We observed similar overall survival, rates of metastasis, and histological prevalence of invasion at sacrifice between KPC and 17KPC mice, suggesting that Trp53 loss can compensate for mir-17~92 deletion. In the KPC model, mice typically develop aggressive PDAC, characterized by local invasion, obstructive symptoms involving the gastrointestinal or biliary systems, and metastasis, which we observe in the KPC animals of this study. In contrast, we find that 17KPC mice exhibit less aggressive primary disease, as demonstrated by longer survival with larger primary tumors in the absence of metastases, and the absence of obstructive gastrointestinal or biliary symptoms. These data suggest that mir-17~92 plays a role in PDAC invasiveness. However, we cannot exclude the possibility that the absence of obstructive disease in the 17KPC mice reflects a difference in the initial anatomical site of these primary tumors compared to KPC tumors. Perhaps the tumors in 17KPC mice arise in the tail of the pancreas, allowing them to reach greater size before obstructing the duodenum or bile duct; whereas tumors occurring in KPC animals predominantly occur in the head of the pancreas, predisposing those animals to early obstructive phenomena. Additional studies analyzing tumors at earlier stages and smaller sizes will be needed in order to clarify whether KPC and 17KPC tumors arise in different locations within the pancreas.