|
rs746763556
|
|
Malignant Neoplasms
|
|
0.010 |
GeneticVariation
|
BEFREE |
Among these impactful variants are rare somatic, clinically actionable variants including EGFR S645C, ARAF S214C and S214F, ERBB2 S418T, and multiple BRAF variants, demonstrating that rare mutations can be functionally important in cancer.
|
27478040 |
2016 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
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 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The response rate to EGFR TKIs, the median progression-free survival (PFS) to TKIs, the percentage of EGFR-T790M TKI resistance and survival had higher trends in EGFR mutant/TP53 wild-type cases when compared to EGFR mutant/TP53 mutant tumors (all p >0.05 without statistical significance); with a significantly longer median PFS in EGFR-exon 19 deletion mutant/TP53 wild-type cancers treated with 1st generation EGFR TKIs (p=0.035).
|
28285689 |
2017 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
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 |
|
rs397517132
|
|
Malignant Neoplasms
|
|
0.090 |
GeneticVariation
|
BEFREE |
In FNA biopsy samples (n=186), immunocytochemical expression of caveolin-1 and BRAF V600E mutation coincided with malignancy.
|
27818286 |
2017 |
|
rs121434568
|
|
Malignant Neoplasms
|
|
0.040 |
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 |
|
rs1057519848
|
|
Malignant Neoplasms
|
|
0.040 |
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 |
|
rs1057519847
|
|
Malignant Neoplasms
|
|
0.040 |
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 |
|
rs121913444
|
|
Malignant Neoplasms
|
|
0.020 |
GeneticVariation
|
BEFREE |
Two frequent cancer-driver mutation sequences (EGFR-L861Q, NRAS-Q61K) were tested.
|
29069899 |
2017 |
|
rs1057519861
|
|
Malignant Neoplasms
|
|
0.020 |
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 |
|
rs35918369
|
|
Malignant Neoplasms
|
|
0.010 |
GeneticVariation
|
BEFREE |
Using NGS, the following mutations were detected: nonsense mutations in four tumor suppressor genes [APC R1114X (molecular argument that the cancer was a primary tumor of colon), TP53 R213X, RB1 E137X and FBWX7 R393X & S282X], mutations in three receptor tyrosine kinases (RET A919V of high transforming activity, EGFR E114K and FLT3 L601I) well known as oncogenes.
|
28730258 |
2017 |
|
rs140516819
|
|
Malignant Neoplasms
|
|
0.010 |
GeneticVariation
|
BEFREE |
Using NGS, the following mutations were detected: nonsense mutations in four tumor suppressor genes [APC R1114X (molecular argument that the cancer was a primary tumor of colon), TP53 R213X, RB1 E137X and FBWX7 R393X & S282X], mutations in three receptor tyrosine kinases (RET A919V of high transforming activity, EGFR E114K and FLT3 L601I) well known as oncogenes.
|
28730258 |
2017 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Non-Small Cell Lung Cancer with Resistance to EGFR-TKI Therapy: CT Characteristics of T790M Mutation-positive Cancer.
|
30015588 |
2018 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Liquid biopsy offers a potential alternative to tissue biopsy for detection of genetic alterations in cancer, and it has been introduced into clinical practice to detect the tyrosine kinase inhibitor (TKI) resistance-conferring T790M mutation of epidermal growth factor receptor (EGFR) in patients with non-small-cell lung cancer (NSCLC).
|
30289575 |
2018 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
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 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
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 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
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 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
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 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
This could further help avoid unnecessary tumor biopsies for T790M mutation testing.<i>Clin Cancer Res; 24(12); 2944-50.©2018 AACR</i>.
|
29535126 |
2018 |
|
rs397517132
|
|
Malignant Neoplasms
|
|
0.090 |
GeneticVariation
|
BEFREE |
Our findings provide evidence of critical survival signals in BRAF non-V600E mutant c</span>ancers, which could pave the way for effective treatment of these cancers.
|
29348459 |
2018 |
|
rs397517132
|
|
Malignant Neoplasms
|
|
0.090 |
GeneticVariation
|
BEFREE |
With advances in RAF inhibitors and second-generation inhibitors including encorafenib and vemurafenib, which have been approved for treating BRAF-V600E malignancies, the combinatorial therapeutic strategies of RAF inhibitors elicit remarkable responses in patients with BRAF-V600E mCRC.
|
30122982 |
2018 |
|
rs397517132
|
|
Malignant Neoplasms
|
|
0.090 |
GeneticVariation
|
BEFREE |
Patients with this cancer have a high frequency (~50%) of oncogenic <i>BRAF</i> mutations, particularly BRAF V600E.
|
29387237 |
2018 |
|
rs556324078
|
|
Malignant Neoplasms
|
|
0.010 |
GeneticVariation
|
BEFREE |
Moreover, we showed that the D717V, G800D, G800R, L840F, G843D, S925F, R1022Q, R1032Q, and S1100F VEGFR2 mutants promote tumor growth in mice.<b>Conclusions:</b> Our study supports WES-cfDNA as a powerful platform for portraying the somatic mutation landscape of cancer and discovery of new resistance mechanisms to cancer therapies.
|
29588308 |
2018 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
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 |
|
rs121434569
|
|
Malignant Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
We reviewed all patients with T790M-positive NSCLC and acquired resistance to initial EGFR-TKIs who were administered osimertinib between March 2016 and January 2018 at the Tokyo Metropolitan Cancer and Infectious Diseases Center in Komagome Hospital, Japan.
|
31372272 |
2019 |