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Comment on “PP2A inhibition sensitizes cancer stem cells to ABL tyrosine kinase inhibitors in BCR-ABL human leukemia”

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Science Translational Medicine  17 Jul 2019:
Vol. 11, Issue 501, eaau0416
DOI: 10.1126/scitranslmed.aau0416

Figures

  • Fig. 1 Effects of protein phosphatase 2A–activating drug and protein phosphatase 2A–inhibiting drug in chronic myeloid leukemia.

    (A) Hematopoietic stem cell (HSC) and progenitor activity after protein phosphatase 2A–activating drug (PAD) or protein phosphatase 2A–inhibiting drug (PID) treatment. (1) Eight PADs were independently tested in nine laboratories. (2) Average of data from Perrotti group’s publications. (3) PAD-induced apoptosis also in BCR-ABL1T315I chronic myeloid leukemia (CML). (4) PID values are from Lai et al. (1). (5) FTY720 and derivatives increase bone marrow (BM) homing of normal but not tumor HSCs. (B) Effects of LB100 on CML cell proliferation and survival. Data are from figures 6 and 8 and figure S8 of Lai et al. (1). TKI, tyrosine kinase inhibitor; CFC, colony-forming cell; LTC-IC, long-term culture-initiating cell; NR, nonresponder; N/A, not applicable; N.S, nonsignificant differences; wk, weeks; DAS, dasatinib; RT-PCR, reverse transcription polymerase chain reaction. NBM, normal bone marrow; CFSEmax, maximum staining with carboxyfluorescein succinimidyl ester; hLSC, human leukemia stem cell; CMPs, common myeloid progenitors; LSK, lineage-negative Sca+ Kit+; DA, dasatinib.

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