rs121913529, KRAS

N. diseases: 144
Source: ALL
Disease Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
Neoplasms
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE The expression of mutant KRAS(G12V) in HPDE cells by retroviral transduction resulted in weak tumorigenic transformation, with tumors formed in 50% of immune-deficient scid mice implanted by these KRAS-transformed cells. 18374152 2008
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE To examine how the MYC and K-ras(G12D) oncogenes cooperate for the initiation and maintenance of tumorigenesis, we generated double conditional transgenic tumor models of lung adenocarcinoma and lymphoma. 18461184 2008
Neoplasms
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Scintigraphic tumor/muscle image intensity ratios for complementary [(111)In](n)-PDAP(m)-KRAS2 G12D probes increased from 3.1 +/- 0.2 at n = 2, m = 1, to 4.1 +/- 0.3 at n = 8, m = 3, to 6.2 +/- 0.4 at n = 16, m = 4, in AsPC1 (G12D) xenografts. 20232877 2010
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE In vitro cytotoxicity studies showed the STO cell line to be resistant to gefitinib and sensitive to sequential treatment with RAD001 and sorafenib; these findings were consistent with the presence of the KRAS mutation G12D in these cells although it was not detectable in the original tumour. 20692828 2010
Neoplasms
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Patients whose tumors had either mutant KRas-Gly12Cys or mutant KRas-Gly12Val had worse progression-free survival compared with patients whose tumors had other mutant KRas proteins or wild-type KRas (P = .046, median survival = 1.84 months) compared with all other mutant KRas (median survival = 3.35 months) or wild-type KRas (median survival = 1.95 months). 22247021 2012
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE A KRAS G12A mutation was found in tumor removed from the finger. 22317887 2012
Neoplasms
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Most of the patients (82.8%) had a KRAS wild type tumor; a p.Gly12Cys was found in three patients and a p.Gly12Val mutation in one. 22668015 2012
Neoplasms
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE We found that the deletion of Ink4a/Arf in K-Ras(G12D) expressing mice led to high expression of PDGF-D signaling pathway in the tumor and tumor-derived cell line (RInk-1 cells). 22806240 2013
Neoplasms
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: 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
CUI: C0027651
Disease: 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
Neoplasms
CUI: C0027651
Disease: 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