|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
Moreover, we use the LITer gene circuit architecture to control gene expression of the cancer oncogene KRAS(G12V) and study its downstream effects through phospho-ERK levels and cellular proliferation.
|
31269201 |
2019 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
G12D and Q61H are among the most prevalent cancer-causing mutations at the P-loop and switch 2 regions of KRAS, respectively.
|
31554397 |
2019 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
Adenoviral vectors containing the specific ribozymes with downstream suicide gene were constructed and then infection with the adenoviruses specifically downregulated KRAS G12V expression and killed KRAS G12V-harboring cancer cells additively upon pro-drug treatment, but it did not affect the growth of wild-type KRAS-expressing cells.
|
28153088 |
2017 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
After subsequent sequence optimization, we successfully generated KRpep-2d (Ac-RRRRCPLYISYDPVCRRRR-NH<sub>2</sub>) that inhibited enzyme activity of K-Ras(G12D) with IC<sub>50</sub> = 1.6 nM and significantly suppressed ERK-phosphorylation, downstream of K-Ras(G12D), along with A427 cancer cell proliferation at 30 μM peptide concentration.
|
28153726 |
2017 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
Thus, the infusion of CD8+ cells targeting mutant KRAS mediated effective antitumor immunotherapy against a cancer that expressed mutant KRAS G12D and HLA-C*08:02.
|
27959684 |
2016 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
In conclusion, our results illustrate that the K-Ras(V14I) activating protein is able to induce cancer, although at a much lower level than the classical K-Ras(G12V) oncogene, and that it can be significantly modulated by both genetic and non-genetic events.
|
27174785 |
2016 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
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 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here, we globally activated a mutant oncogenic K-Ras allele (K-Ras(G12D)) in mice and examined the tissue-specific effects of this activation on cancer pathobiology, Ras signaling, tumor suppressor, DNA damage, and inflammatory responses.
|
22532587 |
2012 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
The codon 12 G12D mutation was found; the same mutation was evident in the primary cancer of the colon and in its liver and lung metastasis.
|
20213843 |
2010 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
0.100 |
GeneticVariation
|
BEFREE |
Moreover, all mice with Kras(G12D) activation and Pten homozygous deletion succumbed to cancer by 3 weeks of age.
|
20807812 |
2010 |
|
rs121913529
|
|
Primary malignant neoplasm
|
|
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 |