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glutamine/meme kanseri

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Sayfa 1 itibaren 314 Sonuçlar

Diverse Roads Taken by 13C-Glucose-Derived Metabolites in Breast Cancer Cells Exposed to Limiting Glucose and Glutamine Conditions.

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In cancers, tumor cells are exposed to fluctuating nutrient microenvironments with limiting supplies of glucose and glutamine. While the metabolic program has been related to the expression of oncogenes, only fractional information is available on how variable precarious nutrient concentrations

Glutamine suppresses PGE2 synthesis and breast cancer growth.

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Reduced natural killer (NK) activity found in tumor-bearing hosts has been associated with high levels of prostaglandin E2 (PGE2) produced by monocytes in vitro. We have previously demonstrated a dependence of NK cell activity on glutamine (GLN) levels in vitro and in vivo. Further, glutathione

The AIB1 glutamine repeat polymorphism is not associated with risk of breast cancer before age 40 years in Australian women.

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BACKGROUND AIB1, located at 20q12, is a member of the steroid hormone coactivator family. It contains a glutamine repeat (CAG/CAA) polymorphism at its carboxyl-terminal region that may alter the transcriptional activation of the receptor and affect susceptibility to breast cancer through altered
OBJECTIVE To evaluate the effects of oral administration of GLN on the oxidative stress in women with breast cancer undergoing neoadjuvant FAC chemotherapy (5 fluouracil 500 mg/m²+Doxorubicin 50 mg/m²+Cyclophosphamide 500 mg/m² body surface area). METHODS Twenty women (mean age: 51.7 years) with

Complement susceptibility in glutamine deprived breast cancer cells.

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BACKGROUND Membrane complement regulatory proteins (mCRPs) inhibit complement-mediated killing of human cells by human complement, a property that confers protection from complement to malignant breast cancer cells and that thwarts some immunotherapies. Metabolic mechanisms may come into play in

Glutamine-β-cyclodextrin for targeted doxorubicin delivery to triple-negative breast cancer tumors via the transporter ASCT2.

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Chemotherapy is the primary therapy for triple-negative breast cancer (TNBC) and the tumor-targeted delivery of chemotherapeutic drugs is necessary to minimize their side effects on normal tissues. TNBC cells display addictions to glutamine in culture, and the levels of the glutamine transporter,

Glutamine deprivation plus BPTES alters etoposide- and cisplatin-induced apoptosis in triple negative breast cancer cells.

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Glutamine provides cancer cells with the energy required to synthesize macromolecules. Methods which block glutamine metabolism in treatment of breast cancer inhibit oncogenic transformation and tumor growth. We investigated whether inhibiting glutamine metabolism produces effects that are

Glutamine affects glutathione recycling enzymes in a DMBA-induced breast cancer model.

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Malignancy depletes host glutathione (GSH) levels to increase treatment-related toxicity and increases itself to resist the treatments. Our previous studies have shown that dietary glutamine (GLN) prevented 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumors through enhancing gut GSH

The effects of enteral glutamine on radiotherapy induced dermatitis in breast cancer.

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OBJECTIVE Radiotherapy is a critical component of breast cancer treatment. Many skin reactions ranging from erythema to moist desquamation and ulceration can be induced by high dose external beam radiotherapy. There is no golden standard for treating radiation dermatitis. Glutamine is an amino acid
OBJECTIVE Sixty patients with breast cancer were randomly assigned to oral glutamine or placebo pre-neoadjuvant chemotherapy (CEF regimen). METHODS Oral glutamine supplementation was continued for at least 12 days. Patients kept a daily record of diarrhea and stomatitis. The plasma glutamine level,

Targeted poly (L-γ-glutamyl glutamine) nanoparticles of docetaxel against folate over-expressed breast cancer cells.

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A novel folate (FA) conjugated poly(l-γ-glutamyl glutamine) (PGG) nanoparticle loaded with docetaxel (DTX) was prepared to take advantage of both targeted drug delivery in breast cancer and reducing the overall side effects due to the adjuvant free formulation in comparison with Taxotere(®).

RhoC GTPase Is a Potent Regulator of Glutamine Metabolism and N-Acetylaspartate Production in Inflammatory Breast Cancer Cells.

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Inflammatory breast cancer (IBC) is an extremely lethal cancer that rapidly metastasizes. Although the molecular attributes of IBC have been described, little is known about the underlying metabolic features of the disease. Using a variety of metabolic assays, including (13)C tracer experiments, we

Oral glutamine (AES-14) supplementation inhibits PI-3k/Akt signaling in experimental breast cancer.

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BACKGROUND 7,12-dimethylbenz [a] anthracene (DMBA) administration to pubertal rats causes breast tumors and inhibits glutathione (GSH) production. Our previous results have established that oral glutamine (GLN) supplementation significantly reduced tumor development, restored the depressed GSH

Effect of dietary glutamine on tumor glutathione levels and apoptosis-related proteins in DMBA-induced breast cancer of rats.

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Glutamine (GLN) is a non-essential amino acid that is present in nearly every biochemical pathway and is the major intraorgan nitrogen carrier. GLN via glutamate, is one of the precursors for the synthesis of glutathione (GSH), the major endogenous antioxidant in mammalian cells, which protects them

The Ephrin-A1/EPHA2 Signaling Axis Regulates Glutamine Metabolism in HER2-Positive Breast Cancer.

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Dysregulation of receptor tyrosine kinases (RTK) contributes to cellular transformation and cancer progression by disrupting key metabolic signaling pathways. The EPHA2 RTK is overexpressed in aggressive forms of breast cancer, including the HER2(+) subtype, and correlates with poor prognosis.
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