Treatment of Ptf1a(cre/+) ;LSL-Kras(G12D/+) ;Tgfbr2(flox/flox) mice with the JNK inhibitor decreased growth of murine pancreatic cancer and prolonged survival of the mice significantly.
We have been investigating the pancreas specific transcription factor, 1a cre-recombinase; lox-stop-lox- Kristen rat sarcoma, glycine to aspartic acid at the 12 codon (Ptf1a<sup>cre/+</sup>;LSL-Kras<sup>G12D/+</sup>) mouse strain as a model of human pancreatic cancer.
In conditional PCa mouse models with selective in vivo blockade of interleukin (IL)-6 signalling (Ptf1a-Cre;LSL-Kras(G12D)/KC interbred with IL6(-/-) or sgp130(tg) mice), SC reactivity, abdominal mechanosensitivity and spinal glial/neuronal activity were quantified.
Although the Ptf1a-Cre; LSL-KrasG12D transgenic mouse is perhaps the most widely utilised animal model for human pancreatic cancer, expression levels of HMGA1 in pancreata from this mouse model have not been characterised.