Pub. Date : 2017 Jun
PMID : 28653879
9 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | TP53 alteration determines the combinational cytotoxic effect of doxorubicin and an antioxidant NAC. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 2 | In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 3 | In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 4 | In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 5 | In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 6 | In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 7 | In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 8 | N-acetylcysteine prevented phosphorylation of P53 protein that had been induced by doxorubicin. | Doxorubicin | tumor protein p53 | Homo sapiens |
| 9 | In conclusion, TP53 genetic alteration is a critical factor that determines the use of antioxidant supplements during doxorubicin treatment. | Doxorubicin | tumor protein p53 | Homo sapiens |