Eph tumour suppression: the dark side of Gleevec

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Gleevec inhibits the oncogenic BCR–ABL tyrosine kinase in chronic myelogenous leukaemia and thus safely and effectively suppresses this human cancer. Gleevec also inhibits the normal cellular ABL, a downstream effector of the Eph-receptors, which mediate repulsive cell–cell interactions to regulate axon guidance, angiogenesis and epithelial homeostasis. New work shows that Eph-dependent tumour suppression requires ABL and is blocked by Gleevec, thus cautioning against the indiscriminate use of this drug in cancer therapy.

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Figure 1: Tumour suppression by EphB4 receptor.

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Wang, J. Eph tumour suppression: the dark side of Gleevec. Nat Cell Biol 8, 785–786 (2006) doi:10.1038/ncb0806-785

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