Rhabdomyosarcoma
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|
0.010 |
GeneticVariation
|
BEFREE |
First, to compare YAP1 S127A and KRAS G12V-driven rhabdomyosarcomas, we re-analysed gene expression microarray datasets from mouse rhabdomyosarcomas caused by these genes.
|
30353028 |
2018 |
Childhood Embryonal Rhabdomyosarcoma
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|
0.010 |
GeneticVariation
|
BEFREE |
Analysis of the relationship between the KRAS G12V oncogene and the Hippo effector YAP1 in embryonal rhabdomyosarcoma.
|
30353028 |
2018 |
Embryonal Rhabdomyosarcoma
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|
0.010 |
GeneticVariation
|
BEFREE |
Analysis of the relationship between the KRAS G12V oncogene and the Hippo effector YAP1 in embryonal rhabdomyosarcoma.
|
30353028 |
2018 |
Tumour budding
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|
0.010 |
GeneticVariation
|
BEFREE |
Our results showed that 21 of 34 tumors with high-grade TB had KRAS mutations (P=.001) and KRAS G12D and PIK3CA exon 9 variants were significantly associated with high-grade TB (P=.002 and .006, respectively); furthermore, tumors with KRAS mutations in exons 3 and 4 tended to have lymphovascular tumor emboli and perineural invasion (P=.044 and .049, respectively).
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28188750 |
2017 |
Tumor Cell Invasion
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|
0.010 |
GeneticVariation
|
BEFREE |
Our results showed that 21 of 34 tumors with high-grade TB had KRAS mutations (P=.001) and KRAS G12D and PIK3CA exon 9 variants were significantly associated with high-grade TB (P=.002 and .006, respectively); furthermore, tumors with KRAS mutations in exons 3 and 4 tended to have lymphovascular tumor emboli and perineural invasion (P=.044 and .049, respectively).
|
28188750 |
2017 |
Carcinoma, Signet Ring Cell
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|
0.010 |
GeneticVariation
|
BEFREE |
The DNA sequencing of the 2 microdissected neoplastic components (adenomatous and SRCC) showed the same G12V KRAS mutation.
|
26997454 |
2016 |
Squamous cell carcinoma of skin
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|
0.010 |
GeneticVariation
|
BEFREE |
MAPK pathway hyperactivation (through Braf(V600E) or Kras(G12D) knockin) and TGFβ signalling ablation (through Tgfbr1 deletion) in LGR5(+ve) stem cells enables rapid cSCC development in the mouse.
|
27558455 |
2016 |
Squamous cell carcinoma
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|
0.010 |
GeneticVariation
|
BEFREE |
We also studied genetically induced SCCs that expressed G12D mutant Kras (Kras G12D) but were deficient for p53.
|
26168291 |
2015 |
Stomach Neoplasms
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|
0.010 |
GeneticVariation
|
BEFREE |
One case had a KRAS G12V (c.35G>T) mutation in both the primary gastric tumor and a post-imatinib recurrence.
|
25427437 |
2015 |
Carcinoma, Spindle-Cell
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|
0.010 |
GeneticVariation
|
BEFREE |
Combining p53(R273H) with KRAS(G12V) activation caused transformation of MOE into high-grade sarcomatoid carcinoma when xenografted into nude mice.
|
25810107 |
2015 |
Pancreatic Ductal Adenocarcinoma
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|
0.010 |
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 |
Hurthle Cell Tumor
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|
0.010 |
GeneticVariation
|
BEFREE |
Using genetically engineered mouse models (GEMMs) for human non-small-cell lung cancer (NSCLC), we found that deletion of the essential autophagy gene, Atg7, in KRAS(G12D)-driven NSCLC inhibits tumor growth and converts adenomas and adenocarcinomas to benign oncocytomas characterized by the accumulation of respiration-defective mitochondria.
|
23959381 |
2013 |
Malignant transformation
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|
0.010 |
GeneticVariation
|
BEFREE |
Taken together, Kras(G12D) - driven PanIN showed the tumorigenic ability, however, did not undergo a malignant transformation, and decreased expression of PPP2R2A in PDACs may provided a new target for pancreatic carcinoma intervention.
|
23887057 |
2013 |
Secondary malignant neoplasm of lung
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|
0.010 |
GeneticVariation
|
BEFREE |
We show that loss of HIF-1α or PLOD2 expression disrupts collagen modification, cell migration, and pulmonary metastasis (but not primary tumor growth) in allograft and autochthonous LSL-Kras(G12D/+); Trp53(fl/fl) murine sarcoma models.
|
23906982 |
2013 |
ADENOMAS AND ADENOCARCINOMAS
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|
0.010 |
GeneticVariation
|
BEFREE |
Using genetically engineered mouse models (GEMMs) for human non-small-cell lung cancer (NSCLC), we found that deletion of the essential autophagy gene, Atg7, in KRAS(G12D)-driven NSCLC inhibits tumor growth and converts adenomas and adenocarcinomas to benign oncocytomas characterized by the accumulation of respiration-defective mitochondria.
|
23959381 |
2013 |
Secondary Neoplasm
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|
0.010 |
GeneticVariation
|
BEFREE |
Further, in order to investigate whether IL-6 deletion contributes to suppression of lung cancer metastasis, we generated Kras(G12D); p53(flox/flox); IL-6(-/-) mice, which developed lung cancer with a trend for reduced metastases and longer survival than Kras(G12D); p53(flox/flox) mice.
|
24260500 |
2013 |
Primary cholangiocarcinoma of intrahepatic biliary tract
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|
0.010 |
GeneticVariation
|
BEFREE |
Tissue-specific activation of Kras(G12D) alone resulted in the development of invasive IHCC with low penetrance and long latency.
|
22266220 |
2012 |
Malignant neoplasm of soft tissue
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|
0.010 |
GeneticVariation
|
BEFREE |
In addition, using FSF-Kras(G12D/+); p53(FRT/FRT) mice, we demonstrate that an adenovirus expressing FlpO recombinase can initiate primary lung cancers and sarcomas in mice. p53(FRT) mice will enable dual recombinase technology to study cancer biology because Cre is available to modify genes specifically in stromal cells to investigate their role in tumor development, progression and response to therapy.
|
22228755 |
2012 |
Primary malignant neoplasm
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|
0.010 |
GeneticVariation
|
BEFREE |
In addition, using FSF-Kras(G12D/+); p53(FRT/FRT) mice, we demonstrate that an adenovirus expressing FlpO recombinase can initiate primary lung cancers and sarcomas in mice. p53(FRT) mice will enable dual recombinase technology to study cancer biology because Cre is available to modify genes specifically in stromal cells to investigate their role in tumor development, progression and response to therapy.
|
22228755 |
2012 |
Intrahepatic Cholangiocarcinoma
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|
0.010 |
GeneticVariation
|
BEFREE |
Tissue-specific activation of Kras(G12D) alone resulted in the development of invasive IHCC with low penetrance and long latency.
|
22266220 |
2012 |
PATENT DUCTUS ARTERIOSUS 1
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|
0.010 |
GeneticVariation
|
BEFREE |
The concomitant expression of oncogenic Kras(G12D) and mutant p53 (Trp53(R172H)) in the murine pancreas results in metastatic PDA that recapitulates the cognate features of human pancreatic cancer providing an excellent animal model to identify genes required for tumor progression.
|
22158044 |
2012 |
Benign Neoplasm
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|
0.010 |
GeneticVariation
|
BEFREE |
Whereas the successive expression of Ras(G12V) and p53(DD) led to highly malignant tumors with metastatic behavior, reminiscent of those formed after the simultaneous introduction of p53(DD) and Ras(G12V), the reverse sequence gave rise only to benign tumors.
|
22589739 |
2012 |
Malignant Neoplasms
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|
0.010 |
GeneticVariation
|
BEFREE |
In addition, using FSF-Kras(G12D/+); p53(FRT/FRT) mice, we demonstrate that an adenovirus expressing FlpO recombinase can initiate primary lung cancers and sarcomas in mice. p53(FRT) mice will enable dual recombinase technology to study cancer biology because Cre is available to modify genes specifically in stromal cells to investigate their role in tumor development, progression and response to therapy.
|
22228755 |
2012 |
Patent ductus arteriosus
|
|
0.010 |
GeneticVariation
|
BEFREE |
The concomitant expression of oncogenic Kras(G12D) and mutant p53 (Trp53(R172H)) in the murine pancreas results in metastatic PDA that recapitulates the cognate features of human pancreatic cancer providing an excellent animal model to identify genes required for tumor progression.
|
22158044 |
2012 |
Malignant neoplasm of esophagus
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|
0.010 |
GeneticVariation
|
BEFREE |
We developed two mouse models of esophageal cancer by inoculating immunocompetent mice with syngeneic esophageal cell lines transformed by cyclin-D1 or mutant HRAS(G12V) and loss of p53.
|
21869822 |
2011 |