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BIOMARKER:

KRAS mutation + EGFR amplification

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Other names: KRAS, KRAS1, KRAS2, Kirsten rat sarcoma viral oncogene homolog, EGFR, ERBB, ERBB1, Epidermal growth factor receptor
Entrez ID:
2years
Circulating tumor DNA profiling and serial analysis in salivary gland carcinomas reveal unique mutational subsets and actionable alterations. (ASCO 2022)
Blood-based liquid biopsy can be applied in salivary gland tumors to detect genomic alterations in ctDNA which may provide opportunities for therapeutic intervention in a cancer with limited treatment options. Additionally, ctDNA testing may be used to identify resistant alterations to potential therapy. Finally, longitudinal assessment of ctDNA may shed light on tumor evolution and additional therapeutic targets may be found.
MSi-H Biomarker • Circulating tumor DNA
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MSI (Microsatellite instability) • HRAS (Harvey rat sarcoma viral oncogene homolog)
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TP53 mutation • KRAS mutation • EGFR mutation • MSI-H/dMMR • BRAF mutation • EGFR amplification • KRAS mutation + EGFR amplification
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Guardant360® CDx
almost4years
Acquired resistance to osimertinib in patients with non-small-cell lung cancer: mechanisms and clinical outcomes. (PubMed, J Cancer Res Clin Oncol)
The study revealed heterogeneous mechanisms of resistance to osimertinib in advanced NSCLC patients and their association with clinical outcomes. Patients who maintained T790M mutation or with EGFR-dependent resistance mechanism had longer clinical outcome benefits.
Clinical • Clinical data • Retrospective data • Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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TP53 mutation • KRAS mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • MET amplification • EGFR T790M • EGFR amplification • EGFR C797S • PIK3CA amplification • EGFR mutation + KRAS mutation • EGFR G724S • BRAF mutation + MET amplification • EGFR T790M + KRAS mutation • EGFR mutation + EGFR T790M • EGFR C796S • EGFR C797S + EGFR C796S • EGFR E758D • EGFR G796S • EGFR V802I • EGFR V834L • EGFR mutation + EGFR T790M + EGFR C797S • KRAS mutation + EGFR amplification
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Tagrisso (osimertinib)
4years
[VIRTUAL] Molecular characterization and prognostic analysis of non-small cell lung cancer: A single centric real-world study. (ASCO 2020)
Only one patient of this group received immunotherapy with pembrolizumab and achieved SD at the 2nd month... More than half of NSCLC patients have targetable genetic variants and more than 30% patients have a molecular signature that can be treated with immunotherapy. Compared with immunotherapy, targeted therapy has higher acceptability in real-world. NGS-based genetic testing may have clinical value to predict the effectiveness of targeted therapy and immunotherapy.
Clinical • Real-World Evidence • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • mTOR (Mechanistic target of rapamycin kinase)
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BRAF V600E • KRAS mutation • EGFR mutation • TMB-H • BRAF V600 • EGFR amplification • ALK rearrangement • TMB-L • ROS1 rearrangement • MTOR mutation • KRAS mutation + EGFR amplification
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Keytruda (pembrolizumab)
4years
[VIRTUAL] Clinical and patho-genomic characteristics of concomitant mutated status of TP53, EGFR, KRAS genes in Chinese patients with resected lung adenocarcinoma. (ASCO 2020)
TP53,EGFR and KRAS mutations and their concomitant mutation status displayed diverse correlation with spatial, clinical and genomic characteristics in resectable LUAD patients. This correlation may indicate complex biological heterogeneity of LUAD which may need further exploration. Research Funding: None
Clinical • Tumor Mutational Burden
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden)
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TP53 mutation • KRAS mutation • EGFR mutation • EGFR amplification • KRAS G13 • KRAS mutation + EGFR amplification