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ascorbic acid/breast neoplasms

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Ascorbic acid and cell survival of adriamycin resistant and sensitive MCF-7 breast tumor cells.

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The ability of human cells to regenerate ascorbic acid from dehydroascorbate is partially dependent on the glutathione redox status of the cell and the relative activity of dehydroascorbate reductases. Mammalian dehydroascorbate reductase activity is associated with two proteins known as

Ascorbic acid supplementation and five year survival rates in women with early breast cancer.

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The effect of long term ascorbic acid (AA) supplementation (3g per day) on 27 women with early breast cancer has been investigated. For comparison a similar but limited study was carried out in patients with benign breast disease. The responses of leucocyte levels of AA to supplementation provided
The levels of ascorbic acid in plasma and in blood cells (erythrocytes, neutrophils, and platelets) was studied in a group of 30 women with recent onset of breast cancer, and they were compared with a group of 30 healthy women, thus establishing the possible correlations between them. At the same

A prospective study of plasma ascorbic acid concentrations and breast cancer (United States).

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OBJECTIVE To investigate the association between prediagnostic plasma ascorbic acid concentrations and subsequent breast cancer risk in a nested case-control study. METHODS Female volunteer residents of Washington County, MD, donated 14,625 non-fasting blood samples in 1989. Incident breast cancer
Current treatments are generally ineffective once breast cancer has metastasized; median survival is reduced to 2-3 yr. Previous research studies demonstrating potent synergistic antitumor activity of lysine, proline, ascorbic acid, and epigallocatechin gallate prompted us to investigate the in vivo

Potassium increases the antitumor effects of ascorbic acid in breast cancer cell lines in vitro.

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Ascorbic acid (A) has been demonstrated to exhibit anti-cancer activity in association with chemotherapeutic agents. Potassium (K) is a regulator of cellular proliferation. In the present study, the biological effects of A and K bicarbonate, alone or in combination (A+K), on breast cancer cell lines
Many studies have demonstrated that the extracellular domain of human epidermal growth factor receptor 2 (HER2 ECD) level in serum can act as a breast cancer biomarker and serve in monitoring neoadjuvant therapy of breast cancer. In this study, we developed a sensitive ascorbic acid (AA)-mediated
Anticancer effects of L-ascorbic acid (Vitamin C, L-AA) have been reported in various types of cancers. L-AA intake reduces breast cancer recurrence and mortality; however, the role of L-AA in the treatment of breast cancer remains poorly understood. In this study, we investigated the effect and
Breast cancer is characterized by overexpression of superoxide dismutase (SOD) and downregulation of catalase and more resistance to hydrogen peroxide (H2O2) than normal cells. Thus, relatively high H2O2 promotes breast cancer cell growth and proliferation. However, excessive intracellular H2O2

Retinoic acid and ascorbic acid act synergistically in inhibiting human breast cancer cell proliferation.

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BACKGROUND Breast cancer is an increasingly common malignancy. Several vitamins such as retinoic acid (RA), ascorbic acid (AA), vitamin D and vitamin E are known to prevent the development and progression of breast cancer. OBJECTIVE We sought to determine whether RA and AA together (RA+AA) acted
The potential role of vitamin C in cancer prevention and treatment remains controversial. While normal human cells obtain vitamin C as ascorbic acid, the prevalent form of vitamin C in vivo, the uptake mechanisms by which cancer cells acquire vitamin C has remained unclear. The aim of this study is

Ascorbic acid and glutathione content in human breast cancer tissue.

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[Serum concentrations of vitamins A, E and ascorbic acid in premenopausal and postmenopausal women with breast cancer].

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Leucocyte ascorbic acid and urinary hydroxyproline levels in patients bearing breast cancer with skeletal metastases.

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