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rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Orthotopic implantation of PDCs carrying the activated Kras(G12D</span>)-allele and shRNA against p16(Ink4a) or Trp53 resulted in tumor growth, metastasis, and reduced survival of NSG mice.
|
25724428 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In conclusion, whilst oncogenic KRAS mutation might activate Yap in other cell types, we could find no evidence for this in myoblasts because the expression of KRAS G12V expression did not change Yap/Taz activity in myoblasts and there was a limited overlap in gene expression between KRAS G12V and YAP1 S127A-driven tumours.
|
30353028 |
2018 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
When the assay was applied to tumor samples with known KRAS or NRAS mutations (G12A, G12D, G12V, and G13D), RAS-mutant and wild-type peptides were successfully detected in 11 of 13 biopsy samples.
|
29684684 |
2018 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Coactivation of BRAF(V600E) and KRAS(G12D) markedly reduced lung tumor numbers and overall tumo</span>r burden compared with activation of BRAF(V600E) alone.
|
26028035 |
2016 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Moreover, we show that KRAS(G12D)- and BRAF(V600E)-induced tumor formation in an orthotopic model requires IGF1R.
|
22871572 |
2012 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Mice with a combined Tsc1-Kras(G12D) mutation had dramatically reduced tumor latency (median survival: 11.6-15.6 weeks) in comparison with Kras(G12D) alone mutant mice (median survival: 27.5 weeks).
|
19966866 |
2010 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
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 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
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 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The tumors that developed differed in their ability to recapitulate normal myogenesis. cdh15:KRAS(G12D) and rag2:KRAS(G12D) fish developed tumors that displayed an inability to complete muscle differentiation as determined by histological appearance and gene expression analyses.
|
23821038 |
2013 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In all components (bilateral serous borderline tumors, low-grade serous carcinoma and mesonephric-like adenocarcinoma), an identical KRAS mutation was detected (NM_004985.4): c.35G>A, p.(G12D) proving a clonal association between the serous and mesonephric-like components and excluding a collision neoplasm.
|
30575604 |
2020 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
When the tumor suppressor Pten is disrupted conditionally in the Kras(G12D)-expressing granulosa cells, granulosa cell tumors fail to develop.
|
19880654 |
2010 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The karyotype is highly complex, with a hypotriploid to hypertriploid modal number (3n+/-) (52 to 77 chromosomes); low level of HER2 gene amplification, TP53 deletion, gain of AURKA were identified; K-RAS G12D mutation were maintained from primary tumor to MT-CHC01 cells.
|
26486326 |
2016 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The percentage of KRAS G12V mutation relative to wild-type sequences in tumor-derived DNA was also determined.
|
27043547 |
2016 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Patients with tumors bearing a KRAS p.G12D mutation showed a strong trend to a more favorable outcome compared to other mutations (overall survival 23.3 vs. 14-18 months; hazard ratio 0.66, range 0.43-1.03).
|
22948721 |
2012 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Notch1 mutations, including exon 34 mutations and recently characterized type 1 and 2 deletions, are detected in 100% of Kras G12D-induced T-ALL tumors.
|
23673656 |
2013 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The median progression-free survival (PFS) and overall survival (OS) for patients with tumors harboring G12V/A KRAS mutation was 6.6 and 16.8 compared to 11.6 and 26.3 months for patients with tumors harboring other KRAS mutation type (p < 0.001 and p < 0.001), while the survival of patients harboring other KRAS mutation types was comparable to those with tumors harboring wild-type KRAS gene.
|
26662311 |
2016 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
However, G12V mutations appeared to be associated with higher rates of tumor regression than G13D mutations (p=0.012).
|
19913317 |
2010 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Significant variations in treatment effects were found for tumor response (P = .005) and PFS (P = .046) in patients with G13D-mutant tumors versus all other mutations (including G12V).
|
22734028 |
2012 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here, we established isogenic cell line models to systematically investigate the impact of KRAS(G12V) on tumor growth in mouse A431 xenograft models as well as on various modes of action triggered by EGFR-Abs in vitro.
|
22496619 |
2012 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The increased cell survival, invasion, intravasation, and specific molecular regulation observed in KRas G12V tumors is consistent with the higher aggressiveness observed in patients with CRC expressing this oncogene.
|
25359494 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The most common mutation K-Ras(G12V), required for tumor proliferation, survival, and metastasis due to its constitutively active GTPase activity, has provided an ideal target for cancer therapy.
|
19014906 |
2009 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
KRAS mutations were detected in 4 (3%) of 117 tumors (3× G12D and 1 G12V mutation).One tumor had a PIK3CA E545K mutation.
|
23158210 |
2013 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
All of the tumors that showed H-ras alteration had G-to-T transversion mutations in the second base of codon 12 (glycine --> valine).
|
10463479 |
1999 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Visible carcinoma was detected as early as day-15 following oncogenic KRAS(G12V) induction alone, and these tumors proliferate rapidly with a median survival of 28-days accompanied with histological reminiscences to human sarcomatoid SDC variants.
|
26289340 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Treatment of Caggs-Cre/FR-Hras(G12V) mice with TPA alone was sufficient to trigger papilloma development with a shorter latency and an ∼10-fold greater tumor burden than DMBA/TPA-treated WT-controls.
|
24240680 |
2014 |