Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs121913529
rs121913529
0.030 GeneticVariation BEFREE In sst2+/- mice, PI3K was activated and signaled via AKT (PKB; protein kinase B); when these mice were crossed with KRAS(G12D) mice, premalignant lesions, tumors, and lymph node metastases developed more rapidly than in KRAS(G12D) mice. 25683115

2015

dbSNP: rs121913529
rs121913529
0.030 GeneticVariation BEFREE Although CA was observed in mammary tumors initiated by c-Myc or K-Ras(G12D), it was detected only in premalignant mammary lesions expressing K-Ras(G12D). 20581865

2010

dbSNP: rs121913529
rs121913529
0.030 GeneticVariation BEFREE Loss, or mutation, of Trp53 allows retention of the Kras(G12D)-expressing cells and drives rapid progression of these premalignant lesions to PDAC. 20018721

2010

dbSNP: rs10759932
rs10759932
0.010 GeneticVariation BEFREE TLR4 rs10759932, but not TLR2 rs3804099 and rs3804100, was associated with risk of premalignant and/or malignant and H. pylori susceptibility. 30301709

2019

dbSNP: rs1179251
rs1179251
0.010 GeneticVariation BEFREE Among the investigated gene variants onlyIL10T-819C, IL-8-251, IL-18RAP917997, IL-22 rs1179251, IL1-B-511, IL1-B-3954, IL4R-398 and IL1RN were identified as predictors for premalignant gastric lesions risk. 31435167

2019

dbSNP: rs3804099
rs3804099
0.010 GeneticVariation BEFREE TLR4 rs10759932, but not TLR2 rs3804099 and rs3804100, was associated with risk of premalignant and/or malignant and H. pylori susceptibility. 30301709

2019

dbSNP: rs3804100
rs3804100
0.010 GeneticVariation BEFREE TLR4 rs10759932, but not TLR2 rs3804099 and rs3804100, was associated with risk of premalignant and/or malignant and H. pylori susceptibility. 30301709

2019

dbSNP: rs6061243
rs6061243
0.010 GeneticVariation BEFREE Two synonymous SNPs (rs6061243 and rs6587239) were associated with progression of premalignant gastric lesions in a dominant-effects model after correction for multiple comparisons (p = 2.63E-07 and p = 7.97E-07, respectively); effect sizes were β = -0.863 and β = -0.815, respectively, where β is an estimate of effect on histopathology scores, which ranged from 1 (normal) to 5 (dysplasia). 27225266

2016

dbSNP: rs6587239
rs6587239
0.010 GeneticVariation BEFREE Two synonymous SNPs (rs6061243 and rs6587239) were associated with progression of premalignant gastric lesions in a dominant-effects model after correction for multiple comparisons (p = 2.63E-07 and p = 7.97E-07, respectively); effect sizes were β = -0.863 and β = -0.815, respectively, where β is an estimate of effect on histopathology scores, which ranged from 1 (normal) to 5 (dysplasia). 27225266

2016

dbSNP: rs104894230
rs104894230
0.010 GeneticVariation BEFREE In sst2+/- mice, PI3K was activated and signaled via AKT (PKB; protein kinase B); when these mice were crossed with KRAS(G12D) mice, premalignant lesions, tumors, and lymph node metastases developed more rapidly than in KRAS(G12D) mice. 25683115

2015

dbSNP: rs727503094
rs727503094
0.010 GeneticVariation BEFREE In sst2+/- mice, PI3K was activated and signaled via AKT (PKB; protein kinase B); when these mice were crossed with KRAS(G12D) mice, premalignant lesions, tumors, and lymph node metastases developed more rapidly than in KRAS(G12D) mice. 25683115

2015

dbSNP: rs752021744
rs752021744
0.010 GeneticVariation BEFREE In sst2+/- mice, PI3K was activated and signaled via AKT (PKB; protein kinase B); when these mice were crossed with KRAS(G12D) mice, premalignant lesions, tumors, and lymph node metastases developed more rapidly than in KRAS(G12D) mice. 25683115

2015

dbSNP: rs10893506
rs10893506
0.010 GeneticVariation BEFREE The polymorphism analysis showed that at SNP rs10893506, genotypes CC and CT of the ST3GAL4 B3 promoter were associated with the presence of premalignant lesions (OR=2.89; 95%CI 1.72-4.85) and cervical cancer (OR=2.23; 95%CI 1.27-3.91). 24606438

2014

dbSNP: rs61748181
rs61748181
0.010 GeneticVariation BEFREE These findings warrant further analysis of A279T expression in esophageal cancers and premalignant esophageal lesions. 24983628

2014

dbSNP: rs9527
rs9527
0.010 GeneticVariation BEFREE In a follow-up analysis of 1,085 individuals with arsenic-induced premalignant skin lesions (the classical sign of arsenic toxicity) and 1,794 controls, we show that one of these five variants (rs9527) is also associated with skin lesion risk (P = 0.0005). 22383894

2012

dbSNP: rs762846821
rs762846821
0.010 GeneticVariation BEFREE Loss, or mutation, of Trp53 allows retention of the Kras(G12D)-expressing cells and drives rapid progression of these premalignant lesions to PDAC. 20018721

2010

dbSNP: rs11191439
rs11191439
0.010 GeneticVariation BEFREE These findings indicate that Met287Thr influences the susceptibility to premalignant As skin lesions and might be at increased risk for other adverse health effects of iAs exposure. 19538983

2009

dbSNP: rs79658334
rs79658334
RET
0.010 GeneticVariation BEFREE CCH associated with V804M RET mutation is a precancerous condition and surgery is recommended. 18299477

2008

dbSNP: rs113488022
rs113488022
0.010 GeneticVariation BEFREE Mutations in the BRAF gene causing a V599E amino acid substitution that enhance the kinase activity have been described in >60% of cutaneous melanomas and premalignant melanocytic lesions. 14522889

2003

dbSNP: rs121913377
rs121913377
0.010 GeneticVariation BEFREE Mutations in the BRAF gene causing a V599E amino acid substitution that enhance the kinase activity have been described in >60% of cutaneous melanomas and premalignant melanocytic lesions. 14522889

2003