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butyl phthalate/tumore della mammella
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 24 risultati
Benzyl butyl phthalate increases the chemoresistance to doxorubicin/cyclophosphamide by increasing breast cancer-associated dendritic cell-derived CXCL1/GROα and S100A8/A9.
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Phthalates are used as plasticizers in the manufacture of flexible vinyl, which is used in food contact applications. Phthalates have been demonstrated to have an adverse impact on human health, particularly in terms of cancer development. In the present study, we showed for the first time that
Inhibitory effect of silver nanoparticles on proliferation of estrogen-dependent MCF-7/BUS human breast cancer cells induced by butyl paraben or di-n-butyl phthalate.
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In this study the effect of silver nanoparticles (AgNPs) on proliferation of estrogen receptor (ER)-positive human breast cancer MCF-7/BUS cells was assessed by means of in vitro assay. The cells were exposed in the absence of estrogens to AgNPs alone or in combination with aluminum chloride
Benzyl butyl phthalate promotes breast cancer stem cell expansion via SPHK1/S1P/S1PR3 signaling.
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Understanding the regulatory mechanisms unique to breast cancer stem cells (BCSCs) is required to control breast cancer metastasis. We found that phthalates promote BCSCs in human breast cancer cell cultures and xenograft tumors. A toxic phthalate, benzyl butyl phthalate (BBP), activated aryl
Xenoestrogens down-regulate aryl-hydrocarbon receptor nuclear translocator 2 mRNA expression in human breast cancer cells via an estrogen receptor alpha-dependent mechanism.
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Environmental chemicals with estrogenic activity, known as xenoestrogens, may cause impaired reproductive development and endocrine-related cancers in humans by disrupting endocrine functions. Aryl-hydrocarbon receptor nuclear translocator 2 (ARNT2) is believed to play important roles in a variety
Combined effect of silver nanoparticles and aluminium chloride, butylparaben or diethylphthalate on the malignancy of MDA-MB-231 breast cancer cells and tumor-specific immune responses of human macrophages and monocyte-derived dendritic cells.
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The aim of this study was to assess whether silver nanoparticles (AgNP) or selected cosmetic ingredients may modify functions of various immunocompetent cell populations. To this end, the effect of two AgNP (size of 15 nm or 45 nm), alone and in combination with aluminium chloride, butyl paraben,
Xenoestrogens modulate vascular endothelial growth factor secretion in breast cancer cells through an estrogen receptor-dependent mechanism.
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Environmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an
PPARγ and PPARGC1B polymorphisms modify the association between phthalate metabolites and breast cancer risk.
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BACKGROUND
Breast cancer (BC) risk has been differentially associated with urinary levels of some phthalate metabolites.
OBJECTIVE
To investigate whether PPARγ and PPARGC1B polymorphisms modulate these associations.
METHODS
208 BC cases were age-matched with 220 population controls. Phthalate
The effects of bisphenol A, benzyl butyl phthalate, and di(2-ethylhexyl) phthalate on estrogen receptor alpha in estrogen receptor-positive cells under hypoxia.
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Endocrine-disrupting chemicals (EDCs) are widely used in various consumer goods. Consequently, humans are constantly exposed to EDCs, which is associated with a variety of endocrine-related diseases. In this study, we demonstrated the effects of bisphenol A (BPA), benzyl butyl phthalate (BBP), and
Lower concentrations of phthalates induce proliferation in human breast cancer cells.
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OBJECTIVE
To explore the effect and pathway of phthalates on the growth of MCF-7 breast cancer cells.
METHODS
MCF-7 cells were treated with benzyl butyl phthalate (BBP), di-n-butyl phthalate (DBP), and di-2-ethylhexyl phthalate (DEHP) (10(-10)-10(-4) mol/l). After incubation for 24, 48, 72, and 92
Phthalates inhibit tamoxifen-induced apoptosis in MCF-7 human breast cancer cells.
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Environmental estrogens represent a class of compounds that can mimic the function or activity of the endogenous estrogen 17 -estradiol (E2). Phthalates including butyl benzyl phthalate (BBP), di(n-butyl) phthalate (DBP), and di(2-ethylhexyl) phthalate (DEHP) are used as plasticizers, and also
Impact of low concentrations of phthalates on the effects of 17β-estradiol in MCF-7 breast cancer cells.
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OBJECTIVE
To explore whether lower concentrations of phthalates interfere with the effects of 17β-estradiol on the growth of MCF-7 breast cancer cells.
METHODS
MCF-7 cells were treated with 17β-estradiol (E2), phthalates, including butyl benzyl phthalate (BBP), di(n-butyl) phthalate (DBP), and
Didymin reverses phthalate ester-associated breast cancer aggravation in the breast cancer tumor microenvironment.
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The present study demonstrated two novel findings. To the best of our knowledge, it is the first study to demonstrate that regulated upon activation, normal T-cell expressed and secreted (RANTES), produced by breast tumor-associated monocyte-derived dendritic cells (TADCs) following breast cancer
Mono(2-ethylhexyl)phthalate and mono-n-butyl phthalate activation of peroxisome proliferator activated-receptors alpha and gamma in breast.
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The phthalates di(2-ethylhexyl)phthalate (DEHP) and di-n-butyl phthalate (DBP) are environmental contaminants with significant human exposures. Both compounds are known reproductive toxins in rodents and DEHP also induces rodent hepatocarcinogenesis in a process believed to be mediated via the
Breast cancer is associated with methylation and expression of the a disintegrin and metalloproteinase domain 33 (ADAM33) gene affected by endocrine‑disrupting chemicals.
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A disintegrin and metalloproteinase domain 33 (ADAM33) gene is a transmembrane glycoprotein that mediates changes in cell adhesion and plays an important role in cancer progression. Since bisphenol A (BPA) and phthalates are epigenetically toxic, the purpose of this study was to examine whether BPA
Environmental estrogen-like endocrine disrupting chemicals and breast cancer.
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BACKGROUND
Estrogen-mimicking endocrine disruptors (EEDs) such as polychlorinated biphenyls (PCBs), bisphenol A (BPA), and phthalates have been found ubiquitously throughout our environment. Although exposure to EEDs has the ability to interfere with endocrine control of reproductive function and
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