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
The in vitro study, reported in the journal Carcinogenesis (Vol. 27, pp. 32-42), showed that vitamin D, in the form of the highly active 1alpha, 25-dihydroxyvitamin D3 (1,25-VD), inhibited the function of protease enzymes that are involved in tumour invasion.
"We found that 1,25-VD decreased matric metalloproteinases (MMP-9) and cathepsins (CPs), while it [also] increased the activity of their counterparts, tissue inhibitors of metalloproteinase-1 (TIMP-1) and cathepsin inhibitors," wrote lead author Bo-Ying Bao from the University of Rochester and Taipei Medical University.
"Mechanistic studies showed that 1,25-VD did not suppress MMP-9 expression at the transcriptional level, but reduced its mRNA stability," said Bao.
A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth.
Bonnet S, Archer SL, Allalunis-Turner J, Haromy A, Beaulieu C, Thompson R, Lee CT, Lopaschuk GD, Puttagunta L, Bonnet S, Harry G, Hashimoto K, Porter CJ, Andrade MA, Thebaud B, Michelakis ED.
Cancer Cell. 2007 Jan;11(1):37-51.
PMID: 17222789
doi:10.1016/j.ccr.2006.10.020
White button mushroom phytochemicals inhibit aromatase activity and breast cancer cell proliferation.
Grube BJ, Eng ET, Kao YC, Kwon A, Chen S.
J Nutr. 2001 Dec;131(12):3288-93.
PMID: 11739882
MedWire News: Intralesional injection of interleukin (IL)-7 and IL-15 enhances the effects of radiofrequency thermal ablation (RFA) in inhibiting tumor development and metastases, animal study results show.
RFA, used for the treatment of solid tumors and known for its localized tumor effects, may activate immune responses and thereby reduce the risk for local tumor recurrence or distant metastases through T cell stimulation.
However, studies have suggested that additional adjuvant immunotherapy may improve the efficacy of RFA.
This preclinical study, reported in Breast Cancer Research and Treatment, was conducted to evaluate the effect of addition of the cytokines IL-7 and IL-15 to RFA in models of breast cancer.
Effects of eicosapentaenoic and docosahexaenoic n-3 fatty acids from fish oil and preferential Cox-2 inhibition on systemic syndromes in patients with advanced lung cancer.
Cerchietti LC, Navigante AH, Castro MA.
Nutr Cancer. 2007;59(1):14-20.
PMID: 17927497
Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors.
Casanova ML, Blázquez C, Martínez-Palacio J, Villanueva C, Fernández-Aceñero MJ, Huffman JW, Jorcano JL, Guzmán M.
J Clin Invest. 2003 Jan;111(1):43-50.
PMID: 12511587
doi:10.1172/JCI16116
MedWire News: Calcitriol, the active form of vitamin D, has been found to induce the tumor-suppressing protein CCAAT enhancer-binding protein (C/EBP)α, which can inhibit the growth of breast cancer cells, researchers report.
DCA is an organic compound, and a byproduct of TCE (trichloroethylene), a chemical that has been a concern in the development of cancer. In January 2007, researchers at the University of Alberta published a study in the journal Cancer Cell suggesting that DCA showed promise in shrinking tumors in lab rats as well as inhibiting growth of cultured human cancer cells. They hypothesized that DCA may be able to change cancer cells back to normal ones by switching them from the aberrant energy pathways they rely on to those used by normal cells.
Research just published in the American Association for Cancer Research's Cancer Prevention Research identifies a class of flavonoids called anthocyanins in black raspberries that's been shown to inhibit cancer cell growth and stimulate apoptosis (the death of cancer cells) in the esophagus of rats treated with an esophageal carcinogen
WARNING: This page was NOT created or approved by any doctor or medical researcher. The purpose of this page is to provide hard-to-find information on copper reduction cancer treatment, a new unapproved and experimental course of cancer treatment whose ef
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
Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression.
Li Y, Liu L, Tollefsbol TO.
FASEB J. 2009 Dec 17. [Epub ahead of print]
PMID: 20019239
doi: 10.1096/fj.09-149328
Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.
Scientists in Japan recently studied some of the glyconutrients from spinach and found they inhibited destruction of DNA, cancer cell growth, and tumor growth. They used the nutrients to suppress the growth of colon adenocarcinoma in mice. After a two week period of ingesting the nutrients, a 56.1% decrease in solid tumor volume occurred without any side effects. And the nutrients reduced the ability of tumors to supply themselves with blood which they need to fuel their growth. Markers of cell proliferation were drastically reduced. (Lipids, August, 2008)
PHILADELPHIA - Researchers at Amgen are testing a fully human monoclonal antibody that inhibits the activity of insulin-like growth factors (IGF-1 and IGF-2) and appears to reduce pancreatic cancer cells in early testing, according to a report in Molecular Cancer Therapeutics, a journal of the American Association for Cancer Research.
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