New Preprints: Using multiomics to study the role of ASXL1 in Bohring Optiz Syndrome and AML

We just published two new preprints— the hard work of Isabella Lin, MSTP student in her PhD 3 year in the lab! These are a long term projects we have exploring the gene regulatory role of ASXL1 in patient-derived cells. here we identify how ASXL1 mutations change the epigenetic landscape and activate Wnt signaling pathtways in differentiated cells. Specifically we highlight both canonical signaling pathways and non-canoncial planar cell polarity pathways are affected by BOS. For the full preprint see here:

Truncating ASXL1 mutations in Bohring-Opitz Syndrome dysregulate canonical and non-canonical Wnt Signaling

We also explored whether the same observations in patient germline syndomes with ASXL1 mutations affect the same pathways in Acute myeloid leukemia with ASXL1 mutations.

ASXL1 mutations that cause Bohring Opitz Syndrome (BOS) or acute myeloid leukemia share epigenomic and transcriptomic signatures