Supplementary Figures and Legends from Targeting CDK6 and BCL2 Exploits the “MYB Addiction” of Ph<sup>+</sup> Acute Lymphoblastic Leukemia

S1. MYB silencing reduces viability and proliferation of Ph+ ALL cell lines; S2. Expression of shMYB-resistant MYB cDNA rescues the effects of MYB silencing; S3. MYB silencing suppresses leukemia in NSG mice injected with BV173 or SUP-B15 cells; S4. MYB silencing alters the expression of cell cycle regulatory genes in SUP-B15 cells; S5. Restoring CDK4 nuclear localization rescues the impaired proliferation of MYB-silenced BV173 cells; S6. CDK6, Cyclin D3 and BCL2 but not p21 cooperate to rescue the cell growth of MYB silenced BV173 cells; S7. MYB regulation of CDK6 but not of BCL2 is dependent on p300/CBP recruitment; S8. Palbociclib reduces Ph+ ALL proliferation in vitro and leukemia formation in vivo; S9. Venetoclax or Sabutoclax in combination with the CDK4/6 inhibitor palbociclib synergistically reduce the viability of Ph+ ALL cells.