Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs587782329
rs587782329
0.010 GeneticVariation BEFREE Lung tumors of 50 uranium miners in Germany were screened by restriction fragment length analysis for the putative hotspot mutation at codon 249 (Arg-->Met) previously detected in a significant fraction of miners from the Colorado Plateau, USA. 9067550

1997

dbSNP: rs1052559
rs1052559
0.010 GeneticVariation BEFREE Functional polymorphisms in XPD (Asp312Asn, rs1799793 and Lys751Gln, rs1052559), a protein required for nucleotide excision repair and with roles in p53-mediated apoptosis, were modestly associated with G:C-->T:A mutations in TP53 in lung tumors [Asp/Asn312 + Asn/Asn312 and/or Lys/Gln751 + Gln/Gln751 versus Asp/Asp312 + Lys/Lys751; odds ratio (OR) 2.73, 95% confidence interval (CI) 0.98-7.61], consistent with the role of this protein in repair of bulky carcinogen-DNA adducts. 15564288

2005

dbSNP: rs13181
rs13181
0.010 GeneticVariation BEFREE Functional polymorphisms in XPD (Asp312Asn, rs1799793 and Lys751Gln, rs1052559), a protein required for nucleotide excision repair and with roles in p53-mediated apoptosis, were modestly associated with G:C-->T:A mutations in TP53 in lung tumors [Asp/Asn312 + Asn/Asn312 and/or Lys/Gln751 + Gln/Gln751 versus Asp/Asp312 + Lys/Lys751; odds ratio (OR) 2.73, 95% confidence interval (CI) 0.98-7.61], consistent with the role of this protein in repair of bulky carcinogen-DNA adducts. 15564288

2005

dbSNP: rs1799793
rs1799793
0.010 GeneticVariation BEFREE Functional polymorphisms in XPD (Asp312Asn, rs1799793 and Lys751Gln, rs1052559), a protein required for nucleotide excision repair and with roles in p53-mediated apoptosis, were modestly associated with G:C-->T:A mutations in TP53 in lung tumors [Asp/Asn312 + Asn/Asn312 and/or Lys/Gln751 + Gln/Gln751 versus Asp/Asp312 + Lys/Lys751; odds ratio (OR) 2.73, 95% confidence interval (CI) 0.98-7.61], consistent with the role of this protein in repair of bulky carcinogen-DNA adducts. 15564288

2005

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: 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: 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: rs121434569
rs121434569
0.060 GeneticVariation BEFREE MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. 18093943

2007

dbSNP: rs121913529
rs121913529
0.080 GeneticVariation BEFREE Importantly, the combined inactivation of both MYC and K-ras(G12D) resulted more frequently in complete lung tumor regression. 18461184

2008

dbSNP: rs121434569
rs121434569
0.060 GeneticVariation BEFREE Nevertheless, several lines of evidence indicate that the T790M mutation confers growth advantage to cancer cells, and it was shown that mice expressing tetracycline-inducible EGFR transgenes harboring the T790M mutation develop lung tumors. 19096299

2009

dbSNP: rs762846821
rs762846821
0.030 GeneticVariation BEFREE Conversely, in lung tumour cell lines expressing Kras(G12D) and lacking p53, p53 restoration led to NF-kappaB inhibition. 19847165

2009

dbSNP: rs1458974438
rs1458974438
0.010 GeneticVariation BEFREE In mice, Lkb1 deletion and activation of Kras(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases. 20541700

2010

dbSNP: rs752021744
rs752021744
0.010 GeneticVariation BEFREE In mice, Lkb1 deletion and activation of Kras(G12D) results in lung tumors with a high penetrance of lymph node and distant metastases. 20541700

2010

dbSNP: rs121913529
rs121913529
0.080 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: 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: rs16906252
rs16906252
0.010 GeneticVariation BEFREE The A allele was selectively methylated in primary lung tumors and cell lines heterozygous for rs16906252. 21355081

2011

dbSNP: rs12072037
rs12072037
0.010 GeneticVariation BEFREE SNP rs12072037 modulates MFSD2A promoter activity and thus might affect MFSD2A levels in normal lung and in lung tumors, representing a candidate ethnically specific genetic factor underlying the association between the MYCL1 locus and lung cancer patients' survival. 21736709

2011

dbSNP: rs121913529
rs121913529
0.080 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: 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: 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 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: rs121434568
rs121434568
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: 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 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: rs1018379423
rs1018379423
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