![]() We hope this review will promote a comprehensive understanding of the role of the PI3K/AKT/mTOR and RAF/MEK/ERK signaling pathways in facilitating tumors and will help direct drug selection for tumor therapy. This review will further comprehensively describe the genetic alterations in normal patients and tumor patients and discuss the role of targeted inhibitors in malignant neoplasm therapy. Furthermore, dual inhibitors provide new insight into antitumor activity. The combination of small molecular inhibitors with traditional regimens has also been explored. Dozens of agents in these two pathways have attracted great attention and have been assessed in clinical trials. Several inhibitors targeting major components of these two pathways have been supported by the FDA. PTEN alterations suppress RAF/MEK/ERK pathway activity via AKT phosphorylation and RAS inhibition. The two pathways interact with each other to participate in tumorigenesis. These mutations resulted in activated cell growth and downregulated cell apoptosis. RAS, B-Raf, PI3K, and PTEN are frequent upstream alternative sites. RAF/MEK/ERK signaling cascades are used to conduct signaling from the cell surface to the nucleus to mediate gene expression, cell cycle processes and apoptosis. The PI3K/AKT/mTOR signaling pathway is dysregulated in nearly all kinds of neoplasms, with the component in this pathway alternations. The PI3K/AKT/mTOR and RAF/MEK/ERK pathways are commonly activated by mutations and chromosomal translocation in vital targets. ![]()
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