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Wang M. Extending the good diet, good health paradigm: modulation of breast cancer resistance protein (BCRP) by flavonoids. Toxicol Sci. 2007 Apr;96(2):203-5. PMID: 17407835 [PubMed - in process]

Phase I clinical trial of a selective inhibitor of CYP17, abiraterone acetate, confirms that castration-resistant prostate cancer commonly remains hormone driven. Attard G, Reid AH, Yap TA, Raynaud F, Dowsett M, Settatree S, Barrett M, Parker C, Martins V, Folkerd E, Clark J, Cooper CS, Kaye SB, Dearnaley D, Lee G, de Bono JS. J Clin Oncol. 2008 Oct 1;26(28):4563-71. Epub 2008 Jul 21. PMID: 18645193 DOI: 10.1200/JCO.2007.15.9749

Tumours with PI3K activation are resistant to dietary restriction. Nada Y. Kalaany & David M. Sabatini Nature. Published online 11 March 2009 doi:10.1038/nature07782

CYP17 blockade by abiraterone: further evidence for frequent continued hormone-dependence in castration-resistant prostate cancer. Ang JE, Olmos D, de Bono JS. Br J Cancer. 2009 Mar 10;100(5):671-5. Epub 2009 Feb 17. PMID: 19223900 doi:10.1038/sj.bjc.6604904

"Berberine is a quaternary ammonium salt from the group of isoquinoline alkaloids. It is found in such plants as Berberis, goldenseal (Hydrastis canadensis), and Coptis chinensis, usually in the roots, rhizomes, stems, and bark. Berberine is strongly yellow colored, which is why in earlier times berberis species were used to dye wool, leather and wood. Wool is still today dyed with berberine in Northern India Berberine (BBR) is a natural compound with up-regulating activity on both low-density-lipoprotein receptor (LDLR) and insulin receptor (InsR). This one-drug-multiple-target characteristic might be suitable for the treatment of metabolic syndrome.[12] Berberine has been tested and used successfully in experimental[13] and human diabetes mellitus.[14][15][16] Berberine has been shown to lower elevated blood glucose as effectively as metformin.[17] The mechanisms include inhibition of aldose reductase,[18] inducing glycolysis,[19] preventing insulin resistance[20] through increasing insulin receptor expression[14] and acting like incretins. Berberine has drawn extensive attention towards its antineoplastic effects.[43][44] It seems to suppress the growth of a wide variety of tumor cells including breast cancer,[45] leukemia, melanoma,[46] epidermoid carcinoma, hepatoma, oral carcinoma, tongue carcinoma,[47] glioblastoma, prostate carcinoma, gastric carcinoma.[48][49] Animal studies have shown that berberine can suppress chemical-induced carcinogenesis, tumor promotion, tumor invasion,[50][51][52][53][54] prostate cancer,[55][56][57][58] neuroblastoma,[59][60] and leukemia.[34][61] It is a radiosensitzer of tumor cells but not of normal cells

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

"Worcester, MA - Current research suggests that TNF-receptor associated protein-1 (TRAP-1) may prevent cancer cell death. The related report by Leav et al, "Cytoprotective Mitochondrial Chaperone TRAP-1 as a Novel Molecular Target in Localized and Metastatic Prostate Cancer," appears in the January 2010 issue of the American Journal of Pathology. Prostate cancer cells are often resistant to cell death. Researchers led by Dr. Dario C. Altieri of the University of Massachusetts Medical School, therefore, explored the role of TRAP-1, a protein thought to regulate cell death, in prostate cancer survival. TRAP-1 was highly expressed in both high-grade human prostate cancer lesions and mouse models of prostate cancer, but not in benign or normal prostate tissue. In addition, TRAP-1 overexpression in non-cancer prostate cells inhibited cell death, whereas TRAP-1-deficient prostate cancer cells had enhanced levels of cell death. Moreover, treatment with Gamitrinib, which inhibits TRAP-1, resulted in prostate cancer cell death, but not death of non-cancerous prostate cells. Therefore, targeting TRAP-1 via Gamitrinib treatment may be a viable therapeutic strategy for patients with advanced prostate cancer."

Cancer immunotherapies, including cancer vaccines, are novel investigational cancer therapies. In contrast to chemotherapy and radiotherapy regimens that are often associated with severe side effects, cancer immunotherapy stimulates the body's immune system and natural resistance to cancer, thus offering a gentler means of cancer treatment that is less damaging to the rest of the body. Surgery is generally (but not always) performed, prior to immunotherapy, to remove most of the tumor (Hanna MG, Jr. et al 2001; Jocham D et al 2004). Vaccination or immunotherapy prompts the immune system to kill residual cancer cells that persist after surgery and could result in the cancer recurring.

Simultaneously Blocking Glycolysis and Fat Metabolism Can the use of DCA and a fatty acid metabolism blocker together force more cancer cells into using aerobic metabolism? Tim McGough used green tea extract, which contains EGCG, in his fantastic response. DCA works by reactivating mitochondria and shifts metabolism from glycolysis to glucose oxidation. Hopefully the cancer cell will then undergo apoptosis. However, cancer cells have an alternate energy source: fat metabolism. This page explores to possibility of blocking fat metabolism to help force the cell into apoptosis. Oral squamous cell carcinoma is a cancer that does not respond well to DCA. This study, Head and Neck Cancer Cell Lines Are Resistant to Mitochondrial-Depolarization-Induced Apoptosis states: "Results: ΔΨm in head and neck cell lines started to show slight loss of ΔΨm, while HL-60 showed significant loss of ΔΨm after 30 min of treatment. All cell lines demonstrated complete mitochondrial depolarization within 24 h, however, only the control cell line HL-60 underwent apoptosis. In addition, HNSCC cell lines did not demonstrate cytoplasmic cytochrome c release despite significant mitochondrial membrane depolarization, while HL-60 cell initiated apoptosis and cytochcrome c release after 24 h of treatment. Conclusions: Head and neck cancer cell lines exhibit defects in mitochondrial-membrane-depolarization-induced apoptosis as well as impaired release of cytochrome c despite significant mitochondrial membrane depolarization. Proximal defects in the mitochondrial apoptosis pathway are a feature of HNSCC.(head and neck squamous cell carcinoma)" Note that although the cell lines were depolarized, apoptosis did not occur. So I checked to see if fatty acid metabolism is used by squamous cell carcinoma.

Artemisinin (pronounced /ɑːtə'misinən/) is a drug used to treat multi-drug resistant strains of falciparum malaria. The compound (a sesquiterpene lactone) is isolated from the plant Artemisia annua. Not all plants of this species contain artemisinin. Apparently it is only produced when the plant is subjected to certain conditions, most likely biotic or abiotic stress. It can be synthesized from artemisinic acid.[1] The drug is derived from a herb used in Chinese traditional medicine, though it is usually chemically modified and combined with other medications. Artemisinin is under early research and testing for treatment of cancer, primarily by researchers at the University of Washington.[7][8] Artemisinin has a peroxide lactone group in its structure. It is thought that when the peroxide comes into contact with high iron concentrations (common in cancerous cells), the molecule becomes unstable and releases reactive oxygen species. It has been shown to reduce angiogenesis and the expression of vascular endothelial growth factor in some tissue cultures.

A proprietary extract prepared from co-cultured mycelia of several species of Basidiomycete mushrooms, including shiitake (Lentinus edodes), active hexose correlated compound (AHCC) is extracted from mushrooms using hot water following an enzyme pretreatment, but specific mushroom source and preparation details have not been fully disclosed. Patients use this to prevent and treat cancer. Animal studies suggest that AHCC has antioxidant effects and may protect against disorders induced by oxidative stress (1) and may also enhance resistance against bacterial (2) (7)and viral infections (3). In healthy humans, AHCC increased dendritic cell number and function (4) In vitro and animal studies show that AHCC exhibits some anticancer activities, but the results of these studies are vague

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.

Integrative Cancer Science and Therapeutics (ICST) is an open access, peer-reviewed online journal interested in attracting high-quality original research and reviews that present or highlight significant advances in all areas of cancer and related biomedical science. The Journal is concerned with basic, translational and clinical research, across different disciplines and areas, enhancing insight in understanding, prevention, diagnosis and treatment of cancer. The journal also prioritizes clinical trials evaluating new treatments, accompanied by research on pharmacology and molecular alterations or biomarkers that predict response or resistance to treatment.