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BIOMARKER:

EGFR mutation + PIK3CA mutation

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Other names: EGFR, ERBB, ERBB1, Epidermal growth factor receptor, PIK3CA, Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, Phosphoinositide-3-kinase, catalytic, alpha polypeptide, Serine/threonine protein kinase PIK3CA, PtdIns-3-kinase subunit P110-alpha, PI3K-alpha, Phosphatidylinositol-4,5-bisphosphate 3-kinase 110 KDa catalytic subunit alpha, Phosphatidylinositol 3-kinase, Catalytic, 110-KD, alpha, PI3-kinase P110 subunit alpha, PI3-kinase subunit alpha, PtdIns-3-kinase subunit alph
Entrez ID:
2d
CAPP-seq analysis of ctDNA was able to identify potentially targetable genetic alterations in patients with osimertinib resistance.
Clinical • Journal • Circulating tumor DNA
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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KRAS mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • EGFR T790M • EGFR C797S • EGFR mutation + PIK3CA mutation
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Tagrisso (osimertinib)
7d
Case1 was a 59-year-old male with a right frontal tumor with IDH1R132H, TP53, and PIK3CA mutations; EGFR, PDGFRA, and KIT amplifications; and methylated MGMT; who expired two days after initiating temozolomide treatment... Co-existence of IDH mutation and EGFR amplification is occasionally seen in gliomas and should be considered in forthcoming classification paradigms. In our small series, all tumors carried the epigenetic signature of an IDH-mutant astrocytoma.
Clinical • Review
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • CDKN2A (Cyclin-dependent kinase inhibitor 2A) • ATRX (ATRX Chromatin Remodeler) • MTAP (Methylthioadenosine Phosphorylase)
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TP53 mutation • EGFR mutation • PIK3CA mutation • EGFR amplification • MYC amplification • KIT mutation • ATRX mutation • PDGFRA mutation • EGFR mutation + PIK3CA mutation
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temozolomide
14d
The existence of coexisting gene mutations may have adverse effects on the prognosis of patients with EGFR mutation. The unknown mutations discovered by NGS may provide new targets for gene targeting therapy, and ctDNA test by NGS is an effective method for making appropriate treatment choices.
Clinical • Journal • Real-world evidence • Next-generation sequencing • Circulating tumor DNA
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NF1 (Neurofibromin 1)
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KRAS mutation • EGFR mutation • PIK3CA mutation • EGFR mutation + PIK3CA mutation
1m
Specifically, increased PD-L1 expression was associated with wildtype EGFR and vascular invasion, and total PD-L1 mRNA levels correlated weakly with protein expression on tumor cells. These data provide insights into driver gene mutations and immune checkpoint status in relation to lung cancer subtypes and suggest that RT-qPCR is useful for assessing PD-L1 levels.
Journal • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • PD-L1 (Programmed death ligand 1) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS)
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PD-L1 expression • EGFR mutation • BRAF mutation • PIK3CA mutation • EGFR mutation + PIK3CA mutation • PD-L1 mutation
2ms
Molecular profiling of liquid biopsies collected upon disease progression using NGS help to identify molecular mechanisms underlying treatment failure.
Clinical • Next-generation sequencing
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EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR3 (Fibroblast growth factor receptor 3) • HRAS (Harvey rat sarcoma viral oncogene homolog) • MAP2K1 (Mitogen-activated protein kinase kinase 1) • GNA11 (G Protein Subunit Alpha 11) • CCND2 (Cyclin D2)
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TP53 mutation • KRAS mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • EGFR T790M • EGFR mutation + PIK3CA mutation
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Oncomine™ Pan-Cancer Cell-Free Assay
2ms
Our results suggest that dd-PCR is a highly sensitive method and could be used for a routine laboratory detection of the important genomic variations to determine the targeted therapy in patients with varied advanced solid tumors.
Clinical • Liquid biopsy • Polymerase Chain Reaction
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • ER (Estrogen receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • EML4 (EMAP Like 4) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha)
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BRAF V600E • KRAS mutation • EGFR mutation • HER-2 amplification • NRAS mutation • BRAF V600 • PIK3CA mutation • EGFR L858R • EGFR T790M • KRAS G12V • ER mutation • KIT mutation • ALK fusion • ROS1 fusion • ALK mutation • PDGFRA mutation • KRAS G12 • EGFR mutation + PIK3CA mutation • ALK-ROS1 fusion
2ms
In the metastatic samples and the local relapse, we found an activating PIK3CA mutation, further copy number gains in chromosome 7 (EGFR), and a putative pathogenic driver mutation in a canonical splice site of FLNA. Our findings demonstrate tumor spread outside the CNS and identify potential genetic drivers of metastatic dissemination outside the CNS, which could be leveraged as therapeutic targets or potential biomarkers.
Clinical • Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • CDKN2A (Cyclin-dependent kinase inhibitor 2A)
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EGFR mutation • PIK3CA mutation • EGFR mutation + PIK3CA mutation
2ms
Our study did not allow the identification of any specific clinical characteristics that might explain the observed heterogeneity. Despite the overall good quality of the included studies, the applicability of these results to patients' general population with CC is still unclear.
Retrospective data • Review • Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • mTOR (Mechanistic target of rapamycin kinase)
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EGFR mutation • PIK3CA mutation • MTOR mutation • EGFR mutation + PIK3CA mutation
2ms
HPV was detected in three OSCC patients and not associated with smoking and drinking habits. NSND OSCC exhibits distinct genomic profiles and further exploration to elucidate the molecular aetiology in these patients is warranted.
Clinical • Journal • Tumor Mutational Burden • BRCA Biomarker
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • BRCA2 (Breast cancer 2, early onset) • CDKN2A (Cyclin-dependent kinase inhibitor 2A)
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TP53 mutation • TMB-H • EGFR mutation • PIK3CA mutation • EGFR amplification • CDKN2A deletion • CDKN2A mutation • BRCA2 deletion • BRCA1 deletion • EGFR mutation + PIK3CA mutation
3ms
Loss of the T790M mutation was associated with early resistance to osimertinib, and this was exacerbated by MET amplification. Further work is needed to fully understand the implications of each resistance mechanism.
Clinical • Journal • Next-generation sequencing
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • RET (Ret Proto-Oncogene)
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KRAS mutation • EGFR mutation • PIK3CA mutation • MET amplification • EGFR T790M • RET fusion • EGFR C797S • RET mutation • MET mutation • EGFR mutation + PIK3CA mutation
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Tagrisso (osimertinib)
3ms
We describe a novel method to measure TF in plasma ctDNA based on aneuploidy, which may overcome some limitations of TF measurement based on VAF. When TF confirms tumor content, sensitivity of F1LCDx for short variant detection is excellent (90%-100%), suggesting reduced value from a reflex to tissue genotyping in the absence of a targetable genomic alteration. When TF is not quantified, sensitivity can be lower and the value of reflex to tissue genotyping may be heightened.
BRCA Biomarker
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • BRCA2 (Breast cancer 2, early onset) • BRCA1 (Breast cancer 1, early onset)
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BRCA1 mutation • BRCA2 mutation • EGFR mutation • PIK3CA mutation • EGFR L858R • EGFR exon 19 deletion • MET exon 14 mutation • MET mutation • EGFR mutation + PIK3CA mutation
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FoundationOne® Liquid CDx
3ms
Our results suggest that dd-PCR is a highly sensitive method and could be used for a routine laboratory detection of the important genomic variations to determine the targeted therapy in patients with varied advanced solid tumors.
Clinical • Liquid biopsy • Polymerase Chain Reaction
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • ER (Estrogen receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • EML4 (EMAP Like 4) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha)
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BRAF V600E • KRAS mutation • EGFR mutation • HER-2 amplification • NRAS mutation • BRAF V600 • PIK3CA mutation • EGFR L858R • EGFR T790M • KRAS G12V • ER mutation • KIT mutation • ALK fusion • ROS1 fusion • ALK mutation • PDGFRA mutation • KRAS G12 • EGFR mutation + PIK3CA mutation • ALK-ROS1 fusion
3ms
The streamlined automated sample preparation workflow has several advantages, including walkaway automation, sample tracking, elimination of toxic xylene, minimal user intervention and less extraction-to-extraction variability. The MagNA Pure 24 System may provide an automated option for DNA extraction from FFPE tissue for somatic mutation testing in oncology.
EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog)
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KRAS mutation • EGFR mutation • NRAS mutation • BRAF mutation • PIK3CA mutation • EGFR mutation + PIK3CA mutation
4ms
Beyond histological classification as well as IDH1/2 mutation, 1p/19q codeletion status, we could incorporate IDH1/2mt combined with TERTpmt, EGFR mutation or amplification and PIK3CA mutation into the diagnostic criteria for DLGGs to supplement WHO 2016 pathological criteria.
Retrospective data • Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • MGMT (6-O-methylguanine-DNA methyltransferase)
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EGFR mutation • PIK3CA mutation • PIK3CA amplification • MGMT promoter methylation • EGFR mutation + PIK3CA mutation
5ms
Histologic transformation and other off-target molecular alterations are frequent early emerging resistance mechanisms to osimertinib and are associated with poor clinical outcomes.
Clinical • Journal
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EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • FGF (Fibroblast Growth Factor)
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KRAS mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • MET amplification • RET fusion • RET mutation • MET mutation • BRAF fusion • EGFR G724S • EGFR mutation + PIK3CA mutation • BRAF amplification • FGF amplification
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Tagrisso (osimertinib)
6ms
Here, we review the literature on specific gene alterations that coexist with EGFR mutations, including common alterations (intra-EGFR [on target] co-mutation, TP53, PIK3CA, and PTEN) and driver gene alterations (ALK, KRAS, ROS1, and MET). We also summarize data for other biomarkers (e.g., PD-L1 expression and BIM polymorphisms) associated with EGFR-TKI efficacy.
Clinical • Review • Journal • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • PD-L1 (Programmed death ligand 1) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS)
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PD-L1 expression • TP53 mutation • KRAS mutation • EGFR mutation • PIK3CA mutation • PTEN mutation • EGFR mutation + PIK3CA mutation
6ms
"TP53 was the most commonly comutated gene across samples. TP53 p.R337H was associated with somatic mutations in EGFR and ERBB2. Most samples had low TMB; only 5.5% of samples had high TMB."
Journal • Clinical
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • STK11 (Serine/threonine kinase 11)
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TP53 mutation • KRAS mutation • TMB-H • EGFR mutation • BRAF mutation • PIK3CA mutation • STK11 mutation • ALK rearrangement • TMB-L • EGFR mutation + PIK3CA mutation • ALK rearrangement + PIK3CA mutation
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FoundationOne® CDx
6ms
Third generation Osimertinib, targeting sensitizing EGFR mutations and the T790M resistance mutation, received FDA approval as first-line therapy following data from the Phase III FLAURA trial...The efficacy of pan-PIM inhibitor (AZD1208) & STAT3 inhibitor BBI608 alone and in combination with erlotinib were quantified using the CellTiter-Blue, cell viability assay, in all cell lines...Treatment with pan-PIM inhibitor (AZD1208) alone and in combination with erlotinib resulted in a decrease in protein kinase phosphorylation in Clone 3 including pSTAT3 (Ser727) & pSTAT3 (Tyr705). Conclusion Based on these results, co-targeting PIM and EGFR may provide a therapeutic strategy for circumventing bypass mechanisms of resistance, inhibiting tumor cell motility and migration and blocking the progression and outgrowth of drug resistant cancer cells significantly improving patient prognosis and survival when EGFR is targeted
Preclinical
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • AXL (AXL Receptor Tyrosine Kinase) • PIM1 (Pim-1 Proto-Oncogene)
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EGFR mutation • HER-2 amplification • BRAF mutation • PIK3CA mutation • MET amplification • EGFR T790M • EGFR C797S • MET mutation • MET expression • EGFR L718Q • EGFR mutation + PIK3CA mutation • BRAF amplification
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erlotinib • Tagrisso (osimertinib) • napabucasin (BBI608) • AZD1208
6ms
Median number of prior EGFR TKIs was 2 (range, 1-4); 49 patients [86%] received prior osimertinib. Efficacy was observed in patients with various mechanisms of EGFR TKI resistance, including EGFR C797S mutation, MET amplification, HER2 mutation, BRAF fusion, and PIK3CA mutation. Conclusion Patritumab deruxtecan at 5.6 mg/kg provides promising evidence of preliminary antitumor activity and safety in heavily pre-treated patients with locally advanced or metastatic EGFRm NSCLC.
Clinical
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase)
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EGFR mutation • HER-2 amplification • BRAF mutation • PIK3CA mutation • MET amplification • EGFR C797S • MET mutation • ERBB3 expression • BRAF fusion • ERBB3 mutation • EGFR mutation + PIK3CA mutation • BRAF amplification
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Tagrisso (osimertinib) • patritumab deruxtecan (U3-1402)
6ms
EGFR-TKI can be selected as one of gefitinib, erlotinib and icotinib. On the contrary, EGFR-TKIs plus pemetrexed did not improve PFS in the non-concomitant alterations cohort (median PFS: 12.2 vs. 11.1 months, p=0.988). Conclusion In sensitive EGFR-mutant NSCLC, the addition of pemetrexed to EGFR-TKIs results in significantly prolonged PFS in patients with concomitant alterations in MLH1 V384D, TP53, KRAS or PIK3CA, but not in patients without theses concomitant alterations.
EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MLH1 (MutL homolog 1)
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TP53 mutation • KRAS mutation • EGFR mutation • PIK3CA mutation • EGFR mutation + PIK3CA mutation • PIK3CA mutation + KRAS mutation
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erlotinib • gefitinib • pemetrexed • Conmana (icotinib)
6ms
Most(20/25) of them had chose chemotherapy ± bevacizumab as first line, while the rest accepted other treatment, including 1 chemotherapy combined with pembrolizumab, 3 Icotinib and 1 vandetanib. At the data cutoff of follow-up (July 31, 2020), OS events were 11 (44%), and median OS was 33.9m(3.2m-64.7m). Conclusion The most common genotype of NSCLC with BRAF mutation was V600E mutation, which was more tendency to have a concomitant mutation, the therapeutic response was well, and overall survival data had showed a promising outcomes.
Clinical • PD(L)-1 Biomarker
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EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase)
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BRAF V600E • TP53 mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • EGFR L858R • MET amplification • MET mutation • EGFR mutation + PIK3CA mutation
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Keytruda (pembrolizumab) • Avastin (bevacizumab) • Caprelsa (vandetanib) • Conmana (icotinib)
6ms
Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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EGFR mutation • PIK3CA mutation • EGFR T790M • RET fusion • EGFR mutation + PIK3CA mutation
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Gilotrif (afatinib)
6ms
EGFR-targeted therapy may be appropriate for treating many epithelial-like cSCCs without PIK3CA-activating mutations. Combined EGFR- and FGFR-targeted therapy may be used to treat cSCCs that show intrinsic or acquired resistance to EGFR inhibitors.
Journal
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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PIK3CA mutation • PIK3CA E545K • PIK3CA E545 • EGFR mutation + PIK3CA mutation
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gefitinib
7ms
The EGFR c.2573T>G;p.(Leu858Arg) mutation and PIK3CA c.3140A>G;p.(His1047Arg) mutation are associated with response to EGFR TKIs and response with PI3K/AKT/mTOR pathway inhibitors, respectively. Conclusion Interactions between PIK3CA/EGFR mutations are not yet clearly interpreted in pulmonary carcinomas and clinical outcome unknown, deserving more data for treatment definition.
Liquid biopsy
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TTF-1 (Thyroid Transcription Factor-1) • VIM (Vimentin)
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EGFR mutation • PIK3CA mutation • EGFR L858R • PIK3CA H1047R • EGFR mutation + PIK3CA mutation
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Idylla™ EGFR Mutation Test • Oncomine™ Lung cfDNA Assay
7ms
The EGFR c.2573T>G;p.(Leu858Arg) mutation and PIK3CA c.3140A>G;p.(His1047Arg) mutation are associated with response to EGFR TKIs and response with PI3K/AKT/mTOR pathway inhibitors, respectively. Conclusion Interactions between PIK3CA/EGFR mutations are not yet clearly interpreted in pulmonary carcinomas and clinical outcome unknown, deserving more data for treatment definition.
Liquid biopsy
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TTF-1 (Thyroid Transcription Factor-1) • VIM (Vimentin)
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EGFR mutation • PIK3CA mutation • EGFR L858R • PIK3CA H1047R • EGFR mutation + PIK3CA mutation
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Idylla™ EGFR Mutation Test • Oncomine™ Lung cfDNA Assay
7ms
The EGFR c.2573T>G;p.(Leu858Arg) mutation and PIK3CA c.3140A>G;p.(His1047Arg) mutation are associated with response to EGFR TKIs and response with PI3K/AKT/mTOR pathway inhibitors, respectively. Conclusion Interactions between PIK3CA/EGFR mutations are not yet clearly interpreted in pulmonary carcinomas and clinical outcome unknown, deserving more data for treatment definition.
Liquid biopsy
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TTF-1 (Thyroid Transcription Factor-1) • VIM (Vimentin)
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EGFR mutation • PIK3CA mutation • EGFR L858R • PIK3CA H1047R • EGFR mutation + PIK3CA mutation
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Idylla™ EGFR Mutation Test • Oncomine™ Lung cfDNA Assay
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