Table 1 An overview of common genetically engineered mouse models of pancreatic cancer and their key characteristics

Pdx1; KRAS^G12D/+

PanIN

PDAC

Yes

Long latency

³⁴³

Ptf1a^+/Cre; KRAS^G12D/+

PanIN

PDAC

Yes

Long latency

³⁴³

KRAS^G12D/+; Ela-TGFa

PanIN

IPMN

Yes (50%)

Moderate latency

³⁵⁰

Pdx1-Cre; LSL-KRAS^G12D/+; Ink4a/Arf^lox/lox

PanIN

PDAC

Yes (21%)

Short latency and high penetrance

³⁴⁶

Pdx1-Cre; LSL-KRAS^G12D/+; LSL-TP53^R172H/+

PanIN

PDAC

Yes (63%)

Accelerated development of metastatic PDAC

³⁴⁵

LSL-KRAS^G12D; TP53^fl/fl (in situ electroporation of Cre recombinase and myrAkt2)

PanIN

PDAC

Yes (>60%)

High efficiency, short latency

³⁸⁴

Co-electroporation of SB13 transposase with a KRAS^G12V-expressing transposon, Cre recombinase and myrAkt2 in TP53^fl/fl mice

PanIN

PDAC

Yes (>70%)

High efficiency, short latency

³⁸⁴

Pdx1-Cre; KRAS^G12D/+; Ink4a^−/− TP53^lox/lox

PanIN

PDAC

Yes (20%)

Short latency and high penetrance

³⁴⁷

Pdx1-Cre; KRAS^G12D/+; Smad^lox/lox

IPMN

PDAC

Yes (38%)

Model of IPMN to PDAC progression

^351,352

Ptf1a^+/Cre; KRAS^G12D/+; Smad^lox/lox

MCN

PDAC

Yes (18%)

MCNs resembling human disease

³⁸⁵

Ptf1a^+/Cre; KRAS^G12D/+; ATM^lox/lox

PanIN

PDAC

Yes (78%)

High metastasis tendency

³⁴⁸