• 1
    Pass HI, Vogelzang N, Hahn S, et al. Malignant pleural mesothelioma. Curr Probl Cancer. 2004; 28: 93174.
  • 2
    Belli C, Fennell D, Giovannini M, et al. Malignant pleural mesothelioma: current treatments and emerging drugs. Expert Opin Emerg Drugs. 2009; 14: 42337.
  • 3
    Sueoka E, Sueoka N, Okabe S, et al. Expression of the tumour necrosis factor alpha gene and early response genes by nodularin, a liver tumour promoter, in primary cultured rat hepatocytes. J Cancer Res Clin Oncol. 1997; 123: 4139.
  • 4
    Tomek S, Emri S, Krejcy K, Manegold C. Chemotherapy for malignant pleural mesothelioma: past results and recent developments. Br J Cancer. 2003; 88: 16774.
  • 5
    Fennell DA, Gaudino G, O'Byrne KJ, et al. Advances in the systemic therapy of malignant pleural mesothelioma. Nat Clin Pract Oncol. 2008; 5: 13647.
  • 6
    Tsiouris A, Gourgoulianis KI, Walesby RK. Current trends in the management of malignant pleural mesothelioma. Expert Rev Anticancer Ther. 2006; 6: 8313.
  • 7
    Martinotti S, Ranzato E, Burlando B. In vitro screening of synergistic ascorbate-drug combinations for the treatment of malignant mesothelioma. Toxicol In Vitro. 2011; 25: 156874.
  • 8
    Verrax J, Calderon PB. Pharmacologic concentrations of ascorbate are achieved by parenteral administration and exhibit antitumoural effects. Free Radic Biol Med. 2009; 47: 3240.
  • 9
    Ranzato E, Biffo S, Burlando B. Selective ascorbate toxicity in malignant mesothelioma: a redox Trojan mechanism. Am J Respir Cell Mol Biol. 2011; 44: 10817.
  • 10
    Ozben T. Oxidative stress and apoptosis: impact on cancer therapy. J Pharmacol Sci. 2007; 96: 218196.
  • 11
    Ahmad N, Feyes DK, Nieminen AL, et al. Green tea constituent epigallocatechin-3-gallate and induction of apoptosis and cell cycle arrest in human carcinoma cells. J Natl Cancer Inst. 1997; 89: 18816.
  • 12
    Nihal M, Ahsan H, Siddiqui IA, et al. (−)-Epigallocatechin-3-gallate (EGCG) sensitizes melanoma cells to interferon induced growth inhibition in a mouse model of human melanoma. Cell Cycle. 2009; 8: 205763.
  • 13
    Kemberling JK, Hampton JA, Keck RW, et al. Inhibition of bladder tumour growth by the green tea derivative epigallocatechin-3-gallate. J Urol. 2003; 170: 7736.
  • 14
    Wu PP, Kuo SC, Huang WW, et al. (−)-Epigallocatechin gallate induced apoptosis in human adrenal cancer NCI-H295 cells through caspase-dependent and caspase-independent pathway. Anticancer Res. 2009; 29: 143542.
  • 15
    Hibasami H, Achiwa Y, Fujikawa T, Komiya T. Induction of programmed cell death (apoptosis) in human lymphoid leukemia cells by catechin compounds. Anticancer Res. 1996; 16: 19436.
  • 16
    Hsieh DS, Wang H, Tan SW, et al. The treatment of bladder cancer in a mouse model by epigallocatechin-3-gallate-gold nanoparticles. Biomaterials. 2011; 32: 763340.
  • 17
    Chen ZP, Schell JB, Ho CT, Chen KY. Green tea epigallocatechin gallate shows a pronounced growth inhibitory effect on cancerous cells but not on their normal counterparts. Cancer Lett. 1998; 129: 1739.
  • 18
    Chen L, Zhang HY. Cancer preventive mechanisms of the green tea polyphenol (−)-epigallocatechin-3-gallate. Molecules. 2007; 3: 94657.
  • 19
    Chen D, Wan SB, Yang H, et al. EGCG, green tea polyphenols and their synthetic analogs and prodrugs for human cancer prevention and treatment. Adv Clin Chem. 2011; 53: 15577.
  • 20
    Yang CS, Wang X. Green tea and cancer prevention. Nutr Cancer. 2010; 62: 9317.
  • 21
    Patra SK, Rizzi F, Silva A, et al. Molecular targets of (−)-epigallocatechin-3-gallate (EGCG): specificity and interaction with membrane lipid rafts. J Physiol Pharmacol. 2008; 59: 21735.
  • 22
    Tan X, Hu D, Li S, et al. Differences of four catechins in cell cycle arrest and induction of apoptosis in LoVo cells. Cancer Lett. 2000; 158: 16.
  • 23
    Kang HG, Jenabi JM, Liu XF, et al. Inhibition of the insulin-like growth factor I receptor by epigallocatechin gallate blocks proliferation and induces the death of Ewing tumour cells. Mol Cancer Ther. 2010; 9: 1396407.
  • 24
    Duhon D, Bigelow RL, Coleman DT, et al. The polyphenol epigallocatechin-3-gallate affects lipid rafts to block activation of the c-Met receptor in prostate cancer cells. Mol Carcinog. 2010; 49: 73949.
  • 25
    Kim CH, Moon SK. Epigallocatechin-3-gallate causes the p21/WAF1-mediated G(1)-phase arrest of cell cycle and inhibits matrix metalloproteinase-9 expression in TNF-alpha-induced vascular smooth muscle cells. Arch Biochem Biophys. 2005; 15: 26472.
  • 26
    Yamakawa S, Asai T, Uchida T, et al. (−)-Epigallocatechin gallate inhibits membrane-type 1 matrix metalloproteinase, MT1-MMP, and tumour angiogenesis. Cancer Lett. 2004; 210: 4755.
  • 27
    Landis-Piwowar KR, Kuhn DJ, Wan SB, et al. Evaluation of proteasome-inhibitory and apoptosis-inducing potencies of novel (−)-EGCG analogs and their prodrugs. Int J Mol Med. 2005; 15: 73542.
  • 28
    Kim J, Zhang X, Rieger-Christ KM, et al. Suppression of Wnt signaling by the green tea compound (−)-epigallocatechin 3-gallate (EGCG) in invasive breast cancer cells. Requirement of the transcriptional repressor HBP1. J Biol Chem. 2006; 281: 1086575.
  • 29
    Tran PL, Kim SA, Choi HS, et al. Epigallocatechin-3-gallate suppresses the expression of HSP70 and HSP90 and exhibits anti-tumour activity in vitro and in vivo. BMC Cancer. 2010; 10: 276.
  • 30
    Sukhthankar M, Alberti S, Baek SJ. (−)-Epigallocatechin-3-gallate (EGCG) post transcriptionally and post-translationally suppresses the cell proliferative protein TROP2 in human colorectal cancer cells. Anticancer Res. 2010; 30: 2497503.
  • 31
    Adachi S, Shimizu M, Shirakami Y, et al. (−)-Epigallocatechin gallate downregulates EGF receptor via phosphorylation at Ser 1046/1047 by p38 MAPK in colon cancer cells. Carcinogenesis. 2009; 30: 154452.
  • 32
    Fujiki H, Suganuma M, Okabe S, et al. Cancer inhibition by green tea. Mutat Res. 1998; 402: 30710.
  • 33
    Yang WH, Fong YC, Lee CY, et al. Epigallocatechin-3-gallate induces cell apoptosis of human chondrosarcoma cells through apoptosis signal-regulating kinase 1 pathway. J Cell Biochem. 2011; 112: 160111.
  • 34
    Shi X, Ding M, Dong Z, et al. Antioxidant properties of aspirin: characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-kappaB activation, and TNF-alpha production. Mol Cell Biochem. 1999; 199: 93102.
  • 35
    Lambert JD, Elias RJ. The antioxidant and pro-oxidant activities of green tea polyphenols: a role in cancer prevention. Arch Biochem Biophys. 2010; 501: 6572.
  • 36
    Li GX, Chen YK, Hou Z, et al. Pro-oxidative activities and dose-response relationship of (−)-epigallocatechin-3-gallate in the inhibition of lung cancer cell growth: a comparative study in vivo and in vitro. Carcinogenesis. 2010; 31: 90210.
  • 37
    Vittal R, Selvanayagam ZE, Sun Y, et al. Gene expression changes induced by green tea polyphenol (−)-epigallocatechin-3-gallate in human bronchial epithelial 21BES cells analyzed by DNA microarray. Mol Cancer Ther. 2004; 3: 10919.
  • 38
    Azam S, Hadi N, Khan NU, Hadi SM. Prooxidant property of green tea polyphenols epicatechin and epigallocatechin-3-gallate: implications for anticancer properties. Toxicol In Vitro. 2004; 18: 55561.
  • 39
    Yamamoto T, Hsu S, Lewis J, et al. Green tea polyphenol causes differential oxidative environments in tumour versus normal epithelial cells. J Pharmacol Exp Ther. 2003; 307: 2306.
  • 40
    Galati G, Lin A, Sultan AM, O'Brien PJ. Cellular and in vivo hepatotoxicity caused by green tea phenolic acids and catechins. Free Radic Biol Med. 2006; 40: 57080.
  • 41
    Hong J, Lu H, Meng X, et al. Stability, cellular uptake, biotransformation, and efflux of tea polyphenol (−)-epigallocatechin-3-gallate in HT-29 human colon adenocarcinoma cells. Cancer Res. 2002; 62: 72416.
  • 42
    Bertino P, Piccardi F, Porta C, et al. Imatinib mesylate enhances therapeutic effects of gemcitabine in human malignant mesothelioma xenografts. Clin Cancer Res. 2008; 14: 5418.
  • 43
    Orengo AM, Spoletini L, Procopio A, et al. Establishment of four new mesothelioma cell lines: characterization by ultrastructural and immunophenotypic analysis. Eur Respir J. 1999; 13: 52734.
  • 44
    Orecchia S, Schillaci F, Salvio M, et al. Aberrant E-cadherin and gamma-catenin expression in malignant mesothelioma and its diagnostic and biological relevance. Lung Cancer. 2004; 45: 3743.
  • 45
    Dickson MA, Hahn WC, Ino Y, et al. Human keratinocytes that express hTERT and also bypass a p16(INK4a)-enforced mechanism that limits life span become immortal yet retain normal growth and differentiation characteristics. Mol Cell Biol. 2000; 20: 143647.
  • 46
    Legrand C, Bour JM, Jacob C, et al. Lactate dehydrogenase (LDH) activity of the cultured eukaryotic cells as marker of the number of dead cells in the medium. J Biotechnol. 1992; 25: 23143.
  • 47
    Yermolaieva O, Brot N, Weissbach H, et al. Reactive oxygen species and nitric oxide mediate plasticity of neuronal calcium signaling. Proc Natl Acad Sci USA. 2000; 97: 44853.
  • 48
    Grynkiewicz G, Poenie M, Tsien RY. A new generation of Ca2+ indicators with greatly improved fluorescence properties. J Biol Chem. 1985; 260: 344050.
  • 49
    Churg A, Roggli V, Galateau-Salle F, et al. Tumours of the pleura: mesothelial tumours. In: Travis WD, Brambilla E, Müller-Hermelink E, et al. editors. World Health Organization classification of tumours, vol 10: pathology and genetics of tumours of the lung, pleura, thymus and heart, Lyon, France: IARC Press; 2004: pp. 12844.
  • 50
    Barnes M, Correll R, Stevens D. A simple spreadsheet for estimating low-effect concentrations and associated logistic dose response curves. Solutions to pollution: Program abstract book. The Society of Environmental Toxicology and Chemistry Asia/Pacific – Australasian Society of Ecotoxicology 2003, SETAC ASE Asia Pacific. 2003.
  • 51
    Nakagawa H, Hasumi K, Woo JT, et al. Generation of hydrogen peroxide primarily contributes to the induction of Fe(II)-dependent apoptosis in Jurkat cells by (−)-epigallocatechin gallate. Carcinogenesis. 2004; 25: 156774.
  • 52
    Lambeth D. NOX enzymes and the biology of reactive oxygen. Nat Rev Immunol. 2004; 4: 1819.
  • 53
    Yin ST, Tang ML, Deng HM, et al. Epigallocatechin-3-gallate induced primary cultures of rat hippocampal neurons death linked to calcium overload and oxidative stress. Naunyn Schmiedebergs Arch Pharmacol. 2009; 379: 55164.
  • 54
    Taylor JT, Zeng XB, Pottle JE, et al. Calcium signaling and T-type calcium channels in cancer cell cycling. World J Gastroenterol. 2008; 14: 498491.
  • 55
    Michels G, Matthes J, Handrock R, et al. Single-channel pharmacology of mibefradil in human native T-type and recombinant Ca(v)3.2 calcium channels. Mol Pharmacol. 2002; 61: 68294.
  • 56
    Obejero-Paz CA, Gray IP, Jones SW. Ni2+ block of CaV3.1 (alpha1G) T-type calcium channels. J Gen Physiol. 2008; 132: 23950.
  • 57
    Joksovic PM, Nelson MT, Jevtovic-Todorovic V, et al. CaV3.2 is the major molecular substrate for redox regulation of T-type Ca2+ channels in the rat and mouse thalamus. J Physiol. 2006; 574: 41530.
  • 58
    Oikawa S, Furukawaa A, Asada H, et al. Catechins induce oxidative damage to cellular and isolated DNA through the generation of reactive oxygen species. Free Radic Res. 2003; 37: 88190.
  • 59
    Sakagami H, Arakawa H, Maeda M, et al. Production of hydrogen peroxide and methionine sulfoxide by epigallocatechin gallate and antioxidants. Anticancer Res. 2001; 21: 263341.
  • 60
    Lopez-Lazaro M, Calderon-Montano JM, Burgos-Moron E, Austin CA. Green tea constituents (−)-epigallocatechin-3-gallate (EGCG) and gallic acid induce topoisomerase I- and topoisomerase II-DNA complexes in cells mediated by pyrogallol-induced hydrogen peroxide. Mutagenesis. 2011; 26: 48998.
  • 61
    Chacon E, Acosta D. Mitochondrial regulation of superoxide by Ca2+: an alternate mechanism for the cardiotoxicity of doxorubicin. Toxicol Appl Pharmacol. 1991; 107: 11728.
  • 62
    Simon HU, Haj-Yehia A, Levi-Schaffer F. Role of reactive oxygen species (ROS) in apoptosis induction. Apoptosis. 2000; 5: 4158.
  • 63
    Peng TI, Jou MJ. Oxidative stress caused by mitochondrial calcium overload. Ann N Y Acad Sci. 2010; 1201: 1838.
  • 64
    Hool LC, Corry B. Redox control of calcium channels: from mechanisms to therapeutic opportunities. Antioxid Redox Signal. 2007; 9: 40935.
  • 65
    Hidalgo C, Bull R, Marengo JJ, et al. SH oxidation stimulates calcium release channels (ryanodine receptors) from excitable cells. Biol Res. 2000; 33: 11324.
  • 66
    Gray LS, Perez-Reyes E, Gomora JC, et al. The role of voltage gated T-type Ca2+ channel isoforms in mediating “capacitative” Ca2+ entry in cancer cells. Cell Calcium. 2004; 36: 48997.
  • 67
    Mariot P, Vanoverberghe K, Lalevee N, et al. Overexpression of an alpha 1H (Cav3.2) T-type calcium channel during neuroendocrine differentiation of human prostate cancer cells. J Biol Chem. 2002; 277: 1082433.
  • 68
    Li Y, Liu S, Lu F, et al. A role of functional T-type Ca2+ channel in hepatocellular carcinoma cell proliferation. Oncol Rep. 2009; 225: 122935.
  • 69
    Heo JH, Seo HN, Choe YJ, et al. T-type Ca2+ channel blockers suppress the growth of human cancer cells. Bioorg Med Chem Lett. 2008; 18: 3899901.