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Letters to the Editor
First, we used lentiviral vectors to overexpress the two most common isoforms of WT1 (KTS+ and KTS-) in human CD34 cells in culture. In the absence of other co- operating oncogenes, WT1 overexpression led to the rapid disappearance of transduced cells (Figure 2A), con- sistent with previous reports that WT1 overexpression
causes differentiation and death of CD34+ cells.11 Next, we asked whether inactivating mutations in WT1 could enhance expansion of CD34+ cells expressing PML- RARA. We transduced CD34+ cells with PML-RARA or empty vector, and 2 days after transduction used CRISPR/Cas9 to generate inactivating indels in WT1, or
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Figure 2. Legend on following page.
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