Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs10146204
rs10146204
0.010 GeneticVariation BEFREE For SNPs rs8021944, rs1256061 and rs10146204, ERβ expression was higher according to the rank sum test in lung tumors from patients with at least one minor allele. 23619141

2013

dbSNP: rs199976573
rs199976573
0.010 GeneticVariation BEFREE Moreover, Klf5 is not required for lung tumor formation in an inducible oncogenic K-Ras(G12D) mouse model of lung tumorigenesis, and non-small cell lung cancer patients expressing high levels of KLF5 (21/258) have a significantly better disease-specific survival than those with intermediate to no KLF5 expression. 20639455

2010

dbSNP: rs1057519783
rs1057519783
ALK
0.010 GeneticVariation BEFREE The autopsied lung tumors harbored ALK G1202R (c. 3604 G>A) and the right renal metastasis harbored ALK G1202R (c. 3604 G>C); the mutation thus comprised different codon changes. 31374369

2019

dbSNP: rs113488022
rs113488022
0.020 GeneticVariation BEFREE Coactivation of BRAF(V600E) and KRAS(G12D) markedly reduced lung tumor numbers and overall tumor burden compared with activation of BRAF(V600E) alone. 26028035

2016

dbSNP: rs113488022
rs113488022
0.020 GeneticVariation BEFREE We combined (L597V)Braf with (G12D)Kras and found that (L597V)Braf modified (G12D)Kras oncogenesis such that fibroblast transformation and lung tumor development were more reminiscent of that driven by the high-activity (V600E)Braf mutant. 22892241

2012

dbSNP: rs121913377
rs121913377
0.020 GeneticVariation BEFREE Coactivation of BRAF(V600E) and KRAS(G12D) markedly reduced lung tumor numbers and overall tumor burden compared with activation of BRAF(V600E) alone. 26028035

2016

dbSNP: rs121913377
rs121913377
0.020 GeneticVariation BEFREE We combined (L597V)Braf with (G12D)Kras and found that (L597V)Braf modified (G12D)Kras oncogenesis such that fibroblast transformation and lung tumor development were more reminiscent of that driven by the high-activity (V600E)Braf mutant. 22892241

2012

dbSNP: rs121913369
rs121913369
0.010 GeneticVariation BEFREE We combined (L597V)Braf with (G12D)Kras and found that (L597V)Braf modified (G12D)Kras oncogenesis such that fibroblast transformation and lung tumor development were more reminiscent of that driven by the high-activity (V600E)Braf mutant. 22892241

2012

dbSNP: rs1174029586
rs1174029586
0.010 GeneticVariation BEFREE Mutant Ki-ras(G12C) expression was sufficient for initial lung tumor transformation, required for maintenance of tumor phenotype, and induced transformation of lung epithelial cells by the activation of multiple effector pathways. 16051643

2005

dbSNP: rs947996134
rs947996134
0.010 GeneticVariation BEFREE Mutant Ki-ras(G12C) expression was sufficient for initial lung tumor transformation, required for maintenance of tumor phenotype, and induced transformation of lung epithelial cells by the activation of multiple effector pathways. 16051643

2005

dbSNP: rs1444669684
rs1444669684
0.020 GeneticVariation BEFREE Conditional deletion of Foxm1 from Kras(G12D)-expressing respiratory epithelium prevented the initiation of lung tumors in vivo. 24213573

2014

dbSNP: rs1444669684
rs1444669684
0.020 GeneticVariation BEFREE Coactivation of BRAF(V600E) and KRAS(G12D) markedly reduced lung tumor numbers and overall tumor burden compared with activation of BRAF(V600E) alone. 26028035

2016

dbSNP: rs3743073
rs3743073
0.010 GeneticVariation BEFREE We found that four of the variants (rs3829787, rs3841324, rs588765 and rs3743073) were associated with differential levels of genetic alterations measured as the levels of hydrophobic DNA adducts in the adjacent histologically normal tissue of the lung cancer patients and as TP53 mutations in their lung tumors. 23011884

2013

dbSNP: rs588765
rs588765
0.010 GeneticVariation BEFREE We found that four of the variants (rs3829787, rs3841324, rs588765 and rs3743073) were associated with differential levels of genetic alterations measured as the levels of hydrophobic DNA adducts in the adjacent histologically normal tissue of the lung cancer patients and as TP53 mutations in their lung tumors. 23011884

2013

dbSNP: rs775514340
rs775514340
0.010 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: rs1242640031
rs1242640031
CRK
0.010 GeneticVariation BEFREE Mutant Ki-ras(G12C) expression was sufficient for initial lung tumor transformation, required for maintenance of tumor phenotype, and induced transformation of lung epithelial cells by the activation of multiple effector pathways. 16051643

2005

dbSNP: rs1057519847
rs1057519847
0.060 GeneticVariation BEFREE Finally, we showed that EGFR(L858R)/Rhob(+/+) mice developed mainly diffuse lung tumors with a lepidic pattern, whereas EGFR(L858R)/Rhob(+/-) and EGFR(L858R)/Rhob(-/-) developed a greater number of tumors, and aggressive adenocarcinomas with invasive properties. 25320360

2014

dbSNP: rs1057519847
rs1057519847
0.060 GeneticVariation BEFREE Interestingly, acute loss of Erbb3 suppressed further growth of established EGFR(L858R)-mediated lung tumors. 25596284

2015

dbSNP: rs1057519847
rs1057519847
0.060 GeneticVariation BEFREE The epidermal growth factor receptor (EGFR), when carrying an activating mutation like del19 or L858R, acts as an oncogenic driver in a subset of lung tumors. 31689114

2019

dbSNP: rs1057519847
rs1057519847
0.060 GeneticVariation BEFREE Pharmacologic inhibition of β-catenin suppressed EGFR-L858R-T790M mutated lung tumor growth, and genetic deletion of the β-catenin gene dramatically reduced lung tumor formation in EGFR-L858R-T790M transgenic mice. 25164010

2014

dbSNP: rs1057519847
rs1057519847
0.060 GeneticVariation BEFREE Similarly, deficiency of Puma impeded the regression of EGFR(L858R)-driven mouse lung tumors upon inactivation of the EGFR-activating mutant. 23532334

2013

dbSNP: rs1057519847
rs1057519847
0.060 GeneticVariation BEFREE Using specific and sensitive IHC assays, we analyzed the expression of anaplastic lymphoma kinase (ALK), EGFR L858R, and EGFR E746-A750del mutations in a subset of lung tumors, including those expressing ROS1. 22661537

2012

dbSNP: rs1057519848
rs1057519848
0.060 GeneticVariation BEFREE Pharmacologic inhibition of β-catenin suppressed EGFR-L858R-T790M mutated lung tumor growth, and genetic deletion of the β-catenin gene dramatically reduced lung tumor formation in EGFR-L858R-T790M transgenic mice. 25164010

2014

dbSNP: rs1057519848
rs1057519848
0.060 GeneticVariation BEFREE Similarly, deficiency of Puma impeded the regression of EGFR(L858R)-driven mouse lung tumors upon inactivation of the EGFR-activating mutant. 23532334

2013

dbSNP: rs1057519848
rs1057519848
0.060 GeneticVariation BEFREE Using specific and sensitive IHC assays, we analyzed the expression of anaplastic lymphoma kinase (ALK), EGFR L858R, and EGFR E746-A750del mutations in a subset of lung tumors, including those expressing ROS1. 22661537

2012