2012
DOI: 10.4161/cc.22852
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p53 expression controls prostate cancer sensitivity to chemotherapy and the MDM2 inhibitor Nutlin-3

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Cited by 93 publications
(91 citation statements)
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References 51 publications
(76 reference statements)
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“…[121][122][123][124][125][126] While the DBD domain is highly conserved among vertebrates and invertebrates, the C terminus varies, resulting in a change from dimeric structure to a tetramer in the vertebrates. [127][128][129] The more ancient members of the family include p73, involved in cancer, 130 neurodevelopment, 131,132 and aging, 133 and p63, involved in epidermal development, 119,[134][135][136] cancer, [137][138][139][140][141] reproduction, 142 and heart development. 143 Understanding the structural restrain of its structure is pivotal to understand the function of p53 [144][145][146] as well as its potential therapeutic exploitation.…”
Section: Discussionmentioning
confidence: 99%
“…[121][122][123][124][125][126] While the DBD domain is highly conserved among vertebrates and invertebrates, the C terminus varies, resulting in a change from dimeric structure to a tetramer in the vertebrates. [127][128][129] The more ancient members of the family include p73, involved in cancer, 130 neurodevelopment, 131,132 and aging, 133 and p63, involved in epidermal development, 119,[134][135][136] cancer, [137][138][139][140][141] reproduction, 142 and heart development. 143 Understanding the structural restrain of its structure is pivotal to understand the function of p53 [144][145][146] as well as its potential therapeutic exploitation.…”
Section: Discussionmentioning
confidence: 99%
“…However, nutlins, in particular, have proved to be highly effective in the preclinical setup and may inhibit cancer growth by pathways other than MDM2 inhibition[156][163]. In order to critically evaluate the mechanism of action and therapeutic potential of a MDM2 inhibitor, the following properties are desirable: ( a ) a high binding affinity and specificity to MDM2, ( b ) potent cellular activity in cancer cells with wild-type p53, and ( c ) a an appropriate pharmacokinetic (PK) profile.…”
Section: Future Directionsmentioning
confidence: 99%
“…Indeed, it has been demonstrated that a number of small-molecule MDM2 inhibitors can disrupt the MDM2-p53 interaction, release p53 from negative control and activate the p53 pathway, leading to cell cycle arrest and apoptosis in a number of solid cancers and haematological malignancies [14][17]. Moreover, many laboratories have shown that MDM2 inhibitors can synergise with conventional chemotherapeutic agents, resulting in enhanced efficacy [18][22]. Interestingly, MDM2 inhibitors have been reported to induce cancer cell apoptosis even without the concomitant application of genotoxic stimuli [17], [18], [20].…”
Section: Introductionmentioning
confidence: 99%