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Glutamate dehydrogenase (GLUD1) expression in breast cancer.

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BACKGROUND Dysregulated cellular metabolism is one of the hallmarks of cancer with some tumours utilising the glutamine metabolism pathway for their sustained proliferation and survival. Glutamate dehydrogenase (GLUD1) is a key enzyme in glutaminolysis converting glutamate to α-ketoglutarate for

Metabolic recycling of ammonia via glutamate dehydrogenase supports breast cancer biomass.

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Ammonia is a ubiquitous by-product of cellular metabolism; however, the biological consequences of ammonia production are not fully understood, especially in cancer. We found that ammonia is not merely a toxic waste product but is recycled into central amino acid metabolism to maximize nitrogen

[Correlation of glutamate dehydrogenase with several tumors].

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Most organisms contain glutamate dehydrogenase (E.C. 1.4.1.2-1.4.1.4). In eukaryotes, the enzyme is mainly present in mitochondria. This enzyme plays a vital role in the metabolism of nitrogen and carbon and the signaling pathway. Studies have found that glutamate dehydrogenase has a certain

Expression of the glutamine metabolism-related proteins glutaminase 1 and glutamate dehydrogenase in canine mammary tumours.

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Glutamine metabolism is an important metabolic pathway for cancer cell survival, and there is a critical connection between tumour growth and glutamine metabolism. Because of their similarities, canine mammary carcinomas are useful for studying human breast cancer. Accordingly, we investigated the

Proteomic Analysis of Stage-II Breast Cancer from Formalin-Fixed Paraffin-Embedded Tissues.

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Breast cancer is the most frequently occurring disease among women worldwide. The early stage of breast cancer identification is the key challenge in cancer control and prevention procedures. Although gene expression profiling helps to understand the molecular mechanism of diseases or disorder in

Blood and Tissue Enzymatic Activities of GDH and LDH, Index of Glutathione, and Oxidative Stress among Breast Cancer Patients Attending Referral Hospitals of Addis Ababa, Ethiopia: Hospital-Based Comparative Cross-Sectional Study.

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The exact cause of breast cancer is unknown; it is a multifactorial disease. It is the most diagnosed and the second killer cancer among women. Breast cancer can be originated from tissues of breast or secondary from other organs via metastasis. Generally, cancer cells show aberrant metabolism and

Expression of glutamine metabolism-related proteins according to molecular subtype of breast cancer.

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The aim of this study was to investigate the expression of glutamine metabolism-related proteins to determine whether glutamine is metabolized differently according to breast cancer molecular subtype. We generated a tissue microarray of 702 breast cancer patients and performed immunohistochemical

Allosteric regulation of glutamate dehydrogenase deamination activity

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Glutamate dehydrogenase (GDH) is a key enzyme interlinking carbon and nitrogen metabolism. Recent discoveries of the GDH specific role in breast cancer, hyperinsulinism/hyperammonemia (HI/HA) syndrome, and neurodegenerative diseases have reinvigorated interest on GDH regulation, which remains poorly

Site-specific metabolic phenotypes in metastatic breast cancer.

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BACKGROUND The purpose of this study was to examine the expression of metabolism-related proteins according to metastatic site in metastatic breast cancer and to assess the implication of site-specific differential expression. METHODS A tissue microarray containing 162 cases of metastatic breast

Decreased sirtuin 4 expression is associated with poor prognosis in patients with invasive breast cancer.

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Aberrant metabolism is a hallmark of human cancer. Glutamine metabolism has been identified as a central metabolic pathway in cancer and thus, targeting glutamine metabolism may exhibit therapeutic potential. Sirtuin 4 (SIRT4) is an important molecule that mediates the blockade of glutamine

Enzyme activities in human breast tumours.

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The activities of six enzymes associated with carbohydrate metabolism were measured both in carcinomas and in normal breast tissues. The following differences were observed. 1. The carcinoma showed higher enzyme activities than the normal mammary tissue. 2. The ratios of glutamate dehydrogenase,

The effect of the oral iron chelator deferiprone on the liver damage induced by tamoxifen in female rats.

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Tamoxifen (TAM) is a non-steroidal antiestrogen used in the treatment and prevention of hormone-dependent breast cancer. Tamoxifen therapy may be accompanied with hepatic injury and iron accumulation in this organ. The present study investigates the influence of the effective oral iron chelator,

CtBP maintains cancer cell growth and metabolic homeostasis via regulating SIRT4.

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Cancer cells rely on glycolysis to maintain high levels of anabolism. However, the metabolism of glucose via glycolysis in cancer cells is frequently incomplete and results in the accumulation of acidic metabolites such as pyruvate and lactate. Thus, the cells have to develop strategies to alleviate

Risk factors associated with Clostridium difficile infection in adult oncology patients.

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OBJECTIVE Clostridium difficile infection (CDI) prevention is particularly important for cancer patients, because diarrhea often results in dose reductions or delays of chemotherapy or radiotherapy. We conducted this study to better ascertain the incidence, susceptibility, and risk factors for CDI

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