Source: ALL

Variant Gene Disease Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Administration of a CXCL16-neutralizing antibody to KRAS(G12D) mice reduced activation of PI3K signaling to AKT and NF-κB, blocking carcinogenesis. 25683115

2015

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Tumorigenesis was measured in the Kras(G12D/+);Ptf1a(Cre/+) mouse model of PDA; these mice were crossed with mice with pancreas-specific disruption of genes encoding PI3K p110α (Pik3ca), p110β (Pik3cb), or RAC1 (Rac1). 25311989

2014

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Through two novel transgenic mouse models, we show that Twist1 cooperates with Kras(G12D) to markedly accelerate lung tumorigenesis by abrogating cellular senescence programs and promoting the progression from benign adenomas to adenocarcinomas. 22654667

2012

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE To evaluate the role of oncogenic RAS mutations in pancreatic tumorigenesis, we directed endogenous expression of KRAS(G12D) to progenitor cells of the mouse pancreas. 14706336

2003

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Here, we demonstrate in an in vivo transgenic model in which atorvastatin reverses and prevents the onset of MYC-induced lymphomagenesis, but fails to reverse or prevent tumorigenesis in the presence of constitutively activated K-Ras (G12D). 17622571

2007

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Foxm1 transcription factor is required for the initiation of lung tumorigenesis by oncogenic Kras(G12D.). 24213573

2014

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE We demonstrated that transient transgenic expression of KRAS(G12V) in putative neural stem and/or progenitor cells induced brain tumorigenesis. 25644510

2015

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Reduced HRAS G12V-Driven Tumorigenesis of Cell Lines Expressing KRAS C118S. 25902334

2015

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE The data suggest that coexpression of BRAF(V600E) and KRAS(G12D) in early tumorigenesis leads to negative selection due to oncogene-induced senescence. 26028035

2016

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE PIK3CA(H1047R) expression alone failed to promote tumor formation, but dramatically enhanced tumorigenesis initiated by KRAS(G12D). 26567140

2015

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
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

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Furthermore, genetic targeting of the Nrf2 pathway impairs K-Ras(G12D)-induced proliferation and tumorigenesis in vivo. 21734707

2011

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE We used these mice to investigate a possible cooperative effect of GNAS(R201H) and Kras(G12D) in pancreatic tumorigenesis. 26257060

2016

dbSNP: rs121913529
rs121913529
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE However, a more rigorous test of the requirement for Notch signaling in lung oncogenesis, crossing the LSL-KRAS(G12D) mouse model with a transgenic with a similarly inducible global dominant-negative suppressor of Notch activity, LSL-DNMAML (dominant-negative mastermind-like), reveals no evidence of Notch pathway requirement for lung tumor initiation or growth in vivo. 21994468

2011

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Mutation in the B RAF at V600E has been well implicated in the carcinogenesis that makes it as an attractive therapeutictarget. 28472910

2017

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE The B-Raf(V600E) mutant, found in 65% of human melanomas, drives constitutive activation of the extracellular signal-regulated kinase (ERK) pathway and is implicated in tumorigenesis. 18071315

2008

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Here we report that BRAF(V600E) expression in neural progenitors (NPs) is insufficient for tumorigenesis and increases NP cellular differentiation as well as apoptosis. 22586120

2012

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE A large number of studies in the past decade have tried to dissect the relevance and the function of the V600E mutation in controlling oncogenesis and progression of thyroid cancer. 24828987

2015

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Here we show decreasing the levels of CTR1 (Cu transporter 1), or mutations in MEK1 that disrupt Cu binding, decreased BRAF(V600E)-driven signalling and tumorigenesis in mice and human cell settings. 24717435

2014

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE To determine the occurrence of BRAF V600E gene mutations and copy number changes of all autosome arms and genes known to be frequently altered in tumorigenesis in primary and metastatic conjunctival melanomas (CoMs). 21693616

2011

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE While the role of BRAF(V600E) in tumorigenesis is well established, its involvement in metastasis that is clinically observed in melanoma patients remains a topic of debate. 27210749

2016

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE The increased incidence of cancer in FDRs of index CRC patients with the p.V600E BRAF mutation may be explained by a genetic predisposition to develop cancer through the serrated pathway of colorectal carcinogenesis. 20570909

2010

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE Interesting, Prof. Peng Hou and colleagues, at the First Affiliated Hospital of Xi'an Jiaotong University in China, identified unknown epigenetic mechanisms and their involvement in the tumorigenesis of B-RAF(V600E)-driven cancer. 28638488

2017

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE In contrast to other Braf-induced mouse models of tumorigenesis (i.e., melanomas and lung), in which knock-in of Braf(V600E) induces mostly benign lesions, Braf-expressing thyrocytes become transformed and progress to invasive carcinomas with a very short latency, a process that is dampened by treatment with an allosteric MEK inhibitor. 21220306

2011

dbSNP: rs121913377
rs121913377
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation BEFREE These results suggest that the B-Raf activation segment mutations other than V599E reported in colorectal tumors do not necessarily contribute to carcinogenesis by increasing kinase and transforming activities. 14678966

2003