Molecular Targets of Arsenic Trioxide in Malignant Cells

Miller, W. H.

doi:10.1634/theoncologist.7-2004-14

Cited by 13 publications

(17 citation statements)

References 7 publications

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“…It is known that ATO induces apoptosis through multiple intracellular targets 32, 33. For this reason we determined the levels of apoptosis after treatment of NB4 cells with ATO at different times.…”

Section: Resultsmentioning

confidence: 99%

A retrospective seven‐year analysis of the use of B cell depletion therapy in systemic lupus erythematosus at university college london hospital: The first fifty patients

Lu¹,

Ng²,

Cambridge³

et al. 2009

Arthritis & Rheumatism

247

146

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Objective. To describe the 6-month clinical outcome and the long-term safety profile of B cell depletion therapy (BCDT) in 50 patients with active systemic lupus erythematosus (SLE), who were nonresponsive or poorly responsive to conventional immunosuppression. Methods. All except 4 of 50 patients with active SLE received 1 gm of rituximab, 750 mg of cyclophosphamide, and 100 -250 mg of methylprednisolone, administered on 2 occasions 2 weeks apart, to achieve B cell depletion. Clinical outcome was assessed using the British Isles Lupus Assessment Group (BILAG) activity index and serial serologic measurements of disease activity. Remission was defined as a change from a BILAG A or B score to a C or D score in every organ system. Partial remission was a change from a BILAG A or B score to a C or D score in at least 1 system, but with the persistence of 1 score of A or B in another system. No improvement was defined as a BILAG A or B score that remained unchanged after treatment. Results. Of the 45 patients available for followup at 6 months, 19 patients (42%) achieved remission, and 21 patients (47%) reached partial remission after 1 cycle of BCDT (mean followup 39.6 months). BCDT resulted in a decrease in median global BILAG scores from 12 to 5 (P < 0.0001) and median anti-double-stranded DNA antibody titers from 106 to 42 IU/ml (P < 0.0001), and an increase in the median C3 level from 0.81 to 0.95 mg/liter (P < 0.02) at 6 months. Five serious adverse events were observed. Conclusion. BCDT is an effective treatment for patients with active SLE whose disease has failed to respond to standard immunosuppressive therapy. Although the safety profile of BCDT is favorable, ongoing monitoring is required.

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Section: Resultsmentioning

confidence: 99%

A retrospective seven‐year analysis of the use of B cell depletion therapy in systemic lupus erythematosus at university college london hospital: The first fifty patients

Lu¹,

Ng²,

Cambridge³

et al. 2009

Arthritis & Rheumatism

247

146

View full text Add to dashboard Cite

show abstract

“…Therefore, compounds that oxidize thiol group and/ or deplete the mitochondrial glutathione pool will cause substantial apoptosis of cancer cells (72,196). Agents like arsenic trioxide (134,166) or isothiocyanates, represented by phenylethyl isothiocyanate (PEITC) (198,217) have been shown to possess relative selectivity in killing cancer cells by upsetting the normal homeostasis in the cellular redox environment. Intriguingly, PEITC has been reported to efficiently kill resistant leukemia cells (197).…”

Section: Class 3 and 4: Thiol Redox Inhibitors And Vdac/ant Targetingmentioning

confidence: 99%

Anticancer Drugs Targeting the Mitochondrial Electron Transport Chain

Rohlena

Dong

Ralph

et al. 2011

Antioxidants & Redox Signaling

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“…Arsenic trioxide (As 2 O 3 ) is toxic to various human cancers [1–5], and has been primarily used in the treatment of acute promyelocytic leukemia (APL). Moreover, its therapeutic effects are also under investigation in other malignancies [6].…”

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide concentration determines the fate of Ewing's sarcoma family tumors and neuroblastoma cells in vitro

et al. 2006

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Arsenic trioxide (As 2 O 3 ) induces both the differentiation and apoptosis of acute promyelocytic leukemia cells in a concentration dependent manner. We assessed the effects of As 2 O 3 in CADO-ES Ewing's sarcoma (ES), JK-GMS peripheral primitive neuroectodermal tumor (PNET), and SH-SY5Y neuroblastoma cells, as they share common histogenetic backgrounds. As 2 O 3 at low concentrations (0.1-1 lM) induced SH-SY5Y differentiation, and whereas PNET cells acquired a slightly differentiated phenotype, change was minimal in ES cells. Extracellular signal-regulated kinase 2 (ERK2) was activated at low As 2 O 3 concentrations, and PD98059, an inhibitor of MEK-1, blocked SH-SY5Y cell differentiation by As 2 O 3 . High concentrations (2-10 lM) of As 2 O 3 induced the apoptosis in all three cell lines, and this was accompanied by the activation of c-jun N-terminal kinase. The generation of H 2 O 2 and activation of caspase 3 were identified as critical components of As 2 O 3 -induced apoptosis in all of the above cell lines. Fibroblast growth factor 2 enhanced As 2 O 3 -induced apoptosis in JK-GMS cells. The overall effects of As 2 O 3 strongly suggest that it has therapeutic potential for the treatment of ES/PNET.

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Molecular Targets of Arsenic Trioxide in Malignant Cells

Abstract: ABSTRACT

Cited by 13 publications

References 7 publications

A retrospective seven‐year analysis of the use of B cell depletion therapy in systemic lupus erythematosus at university college london hospital: The first fifty patients

A retrospective seven‐year analysis of the use of B cell depletion therapy in systemic lupus erythematosus at university college london hospital: The first fifty patients

Anticancer Drugs Targeting the Mitochondrial Electron Transport Chain

Arsenic trioxide concentration determines the fate of Ewing's sarcoma family tumors and neuroblastoma cells in vitro

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