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rs121913529
|
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|
0.100 |
GeneticVariation |
BEFREE |
Hy15549 and Han4.13 cell lines were derived from primary murine PDAC (Ptf1-Cre; LSL-KRAS-G12D; Trp53 Lox/+) on C57BL/6 and FVB strains, respectively.
|
29903803 |
2018 |
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rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
We found that KRAS, whose mutant G12D allele drives the pathogenesis of PDAC, is a target of miR-216b.
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30306823 |
2018 |
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rs121913529
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0.100 |
GeneticVariation |
BEFREE |
Mice harboring a G12D activating Kras mutation are among the most heavily studied models in the field of pancreatic adenocarcinoma (PDAC) research. miRNAs are differentially expressed in PDAC from patients and mouse models of PDAC.
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27541609 |
2017 |
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rs121913529
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0.100 |
GeneticVariation |
BEFREE |
Together, these data demonstrate the role of CXCR2 signaling in KRAS(G12D)-induced growth transformation and progression in PDAC.
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26771140 |
2016 |
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rs121913529
|
|
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0.100 |
GeneticVariation |
BEFREE |
In genetically engineered Kras(G12D) and Kras(G12D):Trp53(R172H) mouse models, pancreas-specific deletion of Yap halted the progression of early neoplastic lesions to PDAC without affecting normal pancreatic development and endocrine function.
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24803537 |
2014 |
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rs121913529
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|
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0.100 |
GeneticVariation |
BEFREE |
PTEN loss leads to acceleration of Kras(G12D)-driven pancreatic ductal adenocarcinoma (PDAC) in mice and these tumours have high levels of mammalian target of rapamycin (mTOR) signalling.
|
24717934 |
2014 |
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rs121913529
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0.100 |
GeneticVariation |
BEFREE |
Compared with control, DNA synthesis and total cell proliferation was significantly increased in human PDCs harboring the PDAC common p53, Rb/p16(INK4a), and K-Ras (G12D) mutations.
|
23555182 |
2013 |
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rs121913529
|
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|
0.100 |
GeneticVariation |
BEFREE |
Our previous study has shown that activation of Notch and NF-κB play a critical role in the development of PDAC in the compound K-Ras(G12D) and Ink4a/Arf deficient transgenic mice.
|
22806240 |
2013 |
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rs121913529
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|
0.100 |
GeneticVariation |
BEFREE |
G12D K-Ras increased cleavage of p35 to p25, a stable and greater activator of CDK5, thus implicating a role for CDK5 in early progression of PDAC.
|
21825040 |
2011 |
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rs121913529
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|
0.100 |
GeneticVariation |
BEFREE |
In situ hybridization analysis indicated miR-21 production to be concentrated in pathologic ductal cells. miR-21 production was regulated by KRAS(G12D) and epidermal growth factor receptor in PDAC-derived cell lines.
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20093556 |
2010 |
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rs121913530
|
|
|
0.010 |
GeneticVariation |
BEFREE |
In explant cells derived from these PDX tumor models with a KRAS G12R mutation, treatment with inhibitors of CDKs (including CDK9) reduced phosphorylation of a marker of CDK9 activity (phospho-RNAPII CTD Ser2/5) and reduced viability/growth of explant cells derived from PDAC PDX models.
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26934555 |
2016 |