Neoplasms
|
|
0.070 |
GeneticVariation
|
BEFREE |
We analyzed tumor growth in mice that expressed the oncogenic form of KRAS (KRAS(G12D)) in pancreatic precursor cells, as well as sst2+/- and sst2-/-, and in crossed KRAS(G12D);sst2+/- and KRAS(G12D);sst2-/- mice.
|
25683115 |
2015 |
Neoplasms
|
|
0.070 |
GeneticVariation
|
BEFREE |
Furthermore, isoform-selective inhibitors showed a similar pattern of the isoform dependence in established Kras(G12D)/PTEN-deficient tumors.
|
24737887 |
2014 |
Neoplasms
|
|
0.070 |
GeneticVariation
|
BEFREE |
Most genes from this signature are also upregulated in poorly differentiated tumors developing in Pten(thyr-/-),Kras(G12D) mice.
|
23509868 |
2013 |
Neoplasms
|
|
0.070 |
GeneticVariation
|
BEFREE |
Treatment of Kras(G12D) mice with either of two distinct small molecule Pak inhibitors (PF3758309 and FRAX597) caused tumor regression and loss of Erk and Akt activity.
|
22983922 |
2012 |
Neoplasms
|
|
0.070 |
GeneticVariation
|
BEFREE |
Finally, m-CT imaging in live Kras(G12D-LSL) mice showed reduction of tumor burdens in PD-0325901-treated animals at sub-MTD dose.
|
22684718 |
2012 |
Neoplasms
|
|
0.070 |
GeneticVariation
|
BEFREE |
Moreover, we show that KRAS(G12D)- and BRAF(V600E)-induced tumor formation in an orthotopic model requires IGF1R.
|
22871572 |
2012 |
Neoplasms
|
|
0.070 |
GeneticVariation
|
BEFREE |
In LSL-K-ras(G12D/+)Pten(loxP/loxP) mice with established intraperitoneal tumor disease, oral administration of NVP-BEZ235 decreased pAkt, p4E-BP1 and Ki67 in tumor tissue, and resulted in significantly longer survival compared to control animals (P < 0.05).
|
21372221 |
2011 |
Neoplasm Metastasis
|
|
0.020 |
GeneticVariation
|
BEFREE |
GTPase-impairing somatic mutations in RAS genes, such as KRAS(G12D), are among the most common oncogenic events in metastatic cancer.
|
26549032 |
2016 |
Secondary Neoplasm
|
|
0.020 |
GeneticVariation
|
BEFREE |
GTPase-impairing somatic mutations in RAS genes, such as KRAS(G12D), are among the most common oncogenic events in metastatic cancer.
|
26549032 |
2016 |
Malignant Neoplasms
|
|
0.020 |
GeneticVariation
|
BEFREE |
Although mutations in known driver genes typically occurred early in cancer evolution, we also identified later subclonal "actionable" mutations, including BRAF (V600E), IDH1 (R132H), PIK3CA (E545K), EGFR (L858R), and KRAS (G12D), which may compromise the efficacy of targeted therapy approaches.
|
25877892 |
2015 |
Carcinogenesis
|
|
0.020 |
GeneticVariation
|
BEFREE |
Administration of a CXCL16-neutralizing antibody to KRAS(G12D) mice reduced activation of PI3K signaling to AKT and NF-κB, blocking carcinogenesis.
|
25683115 |
2015 |
Primary malignant neoplasm
|
|
0.020 |
GeneticVariation
|
BEFREE |
Although mutations in known driver genes typically occurred early in cancer evolution, we also identified later subclonal "actionable" mutations, including BRAF (V600E), IDH1 (R132H), PIK3CA (E545K), EGFR (L858R), and KRAS (G12D), which may compromise the efficacy of targeted therapy approaches.
|
25877892 |
2015 |
Carcinogenesis
|
|
0.020 |
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).
|
25311989 |
2014 |
Tumor Progression
|
|
0.020 |
GeneticVariation
|
BEFREE |
Additionally, we tested efficacy of PD-0325901 in Kras(G12D-LSL) conditional GEMMs (genetically engineered mouse models) which are a valuable tool in translational research to study tumor progression.
|
22684718 |
2012 |
Tumor Progression
|
|
0.020 |
GeneticVariation
|
BEFREE |
We hypothesized that tumor progression was because of concomitant activation of the mitogen-activated protein kinase pathway downstream of Kras(G12D) expression promoting cell survival and that the therapeutic effect of PF-04691502 would be enhanced by combinatory inhibition of MEK using PD-0325901.
|
21632463 |
2011 |
Neoplasm Metastasis
|
|
0.020 |
GeneticVariation
|
BEFREE |
In mice, Lkb1 deletion and activation of Kras(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases.
|
20541700 |
2010 |
Primary malignant neoplasm
|
|
0.020 |
GeneticVariation
|
BEFREE |
Moreover, all mice with Kras(G12D) activation and Pten homozygous deletion succumbed to cancer by 3 weeks of age.
|
20807812 |
2010 |
Secondary Neoplasm
|
|
0.020 |
GeneticVariation
|
BEFREE |
In mice, Lkb1 deletion and activation of Kras(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases.
|
20541700 |
2010 |
Malignant Neoplasms
|
|
0.020 |
GeneticVariation
|
BEFREE |
Moreover, all mice with Kras(G12D) activation and Pten homozygous deletion succumbed to cancer by 3 weeks of age.
|
20807812 |
2010 |
Malignant tumor of colon
|
|
0.010 |
GeneticVariation
|
BEFREE |
We examined the anti-proliferative effect of miR-143#12 and the mechanism in human colon cancer DLD-1 cell (G13D) and other cell types harboring K-Ras mutations.
|
29498789 |
2018 |
Colon Carcinoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
We examined the anti-proliferative effect of miR-143#12 and the mechanism in human colon cancer DLD-1 cell (G13D) and other cell types harboring K-Ras mutations.
|
29498789 |
2018 |
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
KRAS(G12D) T-ALLs do not show constitutive GTP loading of Ras.
|
26549032 |
2016 |
Disseminated Malignant Neoplasm
|
|
0.010 |
GeneticVariation
|
BEFREE |
GTPase-impairing somatic mutations in RAS genes, such as KRAS(G12D), are among the most common oncogenic events in metastatic cancer.
|
26549032 |
2016 |
Secondary malignant neoplasm of lymph node
|
|
0.010 |
GeneticVariation
|
BEFREE |
In sst2+/- mice, PI3K was activated and signaled via AKT (PKB; protein kinase B); when these mice were crossed with KRAS(G12D) mice, premalignant lesions, tumors, and lymph node metastases developed more rapidly than in KRAS(G12D) mice.
|
25683115 |
2015 |
Precancerous Conditions
|
|
0.010 |
GeneticVariation
|
BEFREE |
In sst2+/- mice, PI3K was activated and signaled via AKT (PKB; protein kinase B); when these mice were crossed with KRAS(G12D) mice, premalignant lesions, tumors, and lymph node metastases developed more rapidly than in KRAS(G12D) mice.
|
25683115 |
2015 |