As positive controls for cancer growth, we found that many known drivers of CML and bcCML, such as the developmental regulators cMyc20, Mdm2 (ref. 21), Wnt1 (ref. 22), Pafah1b1 (Lis1)11 and mTor23, were highly depleted.
. In addition, regulators of AML including the developmental and oncogenic signals Nras24 and Wnt1 (ref. 25), the stem cell self-renewal genes Cdc42 and Lis1 (refs. 11,26) and epigenetic regulators Kdm1a, Hmga1 and Smarca4 (refs. 27,28) were highly depleted and tumor suppressors such as Pten were enriched
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