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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.

Use of cannabinoid receptor agonists in cancer therapy as palliative and curative agents. Pisanti S, Malfitano AM, Grimaldi C, Santoro A, Gazzerro P, Laezza C, Bifulco M. Best Pract Res Clin Endocrinol Metab. 2009 Feb;23(1):117-31. PMID: 19285265 doi:10.1016/j.beem.2009.02.001    

The controversial place of vitamin C in cancer treatment. Verrax J, Calderon PB. Biochem Pharmacol. 2008 Dec 15;76(12):1644-52. Epub 2008 Sep 30. Review. PMID: 18938145 doi:10.1016/j.bcp.2008.09.024    

Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs.\nHeaney ML, Gardner JR, Karasavvas N, Golde DW, Scheinberg DA, Smith EA, O'Connor OA.\nCancer Res. 2008 Oct 1;68(19):8031-8.\nPMID: 18829561

Should Vitamin C Be Used as an Adjunctive\nTreatment in Cancer. \nJack Challem. \nMedical Journal Watch 2009 Feb.

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

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

Intravenous vitamin C as a chemotherapy agent: a report on clinical cases.\nRiordan HD, Riordan NH, Jackson JA, Casciari JJ, Hunninghake R, González MJ, Mora EM, Miranda-Massari JR, Rosario N, Rivera A.\nP R Health Sci J. 2004 Jun;23(2):115-8.\nPMID: 15377059

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.

Vitamin C and cancer revisited. Frei B, Lawson S. Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11037-8. Epub 2008 Aug 5. PMID: 18682554

Q. Pan, C. G. Kleer, K. L. van Golen, J. Irani, K. M. Bottema, C. Bias, M. De Carvalho, E. A. Mesri, D. M. Robins, R. D. Dick, G. J. Brewer, and S. D. Merajver Copper Deficiency Induced by Tetrathiomolybdate Suppresses Tumor Growth and Angiogenesis Canc

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

Mice injected with cancer cells experienced significantly elevated levels of C-reactive protein, white blood cells, and lipid peroxidation compared with control mice. These levels were reduced in animals that received cisplatin and/or DHA. While treatment with 125 mg/kg DHA inhibited tumor growth by 38 percent compared to untreated animals, 250 mg/kg suppressed tumor growth by 79 percent, which was a greater effect than that of cisplatin alone (which was associated with a 55 percent reduction). The combination of DHA and cisplatin resulted in an 81 percent inhibition of growth, while reducing elevated white blood cell levels (leukocytosis) to normal levels. Treatment with the higher dose of DHA alone was associated with a similar reduction in white blood cells, which, when elevated, are associated with tumor growth. A strong relationship was observed between tumor growth and white blood cell levels as well as C-reactive protein levels. In another experiment with rats treated with cisplatin, the addition of 250 mg/kg DHA prevented lethal kidney toxicity in 88 percent of the animals that received it, while none of the rats that received cisplatin alone survived.

Prospective study of predictors of vitamin D status and survival in patients with colorectal cancer K Ng, B M Wolpin, J A Meyerhardt, K Wu, A T Chan, B W Hollis, E L Giovannucci, M J Stampfer, W C Willett and C S Fuchs Br J Cancer 101: 916-923; advance online publication, August 18, 2009; doi:10.1038/sj.bjc.6605262

Berberine inhibits metastasis of nasopharyngeal carcinoma 5-8F cells by targeting Rho kinase-mediated Ezrin phosphorylation at threonine 567. Tang F, Wang D, Duan C, Huang D, Wu Y, Chen Y, Wang W, Xie C, Meng J, Wang L, Wu B, Liu S, Tian D, Zhu F, He Z, Deng F, Cao Y. J Biol Chem. 2009 Oct 2;284(40):27456-66. Epub 2009 Aug 3. PMID: 19651779

Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo.\nChen Q, Espey MG, Sun AY, Lee JH, Krishna MC, Shacter E, Choyke PL, Pooput C, Kirk KL, Buettner GR, Levine M.\nProc Natl Acad Sci U S A. 2007 May 22;104(21):8749-54. Epub 2007 May 14.\nPMID: 17502596 \n doi: 10.1073/pnas.0702854104\n

Phase I clinical trial of i.v. ascorbic acid in advanced malignancy. Hoffer LJ, Levine M, Assouline S, Melnychuk D, Padayatty SJ, Rosadiuk K, Rousseau C, Robitaille L, Miller WH Jr. Ann Oncol. 2008 Nov;19(11):1969-74. Epub 2008 Jun 9. Erratum in: Ann Oncol. 2008 Dec;19(12):2095. PMID: 18544557 doi:10.1093/annonc/mdn377

Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. Chen Q, Espey MG, Sun AY, Pooput C, Kirk KL, Krishna MC, Khosh DB, Drisko J, Levine M. Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11105-9. Epub 2008 Aug 4. PMID: 18678913 doi: 10.1073/pnas.0804226105

Elevated levels of the inflammatory marker C-reactive protein (CRP) are associated with an increased risk of death in men with advanced prostate cancer, according to findings from a subanalysis of the ASCENT (AIPC Study of Calcitriol Enhancing Taxotere) t

Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Blázquez C, González-Feria L, Alvarez L, Haro A, Casanova ML, Guzmán M. Cancer Res. 2004 Aug 15;64(16):5617-23. PMID: 15313899