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A glucose-targeted mixed micellar formulation outperforms Genexol in breast cancer cells.

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Breast cancer represents the top cancer among women, accounting 521.000 deaths per year. Development of targeted nanomedicines to breast cancer tissues represents a milestone to reduce chemotherapy side effects. Taking advantage of the over-expression of glucose (Glu) membrane transporters in breast

Safe chemotherapy and hormone therapy for treating early breast cancer in a glucose 6-phosphate dehydrogenase-deficient patient: case report.

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Breast cancer is the leading cause of neoplasia-related deaths among women, but no data are available in the literature on the safe use of oncological treatments in glucose 6-phosphate dehydrogenase (G6PD)-deficient patients. This case report describes, for the first time, the treatment of a

Safe neoadjuvant trastuzumab-based treatment in HER2 + inflammatory early breast cancer in a glucose 6-phosphate dehydrogenase-deficient postmenopausal woman: A case report and review of the literature.

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Glucose 6-phosphate dehydrogenase (G6PD) is a basic antioxidant pathway for erythrocytes, being its deficiency the most common gene mutation worldwide. As breast cancer is one of the most frequent tumors, many of these patients may present with G6PD deficiency prior treatment without

Corrigendum to ''A glucose-targeted mixed micellar formulation outperforms Genexol in breast cancer cells'' [Euro. J. Pharmaceut. Biopharmaceut. 114 (2017) 305-316].

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Prolactin-Stat5 signaling in breast cancer is potently disrupted by acidosis within the tumor microenvironment.

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BACKGROUND Emerging evidence in estrogen receptor-positive breast cancer supports the notion that prolactin-Stat5 signaling promotes survival and maintenance of differentiated luminal cells, and loss of nuclear tyrosine phosphorylated Stat5 (Nuc-pYStat5) in clinical breast cancer is associated with

Insulin resistance, growth factors and cytokine levels in overweight women with breast cancer before and after chemotherapy.

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OBJECTIVE To evaluate insulin values, insulin resistance, growth factors and cytokine levels in women suffering from breast cancer and the effect of chemotherapy on these parameters. METHODS In a prospective study, glucose and insulin values were determined in ten previously undiagnosed diabetic

Interleukin-6 upregulates GP96 expression in breast cancer.

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Interleukin-6 is associated with poor prognosis in breast cancer. Expression of GP96, a glucose regulated stress protein, is related to drug resistance in tumor cells. Interleukin-6 has previously been shown to induce GP96 expression in a murine myeloblastic cell line. BT474 or MDA-MB231 cells were

Lack of metformin effects on different molecular subtypes of breast cancer under normoglycemic conditions: an in vitro study.

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BACKGROUND In the past few years, a considerable number of preclinical studies have been proposed metformin as a potential anticancer agent, but some of these studies suffer from a number of methodological limitations such as assessment of cytotoxicity in the presence of supraphysiological glucose

Comparison of action of the anti-neoplastic drug lonidamine on drug-sensitive and drug-resistant human breast cancer cells: 31P and 13C nuclear magnetic resonance studies.

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Lonidamine (LND) is a relatively new anti-cancer drug, and several clinical trials have indicated that it may be effective in combinations with other therapeutic modalities. LND is classified within the metabolic inhibitor agents. Multidrug resistance (MDR) phenomenon is often associated with

Selective estrogen receptor modulator: A novel polysaccharide from Sparganii Rhizoma induces apoptosis in breast cancer cells.

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A polysaccharide named SpaTA, as novel selective estrogen receptor modulator, was isolated from water extraction of traditional Chinese herbal medicine Sparganii Rhizoma. SpaTA had a backbone consisting of 2-O-grailsine-β-xylose (4→6)-α-glucose (1→4) -β-mannose osamine. There is an aluminium element

The anti-proliferative effect of metformin in triple-negative MDA-MB-231 breast cancer cells is highly dependent on glucose concentration: implications for cancer therapy and prevention.

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BACKGROUND Metformin has been shown to have a strong anti-proliferative effect in many breast cancer cell lines, mainly due to the activation of the energy sensing kinase, AMP-activated protein kinase (AMPK). MDA-MB-231 cells are aggressive and invasive breast cancer cells that are known to be

p300 and p53 levels determine activation of HIF-1 downstream targets in invasive breast cancer.

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In previous studies, we noted that overexpression of hypoxia-inducible factor (HIF)-1alpha in breast cancer, especially the diffuse form, does not always lead to functional activation of its downstream genes. Transcriptional activity of HIF-1 may be repressed by p53 through competition for

2-Deoxy-D-Glucose inhibits aggressive triple-negative breast cancer cells by targeting glycolysis and the cancer stem cell phenotype.

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Due to limited availability of pharmacological therapies, triple-negative breast cancer (TNBC) is the subtype with worst outcome. We hypothesised that 2-Deoxy-D-Glucose (2-DG), a glucose analogue, may hold potential as a therapy for particularly aggressive TNBC. We investigated 2-DG's effects on

Is Lactate an Oncometabolite? Evidence Supporting a Role for Lactate in the Regulation of Transcriptional Activity of Cancer-Related Genes in MCF7 Breast Cancer Cells.

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Lactate is a ubiquitous molecule in cancer. In this exploratory study, our aim was to test the hypothesis that lactate could function as an oncometabolite by evaluating whether lactate exposure modifies the expression of oncogenes, or genes encoding transcription factors, cell division, and cell

Glucose impairs tamoxifen responsiveness modulating connective tissue growth factor in breast cancer cells.

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Type 2 diabetes and obesity are negative prognostic factors in patients with breast cancer (BC). We found that sensitivity to tamoxifen was reduced by 2-fold by 25 mM glucose (High Glucose; HG) compared to 5.5 mM glucose (Low Glucose; LG) in MCF7 BC cells. Shifting from HG to LG ameliorated MCF7

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