| Autor: |
Fregni M; Department of Cellular, Computational, and Integrative Biology (CIBIO), University of Trento, 38123 Povo, TN, Italy., Ciribilli Y; Department of Cellular, Computational, and Integrative Biology (CIBIO), University of Trento, 38123 Povo, TN, Italy., Zawacka-Pankau JE; Center for Hematology and Regenerative Medicine, Department of Medicine, Huddinge, Karolinska Institutet, 141 86 Stockholm, Sweden.; Chair and Department of Biochemistry, Medical University of Warsaw, 02-097 Warsaw, Poland. |
| Abstrakt: |
Despite the recent development of precision medicine and targeted therapies, lung cancer remains the top cause of cancer-related mortality worldwide. The patients diagnosed with metastatic disease have a five-year survival rate lower than 6%. In metastatic disease, EGFR is the most common driver of mutation, with the most common co-driver hitting TP 53. EGFR -positive patients are offered the frontline treatment with tyrosine kinase inhibitors, yet the development of resistance and the lack of alternative therapies make this group of patients only fit for clinical trial participation. Since mutant p53 is the most common co-driver in the metastatic setting, therapies reactivating the p53 pathway might serve as a promising alternative therapeutic approach in patients who have developed a resistance to tyrosine kinase inhibitors. This review focuses on the molecular background of EGFR -mutated lung cancer and discusses novel therapeutic options converging on the reactivation of p53 tumor suppressor pathways. |
