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glucose 6 phosphate dehydrogenase/рак на гърдата

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[Glutathione-dependent enzymes and glucose-6-phosphate dehydrogenase in breast tumors].

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The authors made a comparative analysis of the activity of antioxidative enzymes and a search for a possible relationship between the activity of glutathione reductase and that of glucose-6-phosphate dehydrogenase in the blood and saliva of patients with breast tumors with varying activity of the

Stimulatory effect of 1,25-dihydroxyvitamin D3 on the glucose-6-phosphate dehydrogenase activity in the MCF-7 human breast cancer cell line.

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Human breast cancer cell lines have been shown to possess high affinity receptors for 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and their growth is inhibited by this steroid. The present study examines the effect of 1,25(OH)2D3 on the activity of glucose-6-phosphate dehydrogenase (G6PD) in cells of a

Glucose-6-phosphate dehydrogenase activity in human breast cancer. Lack of association with oestrogen receptor content.

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The correlation between glucose-6-phosphate dehydrogenase activity and different tumour characteristics was investigated in human breast cancer tissue. The enzyme activity was measured by a histochemical method and the oestrogen receptor content by a dextran-coated charcoal assay. The proliferative

Relative value of oestrogen receptor assay, lactoferrin content, and glucose-6-phosphate dehydrogenase activity as prognostic indicators in primary breast cancer.

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Oestrogen receptor content, lactoferrin, hexokinase, and glucose-6-phosphate dehydrogenase levels were measured in cytosol from 25 primary breast cancers and 3 fibroadenomas. Both hexokinase and glucose-6-phosphate dehydrogenase activity were higher in malignant tissue as compared to benign breast

[A study on the relationship among estrogen receptor, progesterone receptor and glucose-6-phosphate dehydrogenase activity in primary breast cancer].

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The relationships among estrogen receptor (ER), progesterone receptor (PgR) and glucose-6-phosphate dehydrogenase (G6PD) activity demonstrated by histochemical technique were studied in 85 cases of primary breast cancer. The ER positive rate was 71.8% and the PgR positive rate was 54.1%. A close

Effects of 17 beta-estradiol and R5020 on glucose-6-phosphate dehydrogenase activity in MCF-7 human breast cancer cells: a cytochemical assay.

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Although increasing levels of glucose-6-phosphate dehydrogenase (G6PD) have been widely reported in human breast tumor tissue, the effects of 17 beta-estradiol and progesterone on this key enzyme of cellular growth processes have not been well documented. Cellular heterogeneity of breast tumor

Role of glucose-6-phosphate dehydrogenase inhibition in the antiproliferative effects of dehydroepiandrosterone on human breast cancer cells.

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Epidemiological and experimental studies suggest that dehydroepiandrosterone (DHEA) exerts a protective effect against breast cancer. It has been proposed that the non-competitive inhibition of glucose-6-phosphate dehydrogenase (G6PD) contributes to DHEA antitumor action. We evaluated the effects of

Histochemical studies of human breast tumors: Activity of alkaline phosphatase, acid phosphatase and glucose-6-phosphate dehydrogenase.

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Histochemical studies of human breast tumors were performed with particular emphasis on the activity of alkaline phosphatase (AIP), acid phosphatase (AcP) and glucose-6-phosphate dehydrogenase (G6PDH). Enzyme activities in benign and malignant lesions were compared. AIP was prominent in normal

Estradiol receptors and glucose-6-phosphate dehydrogenase activity in human breast tumors.

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Estradiol receptors and glucose-6-phosphate dehydrogenase, an enzyme induced by estrogens, were measured in both benign and malignant human breast tumors. The mean glucose-6-phosphate dehydrogenase activity was higher in the malignant tumors than in the benign tumors. Tumors containing estradiol

Glucose-6-phosphate dehydrogenase activity and estrogen receptors in human breast cancer.

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Both estradiol receptors and glucose-6-phosphate dehydrogenase activity (G6PDH) were measured on the same tissue sample from 143 patients who had undergone mastectomy for primary breast cancer. G6PDH activity in the estrogen receptor positive group (ER+) was higher than in the negative one (ER-).

Quantitative cytochemistry of glucose-6-phosphate dehydrogenase in benign and malignant breast tumours.

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Glucose-6-phosphate dehydrogenase (G6PD) activity was quantified cytochemically in mammary epithelial cells within frozen tissue sections from 38 patients with breast cancer and 44 with benign breast disease. G6PD activities were measured under atmospheres of both N2 and O2. The mean (S.E.) G6PD

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

Treatment of a patient with breast cancer and glucose 6-phosphate dehydrogenase deficiency: A case report.

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Glucose 6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymatic disorder of red blood cells that cause hemolytic anemia. Some anticancer drugs are reported to trigger oxidative stress; however, events of hemolysis are rarely discussed in patients with G6PD deficiency

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

Glucose-6-phosphate dehydrogenase and transketolase modulate breast cancer cell metabolic reprogramming and correlate with poor patient outcome.

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The pentose phosphate pathway is a fundamental metabolic pathway that provides cells with ribose and NADPH required for anabolic reactions - synthesis of nucleotides and fatty acids - and maintenance of intracellular redox homeostasis. It plays a key role in tumor metabolic reprogramming and has
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