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Mouse PDACs also display a desmoplastic stroma and inflammatory responses that closely resemble those observed in human patients.
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PDACs also harbor major driver mutations, including Kras (~95%) and p53 (~75%), which may also contribute to apoptosis resistance.
dFdC shows little efficacy in KPC mouse PDAC tumours (Olive et al, 2009).
To test whether TBL1 upregulation is a conserved feature between human and mouse PDAC, we employed p48+/Cre; Kras+/LSL-G12D mice.
KPC cells were established from a mouse PDAC model, carrying pancreas-specific Kras and p53 mutations (KrasLSL-G12D/+ Tr KrasLSL-G12D/+ Tr8- Cre; hence KPC) [ 14].
Seventy-six PDalsolso harboured precursor lesions.
The tumour stroma has a major role in the development and progression of PDAC, also affecting cancer therapy.
In humans and mice, PDAC progression is characterized by the inactivation of the tumor suppressor gene, Smad4[ 4, 8].
The drug trifluoperazine (TFP), which hampers PDAC development in xenografted mice, also binds to those regions.
Eighteen NC mice were also selected.
Uninfected pregnant mice were also observed similarly.
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