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Cancer Pro-oxidant Therapy Through Copper Redox Cycling: Repurposing Disulfiram and Tetrathiomolybdate

Current pharmaceutical design, 2020-01, Vol.26 (35), p.4461-4466

Rieber, Manuel

2020

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Hypoxia, Mn-SOD and H2O2 regulate p53 reactivation and PRIMA-1 toxicity irrespective of p53 status in human breast cancer cells

Biochemical pharmacology, 2012-12, Vol.84 (12), p.1563-1570

2012

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Optimized Multiplex Detection of 7 KRAS Mutations by Taqman Allele-Specific qPCR

PloS one, 2016-09, Vol.11 (9), p.e0163070-e0163070

2016

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Sensitization to radiation-induced DNA damage accelerates loss of bcl-2 and increases apoptosis and autophagy

Cancer biology & therapy, 2008-10, Vol.7 (10), p.1561-1566

2008

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DN‐R175H p53 mutation is more effective than p53 interference in inducing epithelial disorganization and activation of proliferation signals in human carcinoma cells: Role of E‐cadherin

International journal of cancer, 2009-10, Vol.125 (7), p.1604-1612

2009

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Metabolic utilization of exogenous pyruvate by mutant p53 (R175H) human melanoma cells promotes survival under glucose depletion

Cancer biology & therapy, 2011-10, Vol.12 (7), p.647-656

2011

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Abstract 4334: Greater resistance of mutant p53 tumor cells to hypoxia or chloroquine with glucose or pyruvate supplementation is diminished under glucose starvation

Cancer research (Chicago, Ill.), 2014-10, Vol.74 (19_Supplement), p.4334-4334

Rieber, Manuel

2014

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Mcl-1 cleavage and sustained phosphorylation of c-Jun -N-terminal kinase mediate melanoma apoptosis induced by 2-acetyl furanonaphthoquinone : Roles of bcl-2 and p53

Cancer biology & therapy, 2008-08, Vol.7 (8), p.1206-1211

2008

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Role of peroxidases, thiols and Bak/Bax in tumor cell susceptibility to Cu[DEDTC] 2

Biochemical pharmacology, 2007-09, Vol.74 (6), p.841-850

2007

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Suppression of survival in human SKBR3 breast carcinoma in response to metal–chelator complexes is preferential for copper–dithiocarbamate

Biochemical pharmacology, 2006-03, Vol.71 (6), p.722-734

2006

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ERK activation increases nitroprusside induced apoptosis in human melanoma cells irrespective of p53 status: Role of superoxide dismutases

Cancer biology & therapy, 2009-06, Vol.8 (12), p.1173-1182

2009

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p53 inactivation decreases dependence on estrogen/ERK signalling for proliferation but promotes EMT and susceptility to 3-bromopyruvate in ERα+ breast cancer MCF-7 cells

Biochemical pharmacology, 2014-03, Vol.88 (2), p.169-177

2014

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Nitroprusside induces melanoma ferroptosis with serum supplementation and prolongs survival under serum depletion or hypoxia

Biochemical and biophysical research communications, 2020-05, Vol.525 (3), p.626-632

2020

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Cyclin D1 overexpression induces epidermal growth factor-independent resistance to apoptosis linked to BCL-2 in human A431 carcinoma

Apoptosis (London), 2006-01, Vol.11 (1), p.121-129

2006

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Disulfiram anti-cancer efficacy without copper overload is enhanced by extracellular H2O2 generation: antagonism by tetrathiomolybdate

Oncotarget, 2015-10, Vol.6 (30), p.29771-29781

2015

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Hypoxic resistance of KRAS mutant tumor cells to 3-Bromopyruvate is counteracted by Prima-1 and reversed by N-acetylcysteine

BMC cancer, 2016-11, Vol.16 (1), p.902, Article 902

2016

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Abstract 2907: AMPK induction, lysosomal acidification and melanoma survival increased by p53 dysfunction are counteracted by inhibiting autophagy

Cancer research (Chicago, Ill.), 2015-08, Vol.75 (15_Supplement), p.2907-2907

2015

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Abstract 3049: BRAF status and low glutamine/glucose influence glutamine addiction modulated by oxidative stress in human melanoma cells

Cancer research (Chicago, Ill.), 2015-08, Vol.75 (15_Supplement), p.3049-3049

2015

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Abstract C36: Hypoxia or glutathione depletion increase apoptotic response to PRIMA-1 in p53-mutated and nonmutated human breast cancer cells

Molecular cancer therapeutics, 2011-11, Vol.10 (11_Supplement), p.C36-C36

2011

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Abstract 4331: Lowering glucose increases nutlin-3 toxicity against melanomas irrespective of BRAF,NRAS or p53 mutations

Cancer research (Chicago, Ill.), 2014-10, Vol.74 (19_Supplement), p.4331-4331

2014

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Abstract 1107: Mutant p53 increases epithelial mesenchymal transition, estrogen receptor alpha and erbB2/Her2/neu

Cancer research (Chicago, Ill.), 2010-04, Vol.70 (8_Supplement), p.1107-1107

2010

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Abstract 1890: Superoxide modulates tumor cell survival in response to hypoxia and metabolic stress: role of p53 status

Cancer research (Chicago, Ill.), 2013-04, Vol.73 (8_Supplement), p.1890-1890

2013

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Abstract 5435: Increased tumor susceptibility to low glucose under hypoxia is increased by BRAF(V600E) mutation: correlation with persistent phosphoP90RSK activation

Cancer research (Chicago, Ill.), 2013-04, Vol.73 (8_Supplement), p.5435-5435

2013

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Anticancer response to disulfiram may be enhanced by co-treatment with MEK inhibitor or oxaliplatin: modulation by tetrathiomolybdate, KRAS/BRAF mutations and c-MYC/p53 status

Ecancermedicalscience, 2019-01, Vol.13, p.890

2019

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Signalling responses linked to betulinic acid‐induced apoptosis are antagonized by MEK inhibitor U0126 in adherent or 3D spheroid melanoma irrespective of p53 status

International journal of cancer, 2006-03, Vol.118 (5), p.1135-1143

2006

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Cancer Pro-oxidant Therapy Through Copper Redox Cycling: Repurposing Disulfiram and Tetrathiomolybdate

Hypoxia, Mn-SOD and H2O2 regulate p53 reactivation and PRIMA-1 toxicity irrespective of p53 status in human breast cancer cells

Optimized Multiplex Detection of 7 KRAS Mutations by Taqman Allele-Specific qPCR

Sensitization to radiation-induced DNA damage accelerates loss of bcl-2 and increases apoptosis and autophagy

DN‐R175H p53 mutation is more effective than p53 interference in inducing epithelial disorganization and activation of proliferation signals in human carcinoma cells: Role of E‐cadherin

Metabolic utilization of exogenous pyruvate by mutant p53 (R175H) human melanoma cells promotes survival under glucose depletion

Abstract 4334: Greater resistance of mutant p53 tumor cells to hypoxia or chloroquine with glucose or pyruvate supplementation is diminished under glucose starvation

Mcl-1 cleavage and sustained phosphorylation of c-Jun -N-terminal kinase mediate melanoma apoptosis induced by 2-acetyl furanonaphthoquinone : Roles of bcl-2 and p53

Role of peroxidases, thiols and Bak/Bax in tumor cell susceptibility to Cu[DEDTC] 2

Suppression of survival in human SKBR3 breast carcinoma in response to metal–chelator complexes is preferential for copper–dithiocarbamate

ERK activation increases nitroprusside induced apoptosis in human melanoma cells irrespective of p53 status: Role of superoxide dismutases

p53 inactivation decreases dependence on estrogen/ERK signalling for proliferation but promotes EMT and susceptility to 3-bromopyruvate in ERα+ breast cancer MCF-7 cells

Nitroprusside induces melanoma ferroptosis with serum supplementation and prolongs survival under serum depletion or hypoxia

Cyclin D1 overexpression induces epidermal growth factor-independent resistance to apoptosis linked to BCL-2 in human A431 carcinoma

Disulfiram anti-cancer efficacy without copper overload is enhanced by extracellular H2O2 generation: antagonism by tetrathiomolybdate

Hypoxic resistance of KRAS mutant tumor cells to 3-Bromopyruvate is counteracted by Prima-1 and reversed by N-acetylcysteine

Abstract 2907: AMPK induction, lysosomal acidification and melanoma survival increased by p53 dysfunction are counteracted by inhibiting autophagy

Abstract 3049: BRAF status and low glutamine/glucose influence glutamine addiction modulated by oxidative stress in human melanoma cells

Abstract C36: Hypoxia or glutathione depletion increase apoptotic response to PRIMA-1 in p53-mutated and nonmutated human breast cancer cells

Abstract 4331: Lowering glucose increases nutlin-3 toxicity against melanomas irrespective of BRAF,NRAS or p53 mutations

Abstract 1107: Mutant p53 increases epithelial mesenchymal transition, estrogen receptor alpha and erbB2/Her2/neu

Abstract 1890: Superoxide modulates tumor cell survival in response to hypoxia and metabolic stress: role of p53 status

Abstract 5435: Increased tumor susceptibility to low glucose under hypoxia is increased by BRAF(V600E) mutation: correlation with persistent phosphoP90RSK activation

Anticancer response to disulfiram may be enhanced by co-treatment with MEK inhibitor or oxaliplatin: modulation by tetrathiomolybdate, KRAS/BRAF mutations and c-MYC/p53 status

Signalling responses linked to betulinic acid‐induced apoptosis are antagonized by MEK inhibitor U0126 in adherent or 3D spheroid melanoma irrespective of p53 status

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