Group items tagged

Holick MF. Vitamin D: its role in cancer prevention and treatment. Prog Biophys Mol Biol. 2006 Sep;92(1):49-59. Epub 2006 Mar 10. Review. PMID: 16566961 [PubMed - indexed for MEDLINE]

Calcium plus vitamin D supplementation and the risk of colorectal cancer. Wactawski-Wende J, Kotchen JM, Anderson GL, Assaf AR, Brunner RL, O'Sullivan MJ, Margolis KL, Ockene JK, Phillips L, Pottern L, Prentice RL, Robbins J, Rohan TE, Sarto GE, Sharma S, Stefanick ML, Van Horn L, Wallace RB, Whitlock E, Bassford T, Beresford SA, Black HR, Bonds DE, Brzyski RG, Caan B, Chlebowski RT, Cochrane B, Garland C, Gass M, Hays J, Heiss G, Hendrix SL, Howard BV, Hsia J, Hubbell FA, Jackson RD, Johnson KC, Judd H, Kooperberg CL, Kuller LH, LaCroix AZ, Lane DS, Langer RD, Lasser NL, Lewis CE, Limacher MC, Manson JE; Women's Health Initiative Investigators. N Engl J Med. 2006 Feb 16;354(7):684-96. Erratum in: N Engl J Med. 2006 Mar 9;354(10):1102. PMID: 16481636 Conclusions Daily supplementation of calcium with vitamin D for seven years had no effect on the incidence of colorectal cancer among postmenopausal women. The long latency associated with the development of colorectal cancer, along with the seven-year duration of the trial, may have contributed to this null finding. Ongoing follow-up will assess the longer-term effect of this intervention.

Berberine inhibits growth, induces G1 arrest and apoptosis in human epidermoid carcinoma A431 cells by regulating Cdki-Cdk-cyclin cascade, disruption of mitochondrial membrane potential and cleavage of caspase 3 and PARP. Mantena SK, Sharma SD, Katiyar SK. Carcinogenesis. 2006 Oct;27(10):2018-27. Epub 2006 Apr 18. PMID: 16621886 doi:10.1093/carcin/bgl043 In the present investigation, we show that berberine, which is present abundantly in Berberis plant species, significantly inhibits the viability, proliferation and induces cell death in human epidermoid carcinoma A431 cells (Figure 1), but this effect was not found in normal human epidermal keratinocytes under the identical conditions, except for a non-significant reduction in cell viability at higher concentrations of berberine (50 and 75 µM) and treatment of cells for a longer period of time (72 h). These data suggested that berberine may be examined as an effective chemotherapeutic agent against non-melanoma skin cancers. In conclusion, our study indicates that berberine inhibits growth, induces G1 arrest and apoptotic cell death of human epidermoid carcinoma A431 cells. We also provide mechanistic evidences that berberine-induced apoptosis in human epidermoid carcinoma cells is mediated through disruption of mitochondrial membrane potential and activation of caspase 3 pathway, although other pathways may have a role and that require further investigation. Moreover, further in vivo studies are required to determine whether berberine could be an effective chemotherapeutic agent for the prevention of non-melanoma skin cancers.

ScienceDaily (Feb. 8, 2006) - Vitamin D can inhibit the spread of prostate cancer cells by limiting the activity of two specific enzymes, University of Rochester Medical Center scientists report. \n\nThe finding means that vitamin D could provide beneficial treatment to prostate cancer patients with high levels of the enzymes, the scientists said.\n

Intravenously administered vitamin C as cancer therapy: three cases.\nPadayatty SJ, Riordan HD, Hewitt SM, Katz A, Hoffer LJ, Levine M.\nCMAJ. 2006 Mar 28;174(7):937-42.\nPMID: 16567755 \ndoi:10.1503/cmaj.050346.

Phase II study of pomegranate juice for men with rising prostate-specific antigen following surgery or radiation for prostate cancer. Pantuck AJ, Leppert JT, Zomorodian N, Aronson W, Hong J, Barnard RJ, Seeram N, Liker H, Wang H, Elashoff R, Heber D, Aviram M, Ignarro L, Belldegrun A. Clin Cancer Res. 2006 Jul 1;12(13):4018-26. PMID: 16818701

American Society of Clinical Oncology Meeting 2006.

ScienceDaily (July 2, 2006) - Drinking an eight ounce glass of pomegranate juice daily increased by nearly four times the period during which PSA levels in men treated for prostate cancer remained stable, a three-year UCLA study has found.

Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer. Michelakis ED, Webster L, Mackey JR. Br J Cancer. 2008 Oct 7;99(7):989-94. Epub 2008 Sep 2. Review. PMID: 18766181 doi:10.1038/sj.bjc.6604554 The unique metabolism of most solid tumours (aerobic glycolysis, i.e., Warburg effect) is not only the basis of diagnosing cancer with metabolic imaging but might also be associated with the resistance to apoptosis that characterises cancer. The glycolytic phenotype in cancer appears to be the common denominator of diverse molecular abnormalities in cancer and may be associated with a (potentially reversible) suppression of mitochondrial function. The generic drug dichloroacetate is an orally available small molecule that, by inhibiting the pyruvate dehydrogenase kinase, increases the flux of pyruvate into the mitochondria, promoting glucose oxidation over glycolysis. This reverses the suppressed mitochondrial apoptosis in cancer and results in suppression of tumour growth in vitro and in vivo. Here, we review the scientific and clinical rationale supporting the rapid translation of this promising metabolic modulator in early-phase cancer clinical trials More than 40 nonrandomised trials of DCA in small cohorts of patients have been reported, but the first two randomised control trials of chronic oral therapy with DCA in congenital mitochondrial diseases were reported in 2006. In the first, a blinded placebo-controlled study was performed with oral DCA administered at 25 mg kg-1 day-1 in 30 patients with MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) (Kaufmann et al, 2006). Most patients enrolled in the DCA arm developed symptomatic peripheral neuropathy, compared with 4 out of 15 in the placebo arm, leading to the termination of the study. Seventeen out of 19 patients had at least partial resolution of peripheral neurological symptoms by 9 months after discontinuation of DCA. This neurotoxicity res

Anti-aromatase activity of phytochemicals in white button mushrooms (Agaricus bisporus). Chen S, Oh SR, Phung S, Hur G, Ye JJ, Kwok SL, Shrode GE, Belury M, Adams LS, Williams D. Cancer Res. 2006 Dec 15;66(24):12026-34. PMID: 17178902 doi: 10.1158/0008-5472.CAN-06-2206

Molecular immunological approaches to biotherapy of human cancers--a review, hypothesis and implications. Becker Y. Anticancer Res. 2006 Mar-Apr;26(2A):1113-34. Review. PMID: 16619514

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

Developmental toxicity evaluation of berberine in rats and mice. Jahnke GD, Price CJ, Marr MC, Myers CB, George JD. Birth Defects Res B Dev Reprod Toxicol. 2006 Jun;77(3):195-206. PMID: 16634078 DOI: 10.1002/bdrb.20075 BACKGROUND: Berberine, a plant alkaloid, is found in some herbal teas and health-related products. It is a component of goldenseal, an herbal supplement. Berberine chloride dihydrate (BCD) was evaluated for developmental toxicity in rats and mice. METHODS: Berberine chloride dihydrate was administered in the feed to timed-mated Sprague-Dawley (CD) rats (0, 3625, 7250, or 14,500 ppm; on gestational days [GD] 6-20), and Swiss Albino (CD-1) mice (0, 3500, 5250, or 7000 ppm; on GD 6-17). Ingested doses were 0, 282, 531, and 1313 mg/kg/day (rats) and 0, 569, 841, and 1155 mg/kg/day (mice). RESULTS:There were no maternal deaths. The rat maternal lowest observed adverse effect level (LOAEL), based on reduced maternal weight gain, was 7250 ppm. The rat developmental toxicity LOAEL, based on reduced fetal body weight per litter, was 14,500 ppm. In the mouse study, equivocal maternal and developmental toxicity LOAELs were 5250 ppm. Due to scattering of feed in the high dose groups, a gavage study at 1000 mg/kg/day was conducted in both species. CONCLUSIONS: In rats, maternal, but not fetal adverse effects were noted. The maternal toxicity LOAEL remained at 7250 ppm (531 mg/kg/day) based on the feed study and the developmental toxicity NOAEL was raised to 1000 mg/kg/day BCD based on the gavage study. In the mouse, 33% of the treated females died. Surviving animals had increased relative water intake, and average fetal body weight per litter decreased 5-6% with no change in live litter size. The maternal toxicity LOAEL remained at 5250 ppm (841 mg/kg/day) BCD, based on increased water consumption. The developmental toxicity LOAEL was raised to 1000 mg/kg/day BCD based on decreased fetal body weight.

Researchers investigating the role of cannabis in cancer therapy reveal it has the potential to destroy leukaemia cells, in a paper published in the March 2006 edition of Letters in Drug Design & Discovery.  Led by Dr Wai Man Liu, at Barts and the London, Queen Mary's School of Medicine and Dentistry, the team has followed up on their findings of 2005 which showed that the main active ingredient in cannabis, tetrahydrocannabinol, or THC, has the potential to be used effectively against some forms of cancer.  Dr Liu has since moved to the Institute of Cancer in Sutton where he continues his work into investigating the potential therapeutic benefit of new anti-cancer agents.

Singh RP, Agarwal R. Prostate cancer chemoprevention by silibinin: bench to bedside. Mol Carcinog. 2006 Jun;45(6):436-42. Review. PMID: 16637061 [PubMed - indexed for MEDLINE]

High-dose vitamin C therapy: renewed hope or false promise?\nAssouline S, Miller WH.\nCMAJ. 2006 Mar 28;174(7):956-7. \nPMID: 16567756

Sept. 12, 2006 -- Getting the recommended intake of vitamin D from diet, supplements, or even the sun may cut your risk of pancreatic cancer. The results of two large, long-term surveys show that adults who got 300 IU to 449 IU (international units) per day had a 43% lower risk of pancreatic cancer. The recommended intake of vitamin D for adults aged 51-70 is 400 IU per day.

Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006 Jul;84(1):18-28. Review. PMID: 16825677

Giovannucci E, Liu Y, Rimm EB, Hollis BW, Fuchs CS, Stampfer MJ, Willett WC. Prospective study of predictors of vitamin D status and cancer incidence and mortality in men. J Natl Cancer Inst. 2006 Apr 5;98(7):451-9. PMID: 16595781 [PubMed - indexed fo

Fighting cancer with oncolytic viruses. Chernajovsky Y, Layward L, Lemoine N. BMJ. 2006 Jan 21;332(7534):170-2. Review. . PMID: 16424499