Reactive oxygen species: an Achilles’ heel of melanoma?

References

• Jemal A, Siegel R, Ward E et al. Cancer statistics, 2008. CA Cancer J. Clin.58(2), 71–96 (2008).
   PubMed Web of Science ®Google Scholar
• Korn EL, Liu PY, Lee SJ et al. Meta-analysis of Phase II cooperative group trials in metastatic stage IV melanoma to determine progression-free and overall survival benchmarks for future Phase II trials. J. Clin. Oncol.26(4), 527–534 (2008).
   PubMed Web of Science ®Google Scholar
• Quirt I, Verma S, Petrella T, Bak K, Charette M. Temozolomide for the treatment of metastatic melanoma: a systematic review. Oncologist12(9), 1114–1123 (2007).
   PubMed Web of Science ®Google Scholar
• Middleton MR, Grob JJ, Aaronson N et al. Randomized Phase III study of temozolomide versus dacarbazine in the treatment of patients with advanced metastatic malignant melanoma. J. Clin. Oncol.18(1), 158–166 (2000).
   PubMed Web of Science ®Google Scholar
• Kaufmann R, Spieth K, Leiter U et al; Dermatologic Cooperative Oncology Group. Temozolomide in combination with interferon-α versus temozolomide alone in patients with advanced metastatic melanoma: a randomized, Phase III, multicenter study from the Dermatologic Cooperative Oncology Group. J. Clin. Oncol.23(35), 9001–9007 (2005).
   PubMed Web of Science ®Google Scholar
• Sekulic A, Haluska P Jr, Miller AJ et al; Melanoma Study Group of Mayo Clinic Cancer Center. Malignant melanoma in the 21st Century: the emerging molecular landscape. Mayo Clin. Proc.83(7), 825–846 (2008).
   PubMed Web of Science ®Google Scholar
• Winnepenninckx V, Lazar V, Michiels S et al; Melanoma Group of the European Organization for Research and Treatment of Cancer. Gene expression profiling of primary cutaneous melanoma and clinical outcome. J. Natl Cancer Inst.98(7), 472–482 (2006).
   PubMedGoogle Scholar
• Riley PA. Melanin. Int. J. Biochem. Cell Biol.29(11), 1235–1239 (1997).
   PubMed Web of Science ®Google Scholar
• Gidanian S, Mentelle M, Meyskens FL Jr, Farmer PJ. Melanosomal damage in normal human melanocytes induced by UVB and metal uptake – a basis for the pro-oxidant state of melanoma. Photochem. Photobiol.84(3), 556–564 (2008).
   PubMed Web of Science ®Google Scholar
• Wittgen HG, van Kempen LC. Reactive oxygen species in melanoma and its therapeutic implications. Melanoma Res.17(6), 400–409 (2007).
   PubMed Web of Science ®Google Scholar
• Pavel S, van Nieuwpoort F, van der Meulen H et al. Disturbed melanin synthesis and chronic oxidative stress in dysplastic naevi. Eur. J. Cancer40(9), 1423–1430 (2004).
   PubMed Web of Science ®Google Scholar
• Smit NP, van Nieuwpoort FA, Marrot L et al. Increased melanogenesis is a risk factor for oxidative DNA damage – study on cultured melanocytes and atypical nevus cells. Photochem. Photobiol.84(3), 550–555 (2008).
   PubMed Web of Science ®Google Scholar
• Sander CS, Chang H, Hamm F, Elsner P, Thiele JJ. Role of oxidative stress and the antioxidant network in cutaneous carcinogenesis. Int. J. Dermatol.43(5), 326–335 (2004).
   PubMed Web of Science ®Google Scholar
• Meyskens FL Jr, Farmer P, Fruehauf JP. Redox regulation in human melanocytes and melanoma. Pigment Cell Res.14(3), 148–154 (2001).
   PubMedGoogle Scholar
• Eberle J, Kurbanov BM, Hossini AM, Trefzer U, Fecker LF. Overcoming apoptosis deficiency of melanoma – hope for new therapeutic approaches. Drug Resist. Updat.10(6), 218–234 (2007).
   PubMed Web of Science ®Google Scholar
• Fruehauf JP, Meyskens FL Jr. Reactive oxygen species: a breath of life or death? Clin. Cancer Res.13(3), 789–794 (2007).
   PubMed Web of Science ®Google Scholar
• Riley PA. Melanogenesis: a realistic target for antimelanoma therapy? Eur. J. Cancer27, 1172–1177 (1991).
   PubMed Web of Science ®Google Scholar
• Cabello CM, Bair WB 3rd, Wondrak GT. Experimental therapeutics: targeting the redox Achilles heel of cancer. Curr. Opin. Investig. Drugs8(12), 1022–1037 (2007).
   PubMedGoogle Scholar
• Valko M, Leibfritz D, Moncol J, Cronin MT, Mazur M, Telser J. Free radicals and antioxidants in normal physiological functions and human disease. Int. J. Biochem. Cell Biol.39(1), 44–84 (2007).
   PubMed Web of Science ®Google Scholar
• Chandel NS, Vander Heiden MG, Thompson CB, Schumacker PT. Redox regulation of p53 during hypoxia. Oncogene19(34), 3840–3848 (2000).
   PubMed Web of Science ®Google Scholar
• Klimova T, Chandel NS. Mitochondrial complex III regulates hypoxic activation of HIF. Cell Death Differ.15(4), 660–666 (2008).
   PubMed Web of Science ®Google Scholar
• Dahl C, Guldberg P. The genome and epigenome of malignant melanoma. APMIS115(10), 1161–1176 (2007).
   PubMed Web of Science ®Google Scholar
• Salmeen A, Barford D. Functions and mechanisms of redox regulation of cysteine-based phosphatases. Antioxid. Redox Signal.7(5–6), 560–577 (2005).
   PubMed Web of Science ®Google Scholar
• Robertson GP. Functional and therapeutic significance of Akt deregulation in malignant melanoma. Cancer Metastasis Rev.24(2), 273–285 (2005).
   PubMed Web of Science ®Google Scholar
• Meyskens FL Jr, Buckmeier JA, McNulty SE, Tohidian NB. Activation of nuclear factor-κΒ in human metastatic melanoma cells and the effect of oxidative stress. Clin. Cancer Res.5(5), 1197–1202 (1999).
   PubMed Web of Science ®Google Scholar
• Brar SS, Kennedy TP, Whorton AR et al. Reactive oxygen species from NAD(P) H:quinone oxidoreductase constitutively activate NF-κB in malignant melanoma cells. Am. J. Physiol. Cell Physiol.280(3), C659–C676 (2001).
   PubMed Web of Science ®Google Scholar
• Grimm EA, Ellerhorst J, Tang CH, Ekmekcioglu S. Constitutive intracellular production of iNOS and NO in human melanoma: possible role in regulation of growth and resistance to apoptosis. Nitric Oxide19(2), 133–137 (2008).
   PubMed Web of Science ®Google Scholar
• Karin M. Nuclear factor-κB in cancer development and progression. Nature441(7092), 431–436 (2006).
   PubMed Web of Science ®Google Scholar
• Soengas MS, Lowe SW. Apoptosis and melanoma chemoresistance. Oncogene22(20), 3138–3151 (2003).
   PubMed Web of Science ®Google Scholar
• Fecher LA, Amaravadi RK, Flaherty KT. The MAPK pathway in melanoma. Curr. Opin. Oncol.20(2), 183–189 (2008).
   PubMed Web of Science ®Google Scholar
• Gray-Schopfer V, Wellbrock C, Marais R. Melanoma biology and new targeted therapy. Nature445(7130), 851–857 (2007).
   PubMed Web of Science ®Google Scholar
• Gogas HJ, Kirkwood JM, Sondak VK. Chemotherapy for metastatic melanoma: time for a change? Cancer109(3), 455–464 (2007).
   PubMed Web of Science ®Google Scholar
• Sosman JA, Puzanov I. Molecular targets in melanoma from angiogenesis to apoptosis. Clin. Cancer Res.12(7 Pt 2), 2376S–2383S (2006).
   PubMed Web of Science ®Google Scholar
• Bedikian AY, Millward M, Pehamberger H et al; Oblimersen Melanoma Study Group. Bcl-2 antisense (oblimersen sodium) plus dacarbazine in patients with advanced melanoma: the Oblimersen Melanoma Study Group. J. Clin. Oncol.24(29), 4738–4745 (2006).
   PubMed Web of Science ®Google Scholar
• McDermott DF, Sosman JA, Gonzalez R et al. Double-blind randomized Phase II study of the combination of sorafenib and dacarbazine in patients with advanced melanoma: a report from the 11715 Study Group. J. Clin. Oncol.26(13), 2178–2185 (2008).
   PubMed Web of Science ®Google Scholar
• Margolin K, Longmate J, Baratta T et al. CCI-779 in metastatic melanoma: a Phase II trial of the California Cancer Consortium. Cancer104(5), 1045–1048 (2005).
   PubMed Web of Science ®Google Scholar
• Mikhail M, Velazquez E, Shapiro R et al. PTEN expression in melanoma: relationship with patient survival, Bcl-2 expression, and proliferation. Clin. Cancer Res.11(14), 5153–5157 (2005).
   PubMed Web of Science ®Google Scholar
• Lawenda BD, Kelly KM, Ladas EJ, Sagar SM, Vickers A, Blumberg JB. Should supplemental antioxidant administration be avoided during chemotherapy and radiation therapy? J. Natl Cancer Inst.100(11), 773–783 (2008).
   PubMed Web of Science ®Google Scholar
• Fruehauf JP, Zonis S, al-Bassam M et al. Melanin content and downregulation of glutathione S-transferase contribute to the action of L-buthionine-S-sulfoximine on human melanoma. Chem. Biol. Interact.111–112, 277–302 (1998).
   PubMedGoogle Scholar
• Lau AT, Wang Y, Chiu JF. Reactive oxygen species: current knowledge and applications in cancer research and therapeutic. J. Cell Biochem.104(2), 657–667 (2008).
   PubMed Web of Science ®Google Scholar
• Le Bras M, Clément MV, Pervaiz S, Brenner C. Reactive oxygen species and the mitochondrial signaling pathway of cell death. Histol. Histopathol.20(1), 205–219 (2005).
   PubMed Web of Science ®Google Scholar
• Friesen C, Kiess Y, Debatin KM. A critical role of glutathione in determining apoptosis sensitivity and resistance in leukemia cells. Cell Death Differ.11, S73–S85 (2004).
   PubMed Web of Science ®Google Scholar
• Bailey HH, Mulcahy RT, Tutsch KD et al. Phase I clinical trial of intravenous L-buthionine sulfoximine and melphalan: an attempt at modulation of glutathione. J. Clin. Oncol.12, 194–205 (1994).
   PubMed Web of Science ®Google Scholar
• Revesz L, Edgren MR, Wainson AA. Selective toxicity of buthionine sulfoximine (BSO) to melanoma cells in vitro and in vivo. Int. J. Radiat. Oncol. Biol. Phys.29(2), 403–406 (1994).
   PubMed Web of Science ®Google Scholar
• Kable EP, Favier D, Parsons PG. Sensitivity of human melanoma cells to L-dopa and DL-buthionine (S,R)-sulfoximine. Cancer Res.49(9), 2327–2331 (1989).
   PubMed Web of Science ®Google Scholar
• Prezioso JA, FitzGerald GB, Wick MM. Melanoma cytotoxicity of buthionine sulfoximine (BSO) alone and in combination with 3,4-dihydroxybenzylamine and melphalan. J. Invest. Dermatol.99(3), 289–293 (1992).
   PubMed Web of Science ®Google Scholar
• Bailey HH, Mulcahy RT, Tutsch KD. Phase I clinical trial of intravenous L-buthionine sulfoximine and melphalan: an attempt at modulation of glutathione. J. Clin. Oncol.12(1), 194–205 (1994).
   PubMed Web of Science ®Google Scholar
• Bailey HH, Ripple G, Tutsch KD. Phase I study of continuous-infusion L-S, R-buthionine sulfoximine with intravenous melphalan. J. Natl Cancer Inst.89(23), 1789–1796 (1997).
   PubMed Web of Science ®Google Scholar
• Campbell RA, Gordon MS, Betancourt O et al. ATN-224, an orally available small molecule inhibitor of SOD1, inhibits multiple signaling pathways associated with myeloma progression and has antitumor activity in a murine model of refractory myeloma growth. Proc. Am. Assoc. Canc. Res.47, 4859, (2006).
   Google Scholar
• Lowndes SA, Adams A, Timms A et al. Phase I study of ATN-224 in patients (pts) with advanced solid tumours. ASCO Annual Meeting Proceedings Part I. J. Clin. Oncol.24, 18(Suppl.), 2065 (2006).
   PubMed Web of Science ®Google Scholar
• Donate F, Juarez JC, Burnett ME et al. Identification of biomarkers for the antiangiogenic and antitumour activity of the superoxide dismutase 1 (SOD1) inhibitor tetrathiomolybdate (ATN-224). Br. J. Cancer98, 776–783 (2008).
   PubMed Web of Science ®Google Scholar
• Juarez JC, Betancourt O Jr, Pirie-Shepherd SR et al. Copper binding by tetrathiomolybdate attenuates angiogenesis and tumor cell proliferation through the inhibition of superoxide dismutase 1. Clin. Cancer Res.12, 4974–4982 (2006).
   PubMed Web of Science ®Google Scholar
• Juarez JC, Manuia M, Burnett ME et al. Superoxide dismutase 1 (SOD1) is essential for H2O2-mediated oxidation and inactivation of phosphatases in growth factor signaling. Proc. Natl Acad. Sci.105(20), 7147–7152 (2008).
   PubMed Web of Science ®Google Scholar
• Berenson JR, Boccia RV, Bashey A et al. Phase I study of the [Cu, Zn] superoxide dismutase (sod1) inhibitor atn-224 (bis-choline tetrathiomolybdate) in patients (pts) with advanced hematologic malignancies. Blood (ASH Annual Meeting Abstracts)108(11), 2593 (2006).
   Google Scholar
• Doñate F, Lowndes S, Juarez J et al. Translation of in vitro markers of the anti-angiogenic and anti-tumor activity of the SOD1 inhibitor ATN-224 to clinical trials. Eur. J. Cancer4(Suppl.), 43 (2006).
   Google Scholar
• Kim CH, Kim JH, Hsu CY, Ahn YS. Zinc is required in pyrrolidine dithiocarbamate inhibition of NF-κB activation. FEBS Lett.449(1), 28–32 (1999).
   PubMed Web of Science ®Google Scholar
• Erl W, Weber C, Hansson GK. Pyrrolidine dithiocarbamate-induced apoptosis depends on cell type, density, and the presence of Cu2+ and Zn2+. Am. J. Physiol. Cell Physiol.278(6), C1116–C1125 (2000).
   PubMed Web of Science ®Google Scholar
• Shian SG, Kao YR, Wu FY, Wu CW. Inhibition of invasion and angiogenesis by zinc-chelating agent disulfiram. Mol. Pharmacol.64(5), 1076–1084 (2003).
   PubMed Web of Science ®Google Scholar
• Chen D, Cui QC, Yang H, Duo QP. Disulfiram, a clinically used anti-alcoholism drug and copper binding agent, induces apoptotic cell death in breast cancer cultures and xenografts via inhibition of the proteasome activity. Cancer Res.66(21), 10425–10433 (2006).
   PubMed Web of Science ®Google Scholar
• Cen D, Gonzalez RI, Buckmeier JA, Kahlon RS, Tohidian NB, Meyskens FL Jr. Disulfiram induces apoptosis in human melanoma cells: a redox-related process. Mol. Cancer Ther.1, 197–204 (2002).
   PubMed Web of Science ®Google Scholar
• Meyskens FL Jr, Farmer P, Fruehauf JP. Redox regulation in human melanocytes and melanoma. Pigment Cell Res.14(3), 148–154 (2001).
   PubMedGoogle Scholar
• Cen D, Brayton D, Shahandeh B, Meyskens FL Jr, Farmer PJ. Disulfiram facilitates intracellular Cu uptake and induces apoptosis in human melanoma cells. J. Med. Chem.47, 6914–6920 (2004).
   PubMed Web of Science ®Google Scholar
• Brar SS, Grigg C, Wilson KS et al. Disulfiram inhibits activating transcription factor/cyclic AMP-responsive element binding protein and human melanoma growth in a metal-dependent manner in vitro, in mice and in a patient with metastatic disease. Mol. Cancer Ther.3, 1049–1060 (2004).
   PubMed Web of Science ®Google Scholar
• Woo SH, Park IC, Park MJ et al. Arsenic trioxide induces apoptosis through a reactive oxygen species-dependent pathway and loss of mitochondrial membrane potential in HeLa cells. Int. J. Oncol.21(1), 57–63 (2002).
   PubMed Web of Science ®Google Scholar
• Dai J, Weinberg RS, Waxman S, Jing Y. Malignant cells can be sensitized to undergo growth inhibition and apoptosis by arsenic trioxide through modulation of the glutathione redox system. Blood93(1), 268–277 (1999).
   PubMed Web of Science ®Google Scholar
• Yi J, Gao F, Shi G et al. The inherent cellular level of reactive oxygen species: one of the mechanisms determining apoptotic susceptibility of leukemic cells to arsenic trioxide. Apoptosis7, 209–215 (2002).
   PubMed Web of Science ®Google Scholar
• Davison K, Cote S, Mader S, Miller WH. Glutathione depletion overcomes resistance to arsenic trioxide in arsenic-resistant cell lines. Leukemia17(5), 931–940 (2003).
   PubMed Web of Science ®Google Scholar
• Maeda H, Hori S, Ohizumi H et al. Effective treatment of advanced solid tumors by the conbination of arsenic trioxide and L-buthionine-sulfoximine. Cell Death Differ.11(7), 737–746 (2004).
   PubMed Web of Science ®Google Scholar
• Tarhini AA, Kirkwood JM, Tawbi H, Gooding WE, Islam MF, Agarwala SS. Safety and efficacy of arsenic trioxide for patients with advanced metastatic melanoma. Cancer112(5), 1131–1138 (2008).
   PubMed Web of Science ®Google Scholar
• Kim KB, Bedikian AY, Camacho LH, Papadopoulos NE, McCullough C. A Phase II trial of arsenic trioxide in patients with metastatic melanoma. Cancer104(8), 1687–1692 (2005).
   PubMed Web of Science ®Google Scholar
• Bael TE, Peterson BL, Gollob JA. Phase II trial of arsenic trioxide and ascorbic acid with temozolomide in patients with metastatic melanoma with or without central nervous system metastases. Melanoma Res.18(2), 147–151 (2008).
   PubMed Web of Science ®Google Scholar
• Tchounwou PB, Yedjou CG, Dorsey WC. Arsenic trioside-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2). Cell Mol. Biol.49, 1071–1079 (2003).
   PubMed Web of Science ®Google Scholar
• Zheng Y, Shi Y, Tian C et al. Essential role of the voltage-dependent anion channel (VDAC) in mitochondrial permeability transition pore opening and cytochrome C release induced by arsenic trioxide. Oncogene23, 1239–1247, (2004).
   PubMed Web of Science ®Google Scholar
• Li JJ, Tang Q, Li Y et al. Role of oxidative stress in the apoptosis of hepatocellular carcinoma induced by combination of arsenic trioxide and ascorbic acid. Acta Pharmacol. Sin.27, 1078–1084 (2006).
   PubMed Web of Science ®Google Scholar
• Magda D, Miller RA. Motexafin Gadolinium: a novel redox active drug for cancer therapy. Semin. Cancer Biol.16, 466–476 (2006).
   PubMed Web of Science ®Google Scholar
• Magda D, Gerasimchuk N, Lecane P, Miller RA, Biaglow JE, Sessler JL. Motexafin gadolinium reacts with ascorbate to produce reactive oxygen species. Chem. Commun. (Camb.)21(22), 2730–2731 (2002).
   Google Scholar
• Young SW, Sidhu MK, Qing F et al. Preclinical evaluation of gadolinium (III) texaphyrin complex. A new paramagnetic contrast agent for magnetic resonance imaging. Invest. Radiol.29(3), 330–338 (1994).
   PubMed Web of Science ®Google Scholar
• Young SW, Qing F, Harriman A et al. Gadolinium(III) texaphyrin: a tumor selective radiation sensitizer that is detectable by MRI. Proc. Natl Acad. Sci. USA93(13), 6610–6615 (1996).
   PubMed Web of Science ®Google Scholar
• Evens AM, Lecane P, Magda D et al. Motexafin Gadolinium generates reactive oxygen species and induces apoptosis in sensitive and highly resistant multiple myeloma cells. Blood105(3), 1265–1273 (2008).
   Google Scholar
• Kirshner J, Du Z, Kepros J et al. STA-4783 induces apoptosis and enhances the anticancer activity of paclitaxel through induction of oxidative stress. Proc. Int. Conf. Mol. Targets Cancer Ther. AACR-NCI-EORTC,B274 (2007).
   Google Scholar
• Tuma RS. Reactive oxygen species may have antitumor activity in metastatic melanoma. J. Natl Cancer Inst.100(1), 11–12 (2008).
   PubMedGoogle Scholar
• Lawson DH, Gonzalez R, Weber RW et al. 2-year overall survival (OS) results of a Phase II trial of elesclomol (formerly STA-4783) and paclitaxel in stage IV metastatic melanoma (MM). J. Clin. Oncol.26, Abstract 20023 (2008).
   Google Scholar
• Mehta MP, Gervais R, Chabot P et al. Motexafin gadolinium (MGd) combined with prompt whole brain radiation therapy (RT) prolongs time to neurologic progression in non-small cell lung cancer (NSCLC) patients with brain metastases: Results of a Phase III trial. J. Clin. Oncol.24, (2006) (Abstract 7014).
   Web of Science ®Google Scholar