This panel provides drug-protein interaction and their ADRs along with references
| Interacting Drugs |
Toxicity |
Mechanism |
Reference |
|---|
| Arsenic trioxide | Anemia | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Cardiovascular Disease | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Developmental Abnormalities | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Diabetes | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Eosinophilia | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Fibrosis Of Kidney | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Fibrosis Of Liver | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Hearing Loss | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Leukopenia | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Arsenic trioxide | Neurologic And Neurobehavioral Disorder | The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p [ ADR Type 2 ] | Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2)
|
| Chelerythrine chloride | Tumor Cell Toxicity And Growth Delay | In vitro and in vivo activity of protein kinase C inhibitor chelerythrine chloride induces tumor cell toxicity and growth delay in vivo p53-deficient SQ-20B HNSCC cells in vivo. [ ADR Type 2 ] | In vitro and in vivo activity of protein kinase C inhibitor chelerythrine chloride induces tumor cell toxicity and growth delay in vivo
|
| Cidofovir | Apoptosis | Induction of apoptosis in HPV-positive cells by HPMPC was associated with accumulation of the tumor suppressor protein p53 and the cyclin-dependent kinase inhibitor p21/WAF-1. [ ADR Type 2 ] | Induction of apoptosis by cidofovir in human papillomavirus (HPV)-positive cells
|
| Cisplatin | Apoptosis | Wild-type p53 and MDM2 (murine double minute 2) proteins was induced when cis-diamminedichloroplatinum (cisplatin) caused apoptosis in human glioblastoma U87-MG cells [ ADR Type 3 ] | MDM2 protein confers the resistance of a human glioblastoma cell line to cisplatin-induced apoptosis
|
| Didanosine | Tumor Suppression | Those patients with a mutated p53 did not enter remission of tumor suppression following treatment with ddI and patients disease relapse was associated with the selection of a tumor clone carrying mutated inactive p53. [ ADR Type 2 ] | Persistent inhibition of telomerase reprograms adult T-cell leukemia to p53-dependent senescence
|
| Indomethacin | Apoptosis | Differential apoptosis by indomethacin in gastric epithelial cells through the constitutive expression of wild-type p53 and/or up-regulation of c-myc [ ADR Type 2 ] | Differential apoptosis by indomethacin in gastric epithelial cells through the constitutive expression of wild-type p53 and/or up-regulation of c-myc
|
| Methotrexate | Apoptosis | Immunohistochemical overexpression of p53 was detected in the basal layer of the cultures treated with methotrexate,which induces apoptotic cell death in human keratinocytes. [ ADR Type 5 ] | Methotrexate induces apoptotic cell death in human keratinocytes
|
| Paclitaxel | Mitotic Catastrophe | Silencing of the novel p53 target gene serum inducible kinase (Snk/Plk2) leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells [ ADR Type 2 ] | Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells
|
| Zalcitabine | Tumor Suppression | Those patients with a mutated p53 did not enter remission of tumor suppression following treatment with ddC and patients disease relapse was associated with the selection of a tumor clone carrying mutated inactive p53. [ ADR Type 2 ] | Persistent inhibition of telomerase reprograms adult T-cell leukemia to p53-dependent senescence
|
| Zidovudine | Tumor Suppression | Those patients with a mutated p53 did not enter remission of tumor suppression following treatment with AZT and patients disease relapse was associated with the selection of a tumor clone carrying mutated inactive p53. [ ADR Type 2 ] | Persistent inhibition of telomerase reprograms adult T-cell leukemia to p53-dependent senescence
|