Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs1050171
rs1050171
0.010 GeneticVariation BEFREE In exon 20, a variant from CAG to CAA at codon 787 (2361G-> A) was identified in 19 patients, which was a genomic variation of EGFR since it was found in both cancer tissue and white blood cells. 22252115

2012

dbSNP: rs1057519847
rs1057519847
0.030 GeneticVariation BEFREE The results of cancer tissue specimens were identical to those with existing systems (nucleic acid-locked nucleic acid PCR clamp or cycleave PCR), except for two samples that showed both exon 19 deletions and L858R. 22858585

2012

dbSNP: rs1057519847
rs1057519847
0.030 GeneticVariation BEFREE The purpose of this study was to clarify the relationship between the EGFR-L858R mutation and cancer cell invasion ability and to investigate the molecular mechanisms involved in the formation of MPE. 26338423

2015

dbSNP: rs1057519847
rs1057519847
0.030 GeneticVariation BEFREE These conjugates exhibited high antiproliferative potency against a number of cancer cell lines, including the epidermal growth factor receptor (EGFR) L858R/T790M mutant cell. 28236592

2017

dbSNP: rs1057519848
rs1057519848
0.030 GeneticVariation BEFREE These conjugates exhibited high antiproliferative potency against a number of cancer cell lines, including the epidermal growth factor receptor (EGFR) L858R/T790M mutant cell. 28236592

2017

dbSNP: rs1057519848
rs1057519848
0.030 GeneticVariation BEFREE The results of cancer tissue specimens were identical to those with existing systems (nucleic acid-locked nucleic acid PCR clamp or cycleave PCR), except for two samples that showed both exon 19 deletions and L858R. 22858585

2012

dbSNP: rs1057519848
rs1057519848
0.030 GeneticVariation BEFREE The purpose of this study was to clarify the relationship between the EGFR-L858R mutation and cancer cell invasion ability and to investigate the molecular mechanisms involved in the formation of MPE. 26338423

2015

dbSNP: rs1057519861
rs1057519861
0.030 GeneticVariation BEFREE The combination of a MEK inhibitor with AZD9291 restores the sensitivity of AZD9291-resistant cells including those with C797S mutation to undergo apoptosis and growth regression <i>in vitro</i> and <i>in vivo</i><b>Conclusions:</b> Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant NSCLC cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291.<i>Clin Cancer Res; 23(21); 6567-79.©2017 AACR</i>. 28765329

2017

dbSNP: rs1057519861
rs1057519861
0.030 GeneticVariation BEFREE Noteworthy effect of slight variation in aliphatic chain length of trisubstituted imidazole inhibitors against epidermal growth factor receptor L858R/T790M/C797S mutant in cancer therapy. 30582282

2019

dbSNP: rs1057519861
rs1057519861
0.030 GeneticVariation BEFREE We also demonstrated that PE2988 cells, a C797S-independent osimertinib-resistant primary cancer cell line from a lung cancer patient, responded to combined AXL inhibitor and osimertinib treatment. 31162839

2019

dbSNP: rs121434568
rs121434568
0.030 GeneticVariation BEFREE These conjugates exhibited high antiproliferative potency against a number of cancer cell lines, including the epidermal growth factor receptor (EGFR) L858R/T790M mutant cell. 28236592

2017

dbSNP: rs121434568
rs121434568
0.030 GeneticVariation BEFREE The purpose of this study was to clarify the relationship between the EGFR-L858R mutation and cancer cell invasion ability and to investigate the molecular mechanisms involved in the formation of MPE. 26338423

2015

dbSNP: rs121434568
rs121434568
0.030 GeneticVariation BEFREE The results of cancer tissue specimens were identical to those with existing systems (nucleic acid-locked nucleic acid PCR clamp or cycleave PCR), except for two samples that showed both exon 19 deletions and L858R. 22858585

2012

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE In two patients, the ctDNA dynamics suggested the presence of cancer cell populations only with the T790M mutation. 26678713

2016

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE The molecular beacon-based approach enabled rapid and sensitive detection of the EGFR mutation (T790M) in NSCLC with in situ fluorescence imaging, which can be directed to determine various treatment options in patients with cancer. 20805561

2010

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Non-Small Cell Lung Cancer with Resistance to EGFR-TKI Therapy: CT Characteristics of T790M Mutation-positive Cancer. 30015588

2018

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Design and synthesis of diphenylpyrimidine derivatives (DPPYs) as potential dual EGFR T790M and FAK inhibitors against a diverse range of cancer cell lines. 31706682

2020

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE This approach detects mutations as subtle as the drug-resistance-conferring cancer mutation EGFR T790M (a single C → T substitution) with an estimated specificity of 99.99999%, surpassing even the leading PCR-based methods and enabling detection of 1 mutant molecule in a background of at least 1 million wild-type molecules. 30125495

2018

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE While they produce dramatic responses in a subset of patients-primarily those with activating EGFR mutations-remissions are typically limited to several months due to acquired drug resistance, frequently associated with the secondary T790M mutation in EGFR.In this issue of Cancer Cell, Li et al. report that an irreversible EGFR kinase inhibitor, HKI-272, had limited activity in a mouse lung cancer model driven by an EGFR mutant harboring T790M and an activating mutation. 17613432

2007

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE To assess the biological implications of <i>RET</i> fusions in an <i>EGFR</i>-mutant cancer, we expressed CCDC6-RET in PC9 (<i>EGFR</i> del19) and MGH134 (<i>EGFR</i> L858R/T790M) cells and found that CCDC6-RET was sufficient to confer resistance to EGFR tyrosine kinase inhibitors (TKI). 30257958

2018

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE In silico evaluation of the resistance of the T790M variant of epidermal growth factor receptor kinase to cancer drug Erlotinib. 29183267

2018

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE T790M mutations disappeared from cancer cells in the pleural effusion after a break from the treatment drug and cytotoxic agent administration. 30145590

2018

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Following drug resistance in patients with lung cancer treated by EGFR TKIs, a biopsy is required to obtain sufficient cancer tissue for T790M detection in order to select potential beneficiaries suitable for third-generation EGFR TKIs, such as osimertinib. 31407509

2019

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE These conjugates exhibited high antiproliferative potency against a number of cancer cell lines, including the epidermal growth factor receptor (EGFR) L858R/T790M mutant cell. 28236592

2017

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Indeed, the use of plasma testing to screen for epidermal growth factor receptor (<i>EGFR</i>) T790M mutant positive non-small cell lung cancer (NSCLC) patients eligible for treatment with third-generation EGFR inhibitors was recently approved by the U.S. Food and Drug Administration and is incorporated into the most recent version of the National Comprehensive Cancer Center guidelines as an alternative to tissue biopsy. 29184671

2017