Selective toxicity of buthionine sulfoximine (BSO) to melanoma cells in vitro and in vivo

Révész, Láśzló; Edgren, Margareta; Wainson, A. A.

doi:10.1016/0360-3016(94)90298-4

Cited by 27 publications

(4 citation statements)

References 13 publications

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“…For instance, preclinical data shows the potential for metabolic modulators to overcome resistance to BRAF and MEK inhibitors [ 55 ] leading to early phase clinical trials, but no phase 3 trial have been initiated [ 56 , 57 , 58 ]. Evidence also exists that certain drug combinations can render melanoma cells sensitive to systemic chemotherapies, which could expand the treatment options for these patients [ 59 ] significantly due to the ease of access to these chemotherapies in cancer care. This is of interest, especially in the second-line for metastatic or unresectable disease when patients fail first-line therapies.…”

Section: Discussionmentioning

confidence: 99%

Trends in Melanoma Phase 3 Clinical Trials since 2010: Is there Hope for Advanced Melanoma Therapies beyond Approved Treatment Mechanisms?

Kakish

Ahmed

Elshami

et al. 2022

Cancers

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Background: Several drugs and treatment modalities are under investigation to improve current melanoma therapy options. This review profiles the trends in clinical trial investment in late-stage melanoma, and anticipates what changes are expected in melanoma treatment, with a focus on exploratory drug mechanisms. Methods: We reviewed nine international clinical trial databases for registered, interventional, and phase 3 cutaneous melanoma clinical trials since 2010. Results: 73 trials studied drug therapies in late-stage (stage III and IV) melanoma. Exploratory mechanisms were investigated in 32% (23/73) of the late-stage melanoma drug therapy trials. Most exploratory drug trials include immunotherapy drug mechanisms (15/23 trials). Two exploratory mechanisms showed promise: the anti-LAG3 antibody, relatlimab, and the hapten modified vaccine, MVax. Many (52%) trials of exploratory mechanisms are ongoing including the use of adoptive cell transfer immunotherapies, dendritic cell vaccine therapy, and histone deacetylase (HDAC) inhibitors, among others. Conclusions: Since most clinical trials focus on previously approved drug mechanisms, it is likely that paradigm-changing treatments will involve these therapies being used in new treatment contexts or combinations. Only 2 exploratory drug mechanisms studied since 2010 have achieved promising results in the phase 3 setting, though many other trials are ongoing at this time

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Section: Discussionmentioning

confidence: 99%

Trends in Melanoma Phase 3 Clinical Trials since 2010: Is there Hope for Advanced Melanoma Therapies beyond Approved Treatment Mechanisms?

Kakish

Ahmed

Elshami

et al. 2022

Cancers

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“…The release is then triggered in the tumor, minimizing the side effects. It is the observed case in certain skin cancers, such as melanoma [ 3 , 4 ]. Moreover, when skin is exposed to UV light, cells react first by activating antioxidant mechanisms: the level of glutathione (GSH) and its accompanying enzymes is dramatically increased to counteract the appearance of reactive oxygen species [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Three-Step Synthesis of a Redox-Responsive Blend of PEG–block–PLA and PLA and Application to the Nanoencapsulation of Retinol

Gheluwe

Buchy²,

Chourpa

et al. 2020

Polymers

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Smart polymeric nanocarriers have been developed to deliver therapeutic agents directly to the intended site of action, with superior efficacy. Herein, a mixture of poly(lactide) (PLA) and redox-responsive poly(ethylene glycol)–block–poly(lactide) (PEG–block–PLA) containing a disulfide bond was synthesized in three steps. The nanoprecipitation method was used to prepare an aqueous suspension of polymeric nanocarriers with a hydrodynamic diameter close to 100 nm. Retinol, an anti-aging agent very common in cosmetics, was loaded into these smart nanocarriers as a model to measure their capacity to encapsulate and to protect a lipophilic active molecule. Retinol was encapsulated with a high efficiency with final loading close to 10% w/w. The stimuli-responsive behavior of these nanocarriers was demonstrated in vitro, in the presence of l-Glutathione, susceptible to break of disulfide bond. The toxicity was low on human keratinocytes in vitro and was mainly related to the active molecule. Those results show that it is not necessary to use 100% of smart copolymer in a nanosystem to obtain a triggered release of their content.

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“…Alkylating agents exert a cytotoxic effect upon melanoma-derived cell lines, 16 their toxicity being enhanced when intracellular levels of GSH are depleted by buthionine sulfoximine (BSO). 17 The purpose of this study was to determine if blocking the melanogenic pathway at the first stage by inhibiting tyrosinase activity could prevent quinone free radicals from being produced and reduce the HD-induced cytotoxicity seen in cultures containing melanin-producing cells. For this purpose, G361-pigmented melanoma cells were used as the experimental in vitro model, with a nonpigmented SV-40 virus-transformed human keratinocyte line (SVK-14) being used as a control system.…”

Section: Introductionmentioning

confidence: 99%

Kojic acid reduces the cytotoxic effects of sulfur mustard on cultures containing human melanoma cells in vitro

Smith

Lindsay

2001

J of Applied Toxicology

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In vivo experiments have shown that melanocytes are more sensitive than keratinocytes to the cytotoxic effects of sulfur mustard when it is applied topically to pig skin.1 It has been hypothesized that this is caused by the uncoupling of the melanogenic pathway by depletion of cellular glutathione, resulting in the uncontrolled production of cytotoxic quinone free-radical species by tyrosinase.2. In the present study, the feasibility of blocking the melanogenic pathway as a means of reducing the cytotoxicity of sulfur mustard was evaluated using kojic acid. Kojic acid is a topically applied depigmenting agent that exerts its effect by acting as a slow-binding, competitive inhibitor of tyrosinase.3 Preincubation of G361 pigmented melanoma cells and mixed cultures of G361 cells and SVK keratinocytes with 2.5 mM kojic acid resulted in significant increases in the viability of these cultures as determined by neutral red (NR) and gentian violet (GV) dye binding assays for up to 48 h following exposure to 50 microM sulfur mustard. The highest levels of protection were seen in the G361 cultures, with a 26.8% increase in culture viability (NR assay) compared with the sulfur-mustard-only controls at 24 h. Preincubation of SVK cells alone with kojic acid resulted in lower increases in viability (2.5% at 24 h by the NR assay). Inhibition of the melanogenic pathway reduces the sensitivity of cultures containing pigment cells to sulfur mustard.

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Selective toxicity of buthionine sulfoximine (BSO) to melanoma cells in vitro and in vivo

Cited by 27 publications

References 13 publications

Trends in Melanoma Phase 3 Clinical Trials since 2010: Is there Hope for Advanced Melanoma Therapies beyond Approved Treatment Mechanisms?

Trends in Melanoma Phase 3 Clinical Trials since 2010: Is there Hope for Advanced Melanoma Therapies beyond Approved Treatment Mechanisms?

Three-Step Synthesis of a Redox-Responsive Blend of PEG–block–PLA and PLA and Application to the Nanoencapsulation of Retinol

Kojic acid reduces the cytotoxic effects of sulfur mustard on cultures containing human melanoma cells in vitro

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