EXCLI Journal; 20:Doc614; ISSN 1611-2156 2021
DOI: 10.17179/excli2020-3181
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Evaluation of the cytotoxic and immunogenic potential of temozolamide, panabinostat, and Lophophora williamsii extract against C6 glioma cells

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Cited by 7 publications
(6 citation statements)
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“…Amidst the pharmaceutical therapies available for the treatment of glioma and melanoma, we can find the well-known drug temozolomide (TMZ), an oral DNA alkylating agent. 105,127 A study unveiled that the incorporation of a N-ethylselenocyanate group to the amide functionality of TMZ resulted in 40 (Figure 9) that exerted a stronger antitumor activity in both glioma and melanoma mouse models. 105 Of note, this modification did not affect its capacity to penetrate the blood−brain barrier (BBB), as the moiety responsible for this TMZ property and the degradation of active metabolites remains unmodified.…”
Section: Cytarabinementioning
confidence: 99%
“…Amidst the pharmaceutical therapies available for the treatment of glioma and melanoma, we can find the well-known drug temozolomide (TMZ), an oral DNA alkylating agent. 105,127 A study unveiled that the incorporation of a N-ethylselenocyanate group to the amide functionality of TMZ resulted in 40 (Figure 9) that exerted a stronger antitumor activity in both glioma and melanoma mouse models. 105 Of note, this modification did not affect its capacity to penetrate the blood−brain barrier (BBB), as the moiety responsible for this TMZ property and the degradation of active metabolites remains unmodified.…”
Section: Cytarabinementioning
confidence: 99%
“…HDACi appear to have a vital role in DNA damage response, and a radiosensitizing effect of HDACi (vorinostat, panobinostat, VPA, entinostat, scriptaid) has been shown in GB in vitro, with support for vorinostat for GB therapy in combination with heavy ion therapy [ 31 , 33 , 35 , 128 ]. HDACi have been shown to inhibit GB cell growth mediated by cell cycle arrest and apoptosis, as highlighted in Supplementary Table S1 [ 129 , 130 , 131 , 132 , 133 , 134 , 135 ]. The class I/II HDACi trichostatin A (TSA) increased GB apoptosis induction through the p38MAPK-p53 cascade [ 136 ].…”
Section: Current Status Of Hdaci For Gb Therapymentioning
confidence: 99%
“…Nanozyme-catalyzed chemodynamical therapy showed great potential due to its noninvasion, sensitive tumor cell lethal, and immunity regulation . Moreover, CDT, if it synergized with photothermal therapy, could be augmented with improved therapeutic outcomes.…”
mentioning
confidence: 99%
“…30,31 Standard treatment for glioma is surgical resection followed by radiotherapy and chemotherapy using TMZ (a secondgeneration oral alkylating agent, which cannot induce ICD when applied alone). 32 For GBM, the effect of treatment is poor, and there are considerable side effects. Most patients still need to undergo secondary surgery.…”
mentioning
confidence: 99%
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