Group items tagged

Changes of terminal cancer patients' health-related quality of life after high dose vitamin C administration.\nYeom CH, Jung GC, Song KJ.\nJ Korean Med Sci. 2007 Feb;22(1):7-11.\nPMID: 17297243

Differential effects of selenium on benign and malignant prostate epithelial cells: stimulation of LNCaP cell growth by noncytotoxic, low selenite concentrations. Kandaş NO, Randolph C, Bosland MC. Nutr Cancer. 2009;61(2):251-64. PMID: 19235042

For the first time, medical groups have issued guidelines that say healthy older men should consider taking a drug that may reduce their risk of developing prostate cancer, even if they're just among the worried well who go in for regular screenings.\n\nThe drug, finasteride, is already used to treat male pattern baldness and to shrink enlarged prostates. The new guidelines suggest that patients who are already taking finasteride for those conditions or who go for regular prostate cancer screening tests should discuss long-term treatment with the drug with their doctors.

A glass of wine each evening is enough to increase your risk of developing cancer, women are being warned.\nConsuming just one drink a day causes an extra 7,000 cancer cases - mostly breast cancer - in UK women each year, Cancer Research UK scientists say

ScienceDaily (Feb. 25, 2009) - Researchers at Purdue University have precisely measured the impact of a high-fat diet on the spread of cancer, finding that excessive dietary fat caused a 300 percent increase in metastasizing tumor cells in laboratory animals.

Vitamin D may not just be good for you, it may help save your life. Recent research from Johns Hopkins University suggests that higher amounts of vitamin D in your diet decreases your likelihood of dying. Studies found that a vitamin D deficiency increases your risk of death by 26 percent, and vitamin D decreases the mortality rate from almost every type of cancer including breast, colon and prostate. Research also suggests that vitamin D helps prevent diabetes, kidney disease and cardiovascular disease.

Extracts from blueberries may reduce the size of tumours primarily found in infants and children, and improve survival, suggest new findings from a study with mice. According to new results from the Ohio State University, mice fed the blueberry extract doubled their lifespan, and had tumours 60 per cent smaller that in control mice.

ScienceDaily (Feb. 22, 2009) - Cancer cells need a lot of nutrients to multiply and survive. While much is understood about how cancer cells use blood sugar to make energy, not much is known about how they get other nutrients. Now, researchers at the Johns Hopkins University School of Medicine have discovered how the Myc cancer-promoting gene uses microRNAs to control the use of glutamine, a major energy source. The results, which shed light on a new angle of cancer that might help scientists figure out a way to stop the disease, appear Feb. 15 online at Nature

Preoperative treatment with a non-steroidal anti-inflammatory drug (NSAID) increases tumor tissue infiltration of seemingly activated immune cells in colorectal cancer. Lönnroth C, Andersson M, Arvidsson A, Nordgren S, Brevinge H, Lagerstedt K, Lundholm K. Cancer Immun. 2008 Feb 29;8:5. PMID: 18307280 MHC II protein (HLA-DP, -DQ, -DR) levels and infiltration by CD4+ T-helper cells of tumor stroma increased upon NSAID treatment, while CD8+ cytotoxic T-lymphocytes increased in both tumor stroma and epithelium. Molecules associated with immunosuppressive T regulatory cells (FOXP3, IL-10) were significantly decreased in indomethacin-exposed tumors. Standard oral administration of NSAID three days preoperatively was enough to increase tumor infiltration by seemingly activated immune cells. These findings agree with previous information that high pr

Interleukin 2-mediated conversion of ovarian cancer-associated CD4+ regulatory T cells into proinflammatory interleukin 17-producing helper T cells. Leveque L, Deknuydt F, Bioley G, Old LJ, Matsuzaki J, Odunsi K, Ayyoub M, Valmori D. J Immunother. 2009 Feb-Mar;32(2):101-8. PMID: 19238008 doi: 10.1097/CJI.0b013e318195b59e Thus, although the impact of TH17 cells on the evolution of EOC remains to be established, our data suggest that local IL-2 treatment in ovarian cancer may result in the conversion of tumor-associated Treg into TH17 cells, relieve Treg-mediated suppression, and contribute to enhance antitumor immunity.

Selenium and immunocompetence in patients with head and neck cancer. Kiremidjian-Schumacher L, Roy M, Glickman R, Schneider K, Rothstein S, Cooper J, Hochster H, Kim M, Newman R. Biol Trace Elem Res. 2000 Feb;73(2):97-111. PMID: 11049203 DOI: 10.1385/BTER:73:2:97

Vitamin D and intervention trials in prostate cancer: from theory to therapy. Schwartz GG. Ann Epidemiol. 2009 Feb;19(2):96-102. Epub 2008 Jul 10. PMID: 18619854 doi:10.1016/j.annepidem.2008.03.007 This suggests that whereas vitamin D (e.g., cholecalciferol) might prevent prostate cancer, existing prostate tumors likely would require treatment with 1,25(OH)(2)D and/or its analogs. The major obstacle to the use of 1,25(OH)(2)D in patients therapeutically is the risk of hypercalcemia. Several maneuvers to reduce this risk, including pulse dosing and the use of less calcemic 1,25(OH)(2)D analogs, have been explored in Phase I-III clinical trials. Once merely a promise, vitamin D-based therapies for prostate cancer may soon be medical practice.

Watercress supplementation in diet reduces lymphocyte DNA damage and alters blood antioxidant status in healthy adults. Gill CI, Haldar S, Boyd LA, Bennett R, Whiteford J, Butler M, Pearson JR, Bradbury I, Rowland IR. Am J Clin Nutr. 2007 Feb;85(2):504-10. PMID: 17284750

Watercress was declared the latest super food yesterday for being packed with a higher than usual amount of nutrients found in vegetables. Research has shown that eating a packet of raw watercress a day, or a bowl full, for eight weeks increased the ability of cells to resist damage to their DNA, helping to protect against the cell changes that lead to cancer.

Prostate tumor growth and recurrence can be modulated by the omega-6:omega-3 ratio in diet: athymic mouse xenograft model simulating radical prostatectomy. Kelavkar UP, Hutzley J, Dhir R, Kim P, Allen KG, McHugh K. Neoplasia. 2006 Feb;8(2):112-24. PMID: 16611404

ncident invasive breast cancer, geographic location of residence, and reported average time spent outside. Millen AE, Pettinger M, Freudenheim JL, Langer RD, Rosenberg CA, Mossavar-Rahmani Y, Duffy CM, Lane DS, McTiernan A, Kuller LH, Lopez AM, Wactawski-Wende J. Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):495-507. Epub 2009 Feb 3. PMID: 19190147 doi: 10.1158/1055-9965.EPI-08-0652 In conclusion, region of residence and geographic solar irradiance are not consistently related to risk of breast cancer and may not be sufficient proxy measures for sunlight/vitamin D exposure. The observed association between time spent outside and breast cancer risk support the hypothesis that vitamin D may protect against breast cancer.

The role of vitamin D in cancer prevention. Garland CF, Garland FC, Gorham ED, Lipkin M, Newmark H, Mohr SB, Holick MF. Am J Public Health. 2006 Feb;96(2):252-61. Epub 2005 Dec 27. Review. PMID: 16380576 DOI: 10.2105/AJPH.2004.045260 Vitamin D status differs by latitude and race, with residents of the northeastern United States and individuals with more skin pigmentation being at increased risk of deficiency. A PubMed database search yielded 63 observational studies of vitamin D status in relation to cancer risk, including 30 of colon, 13 of breast, 26 of prostate, and 7 of ovarian cancer, and several that assessed the association of vitamin D receptor genotype with cancer risk. The majority of studies found a protective relationship between sufficient vitamin D status and lower risk of cancer. The evidence suggests that efforts to improve vitamin D status, for example by vitamin D supplementation, could reduce cancer incidence and mortality at low cost, with few or no adverse effects.

The role of vitamin D in cancer prevention. Garland CF, Garland FC, Gorham ED, Lipkin M, Newmark H, Mohr SB, Holick MF. Am J Public Health. 2006 Feb;96(2):252-61. Epub 2005 Dec 27. Review. PMID: 16380576 DOI: 10.2105/AJPH.2004.045260 Vitamin D status differs by latitude and race, with residents of the northeastern United States and individuals with more skin pigmentation being at increased risk of deficiency. A PubMed database search yielded 63 observational studies of vitamin D status in relation to cancer risk, including 30 of colon, 13 of breast, 26 of prostate, and 7 of ovarian cancer, and several that assessed the association of vitamin D receptor genotype with cancer risk. The majority of studies found a protective relationship between sufficient vitamin D status and lower risk of cancer. The evidence suggests that efforts to improve vitamin D status, for example by vitamin D supplementation, could reduce cancer incidence and mortality at low cost, with few or no adverse effects

Association between serum 25(OH)D and death from prostate cancer. Tretli S, Hernes E, Berg JP, Hestvik UE, Robsahm TE. Br J Cancer. 2009 Feb 10;100(3):450-4. Epub 2009 Jan 20. PMID: 19156140 doi:10.1038/sj.bjc.6604865 The serum level of 25(OH)D may be involved in disease progression and is a potential marker of prognosis in patients with prostate cancer.

Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells. Mantena SK, Sharma SD, Katiyar SK. Mol Cancer Ther. 2006 Feb;5(2):296-308. PMID: 16505103 doi: 10.1158/1535-7163.MCT-05-0448 The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy. The evaluation of ancient herbal medicines may indicate novel strategies for the treatment of prostate cancer, which remains the leading cause of cancer-related deaths in American men (1). In our present investigation, we show that a naturally occurring isoquinoline alkaloid, berberine, significantly inhibits the proliferation and reduces the viability of DU145 and PC-3 as well as LNCaP cells (Fig. 1), which suggests that berberine may be an effective chemotherapeutic agent against both androgen-sensitive and androgen-insensitive prostate cancer cells. Importantly, we found that berberine did not exhibit toxicity to nonneoplastic human prostate epithelial cells under the conditions used, except for a moderate reduction in cell viability at higher concentrations when cells were treated in vitro for an extended period of time. In conclusion, the results of the present study indicate that berberine inhibits proliferation and induces G1-phase arrest and apoptosis in human prostate cancer cells but not in normal human prostate epithelial cells. In addition, we provide mechanistic evidence that berberine-induced apoptosis in prostate carcinoma cells, particularly hormone-refractory prostate carcinoma cells, is mediated through enhanced expression of Bax, disruption of the mitochondrial membrane potential, and activation of caspase-3.