|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant Neoplasms
|
|
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 |
|
Malignant 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 |