rs121913529
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The data suggest that coexpression of BRAF(V600E) and KRAS(G12D) in early tumorigenesis leads to negative selection due to oncogene-induced senescence.
|
26028035 |
2016 |
rs121913529
|
|
|
0.100 |
GeneticVariation |
BEFREE |
We used these mice to investigate a possible cooperative effect of GNAS(R201H) and Kras(G12D) in pancreatic tumorigenesis.
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26257060 |
2016 |
rs121913529
|
|
|
0.100 |
GeneticVariation |
BEFREE |
PIK3CA(H1047R) expression alone failed to promote tumor formation, but dramatically enhanced tumorigenesis initiated by KRAS(G12D).
|
26567140 |
2015 |
rs121913529
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Reduced HRAS G12V-Driven Tumorigenesis of Cell Lines Expressing KRAS C118S.
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25902334 |
2015 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
Administration of a CXCL16-neutralizing antibody to KRAS(G12D) mice reduced activation of PI3K signaling to AKT and NF-κB, blocking carcinogenesis.
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25683115 |
2015 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
We demonstrated that transient transgenic expression of KRAS(G12V) in putative neural stem and/or progenitor cells induced brain tumorigenesis.
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25644510 |
2015 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
Foxm1 transcription factor is required for the initiation of lung tumorigenesis by oncogenic Kras(G12D.).
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24213573 |
2014 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
Tumorigenesis was measured in the Kras(G12D/+);Ptf1a(Cre/+) mouse model of PDA; these mice were crossed with mice with pancreas-specific disruption of genes encoding PI3K p110α (Pik3ca), p110β (Pik3cb), or RAC1 (Rac1).
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25311989 |
2014 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
Through two novel transgenic mouse models, we show that Twist1 cooperates with Kras(G12D) to markedly accelerate lung tumorigenesis by abrogating cellular senescence programs and promoting the progression from benign adenomas to adenocarcinomas.
|
22654667 |
2012 |
rs121913529
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0.100 |
GeneticVariation |
BEFREE |
Furthermore, genetic targeting of the Nrf2 pathway impairs K-Ras(G12D)-induced proliferation and tumorigenesis in vivo.
|
21734707 |
2011 |
rs121913529
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0.100 |
GeneticVariation |
BEFREE |
However, a more rigorous test of the requirement for Notch signaling in lung oncogenesis, crossing the LSL-KRAS(G12D) mouse model with a transgenic with a similarly inducible global dominant-negative suppressor of Notch activity, LSL-DNMAML (dominant-negative mastermind-like), reveals no evidence of Notch pathway requirement for lung tumor initiation or growth in vivo.
|
21994468 |
2011 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
To examine how the MYC and K-ras(G12D) oncogenes cooperate for the initiation and maintenance of tumorigenesis, we generated double conditional transgenic tumor models of lung adenocarcinoma and lymphoma.
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18461184 |
2008 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
Here, we demonstrate in an in vivo transgenic model in which atorvastatin reverses and prevents the onset of MYC-induced lymphomagenesis, but fails to reverse or prevent tumorigenesis in the presence of constitutively activated K-Ras (G12D).
|
17622571 |
2007 |
rs121913529
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|
|
0.100 |
GeneticVariation |
BEFREE |
To evaluate the role of oncogenic RAS mutations in pancreatic tumorigenesis, we directed endogenous expression of KRAS(G12D) to progenitor cells of the mouse pancreas.
|
14706336 |
2003 |
rs121913240
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|
|
0.010 |
GeneticVariation |
BEFREE |
This system allowed us to rapidly compare the ability of 12 different KRAS mutations (G12A, G12C, G12D, G12F, G12R, G12S, G12V, G13C, G13D, Q61L, Q61R and A146T) to drive pancreatic tumorigenesis in vivo.
|
25065594 |
2015 |
rs121913527
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|
|
0.010 |
GeneticVariation |
BEFREE |
This system allowed us to rapidly compare the ability of 12 different KRAS mutations (G12A, G12C, G12D, G12F, G12R, G12S, G12V, G13C, G13D, Q61L, Q61R and A146T) to drive pancreatic tumorigenesis in vivo.
|
25065594 |
2015 |