Abstract
Over the past few years, significant advances have occurred in both our understanding of the complexity of signal transduction pathways as well as the isolation of specific inhibitors which target key components in those pathways. Furthermore critical information is being accrued regarding how genetic mutations can affect the sensitivity of various types of patients to targeted therapy. Finally, genetic mechanisms responsible for the development of resistance after targeted therapy are being discovered which may allow the creation of alternative therapies to overcome resistance. This review will discuss some of the highlights over the past few years on the roles of key signaling pathways in various diseases, the targeting of signal transduction pathways and the genetic mechanisms governing sensitivity and resistance to targeted therapies.
Highlights
The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/ mTOR pathways are often activated by mutations within individual components of these pathways, as well as the aberrant activation of upstream growth factor receptors
Mutations at KRAS which result in increased mutant Ras activity can interact with increased Wnt expression in lung cancer and lead to a worse prognosis as the tumors arise at an increased incidence and tumors which are larger [13]
The PI3K/PTEN/Akt/mTOR complex 1 (mTORC1) pathway is frequently upregulated in T-ALL, The effects of the novel allosteric Akt inhibitor, MK-2206, on a panel of human T-ALL cell lines and primary cells from T-ALL patients were examined
Summary
The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/ mTOR pathways are often activated by mutations within individual components of these pathways, as well as the aberrant activation of upstream growth factor receptors. Mutations Alter the Activity of the Ras/Raf/MEK/ ERK and PI3K/PTEN/Akt/mTOR pathways. Both studies indicated that sensitivity to inhibitors was often linked with genetic mutations at key elements in the Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and some other pathways.
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