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Transforming growth factor beta usually has an anti-proliferative function; however, during tumourigenesis this effect is reverted (Lasfar and Cohen-Solal, 2010).
Of course, in AT-rich chromosomes this effect is reverted but less pronounced (the difference between genome wide and chromosome probabilities are smaller in AT-rich compared to GC-rich chromosomes), and therefore a higher total number of islands are predicted.
Mutations of RAS and RAF family members are frequently found in human tumors and they are responsible for promoting resistance to PI3K inhibitors; this effect is reverted by the combination of MEK and PI3K inhibitors in mouse models of mutated KRAS lung cancer resulting in synergistic tumor shrinkage [ 31].
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This effect was reverted by introducing the dominant negative form of Rac1.
Subcellular fractionation showed that cobalt treatment reduced both cytoplasmic and nuclear HIPK2 nuclear levels, although HIPK2 nuclear levels were more strongly affected by cobalt and that this effect was reverted by zinc supplementation (Figure 5B).
Interestingly, this effect was reverted by allopregnanolone.
This effect was reverted at a dosage of 1 μM.
This effect was reverted at concentrations of 1 μM MMF.
This effect was reverted by adding either Erbitux® or anti-EREG antibodies.
Upon washout of the drug, this effect was reverted [ Fig. 6(c)].
This effect was reverted by reconstitution of SHP1 expression in the SHP1-KO cells.
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