A5035838280- Cancer-related Molecular Pathways
- Cancer Research and Treatments
- Protein Degradation and Inhibitors
- Cytomegalovirus and herpesvirus research
- Signaling Pathways in Disease
- Melanoma and MAPK Pathways
- Blood donation and transfusion practices
- Cell death mechanisms and regulation
- Apelin-related biomedical research
- Cancer Mechanisms and Therapy
Newcastle University
2018-2019
MAPK and p14ARF⁻MDM2⁻p53 pathways are critical in cutaneous melanomas. Here, synergistic combination of the MEK inhibitor, trametinib, with MDM2 inhibitors, nutlin-3/RG7388/HDM201, mechanistic basis responses, for BRAFV600E p53WT melanoma cells, reported. The treatments induced higher levels p53 target gene transcripts protein products, resulting increased cell cycle arrest apoptosis compared inhibitors alone, suggesting trametinib synergized via upregulation p53-dependent pathways. In...
Emergence of resistance to molecular targeted therapy constitutes a limitation clinical benefits in cancer treatment. Cross-resistance commonly happens with chemotherapeutic agents but might not agents. In the current study, TP53 wild-type cell lines druggable MAPK pathway mutations [BRAFV600E (WM35) or NRAS Q61K (SJSA-1)] were compared their mutant sublines (WM35-R, SN40R2) derived by selection for MDM2/p53 binding antagonists. The continued presence targets (TP53MUT) WM35-R and SN40R2...
Abstract Emergence of resistance to molecular targeted therapy constitutes a potential limitation clinical benefits in cancer treatment. Cross-resistance commonly happens with chemotherapeutic agents but might not agents. In the current study, TP53 wild -type cell lines druggable MAPK pathway mutations (BRAFV600E (WM35) or NRAS Q61K (SJSA-1)) were compared their mutant sublines (WM35-R, SN40R2) derived by selection for MDM2/p53 binding antagonists. The continued presence targets (TP53MUT)...
Introduction MAPK and ARF-MDM2-p53 pathways are critical in cutaneous melanomas. This study examined the combination treatment of MEK inhibitor, trametinib, with MDM2 inhibitors, nutlin-3/RG7388/HDM201, BRAFV600E mutant p53 wild-type (p53WT) melanoma cell lines explored mechanistic basis these responses. Material methods Two p53WT lines, A375 WM35, were treated either trametinib or combinations. Results discussions The both WM35 showed additive to synergistic effects by Chou-Talalay median...
Emergence of resistance to molecular targeted therapy constitutes a potential limitation clinical benefits in cancer treatment. Cross-resistance commonly happens with chemotherapeutic agents but might not agents. In the current study, TP53 wild -type cell lines druggable MAPK pathway mutations (BRAFV600E (WM35) or NRAS Q61K (SJSA-1)) were compared their mutant sublines (WM35-R, SN40R2) derived by selection for MDM2/p53 binding antagonists. The continued presence targets (TP53MUT) WM35-R and...