Skip to main content
. Author manuscript; available in PMC: 2018 Nov 30.
Published in final edited form as: Oncogene. 2018 May 30;37(38):5221–5232. doi: 10.1038/s41388-018-0299-8

Figure 5. Model of UHRF1-ROR1 regulatory mechanism.

Figure 5

The 1;19 fusion product leads to cell arrest and constitutively active pre-BCR signaling (top). This signaling can be suppressed by small-molecule inhibitors, such as dasatinib, but kinase inhibition is rescued by increased ROR1 expression (middle). Targeting the UHRF1-ROR1 mechanism with compounds such as naphthazarin can suppress baseline ROR1 levels. In combination with pre-BCR inhibition (via dasatinib), naphthazarin helps to prevent upregulation of ROR1 to maximize t(1;19) pre B-ALL apoptotic cell death (bottom).