnbaum ◽  
Daniel Pomp ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Blood Glucose ◽  
Estrogenic Activity ◽  
Fasting Blood Glucose ◽  
Growth Spurt ◽  
Cancer Model ◽  
Serum Triglycerides ◽  
Cancer Models

Diets high in fat are associated with increased susceptibility to obesity and metabolic syndrome. Increased adipose tissue that is caused by high-fat diets (HFD) results in altered storage of lipophilic toxicants like 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD), which may further increase susceptibility to metabolic syndrome. Because both TCDD and HFD are associated with increased breast cancer risk, we examined their effects on metabolic syndrome-associated phenotypes in three mouse models of breast cancer: 7,12-dimethylbenz[a]anthracene (DMBA), Tg(MMTV-Neu)202Mul/J (HER2), and TgN(MMTV-PyMT)634Mul/J (PyMT), all on an FVB/N genetic background. Pregnant mice dosed with 1 μg/kg of TCDD or vehicle on gestational day 12.5 were placed on a HFD or low-fat diet (LFD) at parturition. Body weights, percent body fat, and fasting blood glucose were measured longitudinally, and triglycerides were measured at study termination. On HFD, all cancer models reached the pubertal growth spurt ahead of FVB controls. Among mice fed HFD, the HER2 model had a greater increase in body weight and adipose tissue from puberty through adulthood compared with the PyMT and DMBA models. However, the DMBA model consistently had higher fasting blood glucose levels than the PyMT and HER2 models. TCDD only impacted serum triglycerides in the PyMT model maintained on HFD. Because the estrogenic activity of the HFD was three times lower than that of the LFD, differential dietary estrogenic activities did not drive the observed phenotypic differences. Rather, the HFD-dependent changes were cancer model dependent. These results show that cancer models can have differential effects on metabolic syndrome-associated phenotypes even before cancers arise.

scholarly journals Post-Translational Modifications of Nuclear Receptors and Human Disease

2012 ◽  
Vol 10 (1) ◽  
pp. nrs.10001 ◽  
Author(s):  
Muralidharan Anbalagan ◽  
Brandy Huderson ◽  
Leigh Murphy ◽  
Brian G. Rowan
Keyword(s):  
Breast Cancer ◽  
Prostate Cancer ◽  
Clinical Outcome ◽  
Nuclear Receptors ◽  
Inflammatory Diseases ◽  
Peroxisome Proliferator ◽  
Additional Measure ◽  
Peroxisome Proliferator Activated Receptor ◽  
Post Translational Modifications ◽  
Pparγ Phosphorylation

Nuclear receptors (NR) impact a myriad of physiological processes including homeostasis, reproduction, development, and metabolism. NRs are regulated by post-translational modifications (PTM) that markedly impact receptor function. Recent studies have identified NR PTMs that are involved in the onset and progression of human diseases, including cancer. The majority of evidence linking NR PTMs with disease has been demonstrated for phosphorylation, acetylation and sumoylation of androgen receptor (AR), estrogen receptor α (ERα), glucocorticoid receptor (GR) and peroxisome proliferator activated receptor γ (PPARΓ). Phosphorylation of AR has been associated with hormone refractory prostate cancer and decreased disease-specific survival. AR acetylation and sumoylation increased growth of prostate cancer tumor models. AR phosphorylation reduced the toxicity of the expanded polyglutamine AR in Kennedy's Disease as a consequence of reduced ligand binding. A comprehensive evaluation of ERα phosphorylation in breast cancer revealed several sites associated with better clinical outcome to tamoxifen therapy, whereas other phosphorylation sites were associated with poorer clinical outcome. ERα acetylation and sumoylation may also have predictive value for breast cancer. GR phosphorylation and acetylation impact GR responsiveness to glucocorticoids that are used as anti-inflammatory drugs. PPARγ phosphorylation can regulate the balance between growth and differentiation in adipose tissue that is linked to obesity and insulin resistance. Sumoylation of PPARγ is linked to repression of inflammatory genes important in patients with inflammatory diseases. NR PTMs provide an additional measure of NR function that can be used as both biomarkers of disease progression, and predictive markers for patient response to NR-directed treatments.

Dexamethasone decreases the autotaxin‐lysophosphatidate‐inflammatory axis in adipose tissue: implications for the metabolic syndrome and breast cancer

2018 ◽  
Vol 33 (2) ◽  
pp. 1899-1910 ◽  
Author(s):  
Guanmin Meng ◽  
Xiaoyun Tang ◽  
Zelei Yang ◽  
Yuan Yuan Zhao ◽  
Jonathan M. Curtis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
The Metabolic Syndrome

scholarly journals Lipogranulomas of the mammary glands: diagnosis and treatment

2021 ◽  
Vol 70 (2) ◽  
Author(s):  
Natalia Cara ◽  
◽  
Veronica Svet ◽  
Ion Mereuta ◽  
◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Mammary Gland ◽  
Inflammatory Process ◽  
Pathological Condition ◽  
Scar Tissue ◽  
Mammary Glands ◽  
Diagnosis And Treatment ◽  
Breast Lesions ◽  
Fat Necrosis

Steatonecrosis of the mammary gland is necrosis of its adipose tissue, followed by replacement with scar tissue. Lipogranuloma is known as a benign inflammatory process, necrosis of breast fat occurs due to iatrogenic breast trauma. Most often, fatty necrosis is seen in women with large breasts – in women with small breasts, it develops much less often. It is important to diagnose lipogranulomas because it can often mimic breast cancer. Fat necrosis of the breast is a common pathological condition, with a wide variety of presentations on mammography, ultrasound and MRI. The incidence of fatty necrosis of the breast is estimated at 0.6%, representing 2.75% of all breast lesions.

scholarly journals Obesity and Breast Cancer: The Role of Crown-Like Structures in Breast Adipose Tissue in Tumor Progression, Prognosis, and Therapy

2020 ◽  
Vol 23 (3) ◽  
pp. 233 ◽  
Author(s):  
Sara Socorro Faria ◽  
Luís Henrique Corrêa ◽  
Gabriella Simões Heyn ◽  
Lívia Pimentel de Sant'Ana ◽  
Raquel das Neves Almeida ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Tumor Progression ◽  
Breast Adipose Tissue ◽  
Breast Adipose

scholarly journals The effect of adipocyte–macrophage crosstalk in obesity-related breast cancer

2019 ◽  
Vol 62 (3) ◽  
pp. R201-R222 ◽  
Author(s):  
Ayse Basak Engin ◽  
Atilla Engin ◽  
Ipek Isik Gonul
Keyword(s):  
Breast Cancer ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Cancer Cells ◽  
Inflammatory Cytokines ◽  
Breast Cancer Cells ◽  
Sirtuin 1 ◽  
Aromatase Activity ◽  
Breast Adipose Tissue ◽  
Mtorc1 Signaling

Adipose tissue is the primary source of many pro-inflammatory cytokines in obesity. Macrophage numbers and pro-inflammatory gene expression are positively associated with adipocyte size. Free fatty acid and tumor necrosis factor-α involve in a vicious cycle between adipocytes and macrophages aggravating inflammatory changes. Thereby, M1 macrophages form a characteristic ‘crown-like structure (CLS)’ around necrotic adipocytes in obese adipose tissue. In obese women, CLSs of breast adipose tissue are responsible for both increase in local aromatase activity and aggressive behavior of breast cancer cells. Interlinked molecular mechanisms between adipocyte–macrophage–breast cancer cells in obesity involve seven consecutive processes: Excessive release of adipocyte- and macrophage-derived inflammatory cytokines, TSC1–TSC2 complex–mTOR crosstalk, insulin resistance, endoplasmic reticulum (ER) stress and excessive oxidative stress generation, uncoupled respiration and hypoxia, SIRT1 controversy, the increased levels of aromatase activity and estrogen production. Considering elevated risks of estrogen receptor (E2R)-positive postmenopausal breast cancer growth in obesity, adipocyte–macrophage crosstalk is important in the aforementioned issues. Increased mTORC1 signaling in obesity ensures the strong activation of oncogenic signaling in E2Rα-positive breast cancer cells. Since insulin and insulin-like growth factors have been identified as tumor promoters, hyperinsulinemia is an independent risk factor for poor prognosis in breast cancer despite peripheral insulin resistance. The unpredictable effects of adipocyte-derived leptin–estrogen–macrophage axis, and sirtuin 1 (SIRT1)–adipose-resident macrophage axis in obese postmenopausal patients with breast cancer are unresolved mechanistic gaps in the molecular links between the tumor growth and adipocytokines.

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