|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
44% of the tumors were positive for G12D, 20% for G12V, and 10% for G12C.
|
27591291 |
2016 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
A KRAS G12A mutation was found in tumor removed from the finger.
|
22317887 |
2012 |
|
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 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Analysis of a tumor biopsy revealed an activating KRAS mutation (G12D) and the patient was started on first-line treatment with Reolysin in combination with gemcitabine in March 2012.
|
26156229 |
2015 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Because of the potent anti-proliferative effects of KRAS(G12D) in granulosa cells, we sought to determine whether KRAS(G12D) would block precancerous lesion and tumor formation in follicles of the CTNNB1-mutant mice.
|
21860425 |
2012 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Co-administration of BI-2536 and fasudil either in the LSL-KRAS(G12D) mouse model or in a patient tumour explant mouse model of KRAS-mutant lung cancer suppresses tumour growth and significantly prolongs mouse survival, suggesting a strong synergy in vivo and a potential avenue for therapeutic treatment of KRAS-mutant cancers.
|
27193833 |
2016 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Co-expression of Kras(G12V) and Braf(D631A) in mouse lung cells markedly enhances tumour initiation, a phenomenon mediated by Craf kinase activity, and effectively accelerates tumour progression when activated in advanced lung adenocarcinomas.
|
28783725 |
2017 |
|
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 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Consistent with previous findings in vitro, Glut1 transcript and protein expression was up-regulated in the tumors of G22Cre;Apc (flox/flox) ; Kras(G12D) mice.
|
26361962 |
2016 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Correspondingly, tumors with a constitutively activated K-Ras (G12D) did not exhibit dephosphorylation of ERK1/2 and MYC.
|
17622571 |
2007 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Disruption of Acvr1b in LSL-KRAS(G12D);Pdx1-Cre mice accelerated the growth of pancreatic IPMNs compared with LSL-KRAS(G12D);Pdx1-Cre mice, but did not alter growth of pancreatic intraepithelial neoplasias.
|
26408346 |
2016 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Ectopic expression of K-Ras(G12D) largely rescued let-7g mediated tumor suppression, whereas ectopic expression of HMGA2 was less effective.
|
18308936 |
2008 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Even though robust Erk1/2 signaling is activated in all the tissues examined, the pErk1/2 distribution remains largely cytoplasmic in K-Ras(G12D)-refractory tissues (pancreas, liver, and intestines) as opposed to a predominantly nuclear localization in K-Ras(G12D)-induced neoplasms of lung, oral, and gastric mucosa.
|
22532587 |
2012 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Finally, excision of the Men1 gene markedly accelerates the K-Ras(G12D)-induced tumor formation in the Men1(f/f);K-Ras(G12D/+);Cre ER mouse model.
|
23027861 |
2012 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Furthermore, we observe an in vivo reduction in tumor size of gallbladder xenografts in response to Afatinib is paralleled by a reduction in the amounts of phospho-ERK, in tumors harboring KRAS (G13D) mutation but not in KRAS (G12V) mutation, supporting an essential role of the ErbB pathway.
|
30304546 |
2019 |
|
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 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
High-dose vitamin C impairs tumor growth in Apc/Kras(G12D) mutant mice.
|
26541605 |
2015 |
|
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 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Importantly, FGTI-2734 inhibited the growth of xenografts derived from four patients with pancreatic cancer with mutant KRAS (2 G12D and 2 G12V) tumors.
|
31227505 |
2019 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Importantly, intratumoral injection of the adenoviruses with pro-drug treatment specifically and significantly impeded the growth of xenografted tumors harboring KRAS G12V through a trans-splicing reaction with the target RNA.
|
28153088 |
2017 |
|
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 |
|
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 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In combination with p53 silencing, KRAS(G12V) alone was sufficient to fully transform the immortalized HPDECs, and MYC markedly accelerated the development of tumors.
|
24858378 |
2014 |
|
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 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In this report, we reveal a previously unidentified tumor cell-autonomous role of KRAS(G12D)-induced CXCR2 signaling in mediating growth of neoplastic PDAC cells.
|
26771140 |
2016 |