Source: ALL
Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs1979277
rs1979277
SHMT1
0.010 GeneticVariation BEFREE A comprehensive search was conducted to identify all eligible studies of the SHMT1 rs1979277 polymorphism and solid tumor</span> risk. 26125758

2015
dbSNP: rs11547328
rs11547328
CDK4
0.010 GeneticVariation BEFREE Absence of R24C mutation of the CDK4 gene in leukemias and solid tumors. 12731669

2003
dbSNP: rs771138120
rs771138120
CDKN2A
0.010 GeneticVariation BEFREE Absence of R24C mutation of the CDK4 gene in leukemias and solid tumors. 12731669

2003
dbSNP: rs121434592
rs121434592
AKT1
0.030 GeneticVariation BEFREE AKT1(E17K) mutations occur at low frequency in a variety of solid tumors, including those of the breast and urinary bladder. 26351323

2015
dbSNP: rs886039463
rs886039463
PTPN11
0.010 GeneticVariation BEFREE Although rare in solid tumors, the identified T507K SHP-2 represents a distinct class of SHP-2 mutants with oncogenic RAS-like transforming activity, which could contribute to the development of solid tumors. 18223690

2008
dbSNP: rs61754966
rs61754966
NBN
0.010 GeneticVariation BEFREE Among children with solid tumors only in 1 child with medulloblastoma I171V variant has been found. 21436738

2011
dbSNP: rs1042522
rs1042522
TP53
0.010 GeneticVariation BEFREE Among the natural sequence variants of TP53, rs1042522 (R72P) modifies the risk for solid tumors. 19837266

2009
dbSNP: rs1131691014
rs1131691014
TP53
0.010 GeneticVariation BEFREE Among the natural sequence variants of TP53, rs1042522 (R72P) modifies the risk for solid tumors. 19837266

2009
dbSNP: rs1353702185
rs1353702185
MDM2
0.010 GeneticVariation BEFREE Among the natural sequence variants of TP53, rs1042522 (R72P) modifies the risk for solid tumors. 19837266

2009
dbSNP: rs878854066
rs878854066
TP53
0.010 GeneticVariation BEFREE Among the natural sequence variants of TP53, rs1042522 (R72P) modifies the risk for solid tumors. 19837266

2009
dbSNP: rs11614913
rs11614913
HOXC6 ; MIR196A2
0.010 GeneticVariation BEFREE As there are no previous studies on the miR-196a2 variant or expression in any type of cancer among our population, we aimed to determine the expression profile of mature miR-196a2 in various types of solid tumors and to analyze the impact of its polymorphism (rs11614913; C/T) on the expression levels. 27342110

2016
dbSNP: rs6674079
rs6674079 		0.010 GeneticVariation BEFREE ENCODE ChIP-seq data at 1q22 for normal ovary show evidence of histone modification around RP11-284F21.8, and rs6674079 is perfectly correlated with another SNP within the super-enhancer MEF2D, expression levels of which were reportedly associated with prognosis in another solid tumor. 26152742

2015
dbSNP: rs758272654
rs758272654
GNAS
0.020 GeneticVariation BEFREE GNAS T393C has been shown to predict the postoperative course in solid tumors and may therefore be useful for treatment stratification. 24986238

2014
dbSNP: rs121434592
rs121434592
AKT1
0.030 GeneticVariation BEFREE Here, we selectively disrupt the ability of rapidly proliferating cancer cells to spawn AKT1<sup>low</sup> daughter cells that are rare, slowly proliferating, tumor-initiating, and chemotherapy-resistant, using β1-integrin activation and the AKT1-E17K-mutant oncoprotein as experimental tools <i>in vivo</i> Surprisingly, we find that selective depletion of AKT1<sup>low</sup> slow proliferators actually reduces the growth of a molecularly diverse panel of human cancer cell xenograft models without globally altering cell proliferation or survival <i>in vivo</i> Moreover, we find that unusual cancer patients with AKT1-E17K-mutant solid tumors also fail to produce AKT1<sup>low</sup> quiescent cancer cells and that this correlates with significantly prolonged survival after adjuvant treatment compared with other patients. 29054988

2018
dbSNP: rs1284806277
rs1284806277
MOK
0.010 GeneticVariation BEFREE Moreover, the most recent data reveal that expression of S100P is up-regulated by activation of glucocorticoid receptor suggesting that S100P could play a role in therapy resistance mediated by glucocorticoids in solid tumors. 20155429

2011
dbSNP: rs1285136498
rs1285136498
NR3C1
0.010 GeneticVariation BEFREE Moreover, the most recent data reveal that expression of S100P is up-regulated by activation of glucocorticoid receptor suggesting that S100P could play a role in therapy resistance mediated by glucocorticoids in solid tumors. 20155429

2011
dbSNP: rs113488022
rs113488022
BRAF
0.030 GeneticVariation BEFREE Our results reveal a common BRAF(V600E)-directed transcriptional regulatory pathway that mediates epigenetic silencing in unrelated solid tumors and provide strong support for an instructive model of oncoprotein-directed epigenetic silencing. 26787892

2016
dbSNP: rs121913377
rs121913377
BRAF
0.030 GeneticVariation BEFREE Our results reveal a common BRAF(V600E)-directed transcriptional regulatory pathway that mediates epigenetic silencing in unrelated solid tumors and provide strong support for an instructive model of oncoprotein-directed epigenetic silencing. 26787892

2016
dbSNP: rs113488022
rs113488022
BRAF
0.030 GeneticVariation BEFREE Precision Medicine Intelligence - evidence scoring evaluating the clinical actionability of BRAF V600E in multiple non-melanoma solid tumors. 27540599

2016
dbSNP: rs121913377
rs121913377
BRAF
0.030 GeneticVariation BEFREE Precision Medicine Intelligence - evidence scoring evaluating the clinical actionability of BRAF V600E in multiple non-melanoma solid tumors. 27540599

2016
dbSNP: rs758272654
rs758272654
GNAS
0.020 GeneticVariation BEFREE Recent studies have shown an association between the GNAS1 T393C polymorphism and clinical outcome for various solid tumors. 19274060

2009
dbSNP: rs121434592
rs121434592
AKT1
0.030 GeneticVariation BEFREE Results In patients with AKT1 E17K-mutant tumors (n = 52) and a median of five lines of prior therapy, the median PFS was 5.5 months (95% CI, 2.9 to 6.9 months), 6.6 months (95% CI, 1.5 to 8.3 months), and 4.2 months (95% CI, 2.1 to 12.8 months) in patients with estrogen receptor-positive breast, gynecologic, and other solid tumors, respectively. 28489509

2017
dbSNP: rs762292600
rs762292600
ESR1
0.010 GeneticVariation BEFREE Results In patients with AKT1 E17K-mutant tumors (n = 52) and a median of five lines of prior therapy, the median PFS was 5.5 months (95% CI, 2.9 to 6.9 months), 6.6 months (95% CI, 1.5 to 8.3 months), and 4.2 months (95% CI, 2.1 to 12.8 months) in patients with estrogen receptor-positive breast, gynecologic, and other solid tumors, respectively. 28489509

2017
dbSNP: rs2736100
rs2736100
TERT
0.010 GeneticVariation BEFREE TERT rs2736100_C polymorphism predisposes to the development of BCR-ABL1-negative MPN with the co-occurrence of solid tumors, especially with the usage of cytoreductive treatment. 26487696

2016
dbSNP: rs121913409
rs121913409
CTNNB1
0.010 GeneticVariation BEFREE The p.S45F activating mutation was found in a variety of solid tumors, and accounts for 3.3 to 10.4% of all known β-catenin mutations. 28725522

2017