<b>Purpose:</b> To confirm the hypothesis that PDX1 in PDAC plays suppressor role of epithelial-mesenchymal transition (EMT), and to study its possible ability to inhibit metastasis.
JTC801 was administered by gavage to mice with xenograft tumors, C57BL/6 mice with orthographic pancreatic tumors grown from Pdx1-Cre;KRas<sup>G12D/+</sup>;Tp53<sup>R172H/+</sup> (KPC) cells, mice with metastases following tail-vein injection of KPC cells, and Pdx-1-Cre;Kras<sup>G12D/+</sup> mice crossed with Hmgb1<sup>flox/flox</sup> mice (KCH mice).
During the progression from primary tumors to metastases, the wild-type allele of Kras was progressively lost (loss of heterozygosity at Kras or LOH at Kras) in p16flox/flox; LSL- KrasG12D; Pdx1-Cre mice.
PDX-1 expression did not correlate with biochemical recurrence, but decreased with higher Gleason pattern (p<0.001) and in metastases vs primary PCa (p<0.001).
Immunohistochemistry confirmed high metastasisPDX-1 expression, lower levels in the primary tumor, and the presence of only traces of PDX-1 in normal colon tissue.