breast cancer

Promising cytotoxic activity profile of fermented wheat germ extract (Avemar®) in human cancer cell lines

Avemar is a fermented wheat germ extract with potent antimetastatic, antiproliferative and immunomodulatory activities. Chemically, it is a complex mixture of biologically active molecules including 2-methoxy-p-benzoquinone and 2,6-dimethoxy-p-benzoquinone which were supposed to be responsible for the main biological properties of Avemar. Despite its ubiquitous use as nutrition supplement for cancer patients in some countries only limited data are available on its activity in human cancer or in combination with chemotherapy.

Avemar Inhibits the Growth of Mouse and Human Xenograft Mammary Carcinomas Comparable To Endocrine Treatments

Background: An in vitro study demonstrated that Avemar increased the effect of Tamoxifen on MCF7 (ER+) mammary carcinoma cells. Methods: MXT (ER+) mouse mammary tumor tissue was transplanted s.c. into BDF1 mice. The tumor bearing animals were treated p.o. with Avemar. Then the most effective Avemar dose (3.0 g/kg), Tamoxifen (0.5 mg/kg s.c.), Examestane (10 mg/kg i.p.) and Anastrasol (5 mg/kg i.p.) monotherapies and their combinations with Avemar was compared. All treatments were given once daily, for 10 days, starting 7 days after the tumor transplantation.

The efficacy of tamoxifen in estrogen receptor-positive breast cancer cells is enhanced by a medical nutriment

Avemar, a fermented wheat germ extract, has been applied in the supplementary therapy of human cancers. Because tamoxifen is commonly used in the therapy of ER+ breast cancer, in this study the combined effect of tamoxifen and Avemar treatment was investigated on MCF-7 breast cancer cells, in order to detect a possible agonistic or antagonistic action.

Chemoprevention with Tamoxifen and Avemar by inducing apoptosis on MCF-7 (ER+) Breast cancer cells

In the present study the combined effect of in vitro tamoxifen and Avemar treatment was studied on MCF-7 (ER+) breast cells as a model of a breast cancer situation. Cells were transformed for 24, 48 and 72 hours, cytotoxicity was measured by MTT assay, the percentage of apoptosis and cell proliferation was determined by flow cytometry, hematoxilin/cosin staining and by immunochemistry using the ApopTag reaction. Estrogen receptor activation was studied by semi-quantitative determination of the estrogen-responsive pS2 gene mRNA production.

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