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Oncogenic KRAS can activate numerous effector pathways to drive malignant progression.
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Moreover, numerous studies have targeted Ras downstream effector pathways such as Raf kinases, MEK or PI3Ks [ 36, 37].
Both the activity of drug effector pathways and drug non-effector pathways could affect therapeutic effects of target drugs.
In the case with good drug effect, drug effector pathways are abnormally activated, which could be caused by two different mutant oncogenes in this pathway.
Numerous effector functions have been attributed to IL-18.
Here again, the range of potential effector pathways is open to speculation.
Ras effector pathways have key roles in p27 proteolysis [ 87- 89].
T-cell effector pathways in RA are complex.
DCs produce cytokines that influence the Th effector pathways.
One of the best-characterized effector pathways trigged by Ras activation is the MAPK pathway.
Ras mediates the activation of several effector pathways like PI3K/Akt and MAPK pathways.
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