Oncology Commons^™

High Dietary Level Of Synthetic Vitamin E On Lipid Peroxidation, Membrane Fatty Acid Composition And Cytotoxicity In Breast Cancer Xenograft And In Mouse Host Tissue, Ivan L. Cameron, Jesus Munoz, Christopher J. Barnes, W. Elaine Hardman

Biochemistry and Microbiology

Background

d-α-tocopherol is a naturally occurring form of vitamin E not previously known to have antitumor activity. Synthetic vitamin E (sE) is a commonly used dietary supplement consisting of a mixture of d-α-tocopherol and 7 equimolar stereoisomers. To test for antilipid peroxidation and for antitumor activity of sE supplementation, two groups of nude mice bearing a MDA-MB 231 human breast cancer tumor were fed an AIN-76 diet, one with and one without an additional 2000 IU/kg dry food (equivalent to 900 mg of all-rac-α-tocopherol or sE). This provided an intake of about 200 mg/kg body weight per day. The mice …

Synergistic Interactions Of Chlorambucil, Dha, And Trail In Jurkat And H460 Human Cancer Cells, Jennifer Ellen Bush-O'Donnell

Theses, Dissertations and Capstones

Traditional chemotherapeutic drugs are prone to toxicity and may result in secondary cancers. In recent years much attention has been garnered by alternate methods of cancer treatment with fewer side effects, including immunotherapy and administration of ω-3 fatty acids, both of which have been shown to cause apoptosis in cancer cells. Docosahexaenoic acid (DHA), a fatty acid, is a normal component of cell membranes and is safe for systemic administration. The cytokine TRAIL (tumor necrosis factorrelated apoptosis-inducing ligand) is able to induce apoptosis in cancer cells while sparing normal tissue. In this study, the alkylating agent chlorambucil (CLB) was combined …

The Role Of Ap-1 Transcription Complex In Retinoic Acid-Dependent B16 Melanoma Cell Growth Arrest And Differentiation, Ying Huang

Theses, Dissertations and Capstones

Our laboratory has been studying the effects of all-trans retinoic acid (atRA) on the growth and differentiation of the B16 mouse melanoma cells. RA inhibits both anchorage-dependent and –independent growth and stimulates melanin production in B16 cells, which are accompanied by an increase in AP-1 activity. To further investigate the RA-induced AP-1 activity, I established clones of B16 stably expressing an AP-1-luciferase reporter gene. Treatment of these clones with phorbol dibutyrate (PDB), a known activator of AP-1, rapidly increased AP-1 activity which reached its maximum level at 2-4 h and returned to baseline level by 24 h. In contrast, RA …