BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

Coordinated BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. Persistence of oncogenic p27 functions despite effective inhibition of BCR-ABL1 may contribute to resistance to tyrosine kinase inhibitors. Overall design: BCR-ABL1 induced p27 versus knockout, controlling with Empty vector p27 versus knock out

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Agarwal A, Mackenzie RJ, Besson A, Jeng S, Carey A, LaTocha DH, Fleischman AG, Duquesnes N, Eide CA, Vasudevan KB, Loriaux MM, Firpo E, Cortes JE, McWeeney S, O'Hare T, Roberts JM, Druker BJ, Deininger MW