rs113488022
|
|
|
0.030 |
GeneticVariation |
BEFREE |
This study evaluated the safety and tolerability, pharmacokinetics (PK) and preliminary efficacy of dabrafenib 150 mg b.i.d. plus trametinib 2 mg q.d. in Japanese patients with BRAF V600E/K mutant solid tumors (phase 1) and melanoma (phase 2).
|
29399853 |
2018 |
rs121434592
|
|
|
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 |
rs121913377
|
|
|
0.030 |
GeneticVariation |
BEFREE |
This study evaluated the safety and tolerability, pharmacokinetics (PK) and preliminary efficacy of dabrafenib 150 mg b.i.d. plus trametinib 2 mg q.d. in Japanese patients with BRAF V600E/K mutant solid tumors (phase 1) and melanoma (phase 2).
|
29399853 |
2018 |
rs121434592
|
|
|
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 |
rs113488022
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|
|
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 |
rs113488022
|
|
|
0.030 |
GeneticVariation |
BEFREE |
Precision Medicine Intelligence - evidence scoring evaluating the clinical actionability of BRAF V600E in multiple non-melanoma solid tumors.
|
27540599 |
2016 |
rs121913377
|
|
|
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 |
rs121913377
|
|
|
0.030 |
GeneticVariation |
BEFREE |
Precision Medicine Intelligence - evidence scoring evaluating the clinical actionability of BRAF V600E in multiple non-melanoma solid tumors.
|
27540599 |
2016 |
rs121434592
|
|
|
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 |
rs758272654
|
|
|
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 |
rs758272654
|
|
|
0.020 |
GeneticVariation |
BEFREE |
Recent studies have shown an association between the GNAS1 T393C polymorphism and clinical outcome for various solid tumors.
|
19274060 |
2009 |
rs121913409
|
|
|
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 |
rs762292600
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|
|
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 |
rs11614913
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|
|
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 |
rs2736100
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|
|
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 |
rs1799945
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|
|
0.010 |
GeneticVariation |
BEFREE |
Therefore, this meta-analysis was conducted to summarize the effect of the H63D variant on the incidence of solid tumor.
|
26535689 |
2015 |
rs1979277
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|
|
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 |
rs6674079
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|
|
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 |
rs10889677
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|
|
0.010 |
GeneticVariation |
BEFREE |
These findings demonstrated that the IL-23R rs10889677</span> genetic variant might play an important part during malignant transformation of multiple solid tumors.
|
24278297 |
2013 |
rs1284806277
|
|
|
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 |
rs1285136498
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|
|
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 |
rs61754966
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|
|
0.010 |
GeneticVariation |
BEFREE |
Among children with solid tumors only in 1 child with medulloblastoma I171V variant has been found.
|
21436738 |
2011 |
rs1042522
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Among the natural sequence variants of TP53, rs1042522 (R72P) modifies the risk for solid tumors.
|
19837266 |
2009 |
rs1057519865
|
|
|
0.010 |
GeneticVariation |
BEFREE |
The specificity of the FOXL2 c.402C>G somatic mutation: a survey of solid tumors.
|
19956657 |
2009 |
rs1131691014
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Among the natural sequence variants of TP53, rs1042522 (R72P) modifies the risk for solid tumors.
|
19837266 |
2009 |