Group items tagged

It was concluded that omega-3 fatty acid could inhibit the proliferation of pancreatic cancer cell line SW1990 cells and promote their apoptosis. The down-regulation of the cyclin E expression by omega-3 fatty acid might be one of the mechanisms for its anti-tumor effect on pancreatic cancer. \n\nModulatory effects of EPA and DHA on proliferation and apoptosis of pancreatic cancer cells.\nZhang W, Long Y, Zhang J, Wang C.\nJ Huazhong Univ Sci Technolog Med Sci. 2007 Oct;27(5):547-50.\nPMID: 18060632

Scroll past the 20 photos on foodborne illness to reach the "Anti-Cancer Diet" Photos. Truly worth the effort

"There are very few large, well-designed human studies testing the health effects of DHEA supplements. For example, there is not enough scientific evidence to rate the effectiveness of DHEA supplements in treating adrenal insufficiency, metabolic syndrome, depression, HIV/AIDS, Addison's disease, chronic fatigue syndrome, menopausal symptoms, heart disease, breast cancer, infertility, diabetes, or Parkinson's disease according to the National Institutes of Health (NIH). In addition, there isn't enough evidence to support the use of DHEA supplements as an anti-aging remedy or weight-loss aid. The NIH also cautions that DHEA supplements appear to be ineffective for boosting libido, enhancing muscle strength in elderly people, protecting against Alzheimer's disease and improving thinking in healthy older people."

Anticancer properties of oxidation products of docosahexaenoic acid.\nSiddiqui RA, Harvey K, Stillwell W.\nChem Phys Lipids. 2008 May;153(1):47-56. Epub 2008 Feb 23. Review.\nPMID: 18343223

The precise mechanism of the anti-tumor effect of imiquimod in BCC is not known. It has been postulated that ultraviolet radiation induces mutations in the tumor-suppressor genes and alters the immuno-surveillance, so that tumor cells escape from cytotoxic T cells and apoptosis.[1] Th-2 cytokines, that downregulate tumor surveillance, are raised in BCC.[1],[5] Imiquimod acts on toll-like receptor-7 (TLR-7) present on dendritic cells, macrophages and monocytes and induces expression of interferons, Th-1 cytokines (IL-1, IL-6, IL-10 and IL-12), tumor necrosis factor-a and G-CSF, thereby counteracting Th2 cytokines and promoting tumor surveillance.[1],[5] It also enhances the activity of natural killer cells and epidermal Langerhans' cells. The tumor regression is achieved probably by induction of Fas receptors on the tumor cells resulting in their apoptosis.[10]