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BIOMARKER:

EGFR mutation + PIK3CA mutation

i
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:
25d
PIK3CA mutation as an acquired resistance driver to EGFR-TKIs in non-small cell lung cancer: clinical challenges and opportunities. (PubMed, Pharmacol Res)
We highlight the role of PIK3CA mutation as an acquired resistance mechanism against EGFR-TKIs in EGFR-mutant NSCLC. Crucially, we explore therapeutic strategies targeting PIK3CA-mediated resistance to EGFR TKIs in lung cancer, aiming to optimize the effectiveness of treatment.
Preclinical • Review • Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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EGFR mutation • PIK3CA mutation • EGFR mutation + PIK3CA mutation
6ms
Preceding plasma EGFR vs upfront tissue NGS for advanced NSCLC in the Chinese population: A single centre experience in Hong Kong (ESMO Asia 2023)
The liquid-first approach enhances the yield of rare mutations by tissue NGS which is resource-dependent. It benefits regions where tissue biopsy is a rate limiting factor and EGFR mutations are prevalent.
Clinical • Next-generation sequencing • Metastases
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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) • ALK (Anaplastic lymphoma kinase) • 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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TP53 mutation • BRAF mutation • PIK3CA mutation • EGFR T790M • EGFR exon 20 insertion • MET exon 14 mutation • MET mutation • EGFR exon 20 mutation • EGFR negative • EGFR mutation + PIK3CA mutation • EGFR exon 20 insertion + EGFR T790M • HER-2 exon 23 mutation
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cobas® EGFR Mutation Test v2 • Oncomine Precision Assay
6ms
Real-world performance of a comprehensive next-generation sequencing (NGS) panel for patients (pts) with solid tumors from Asia and the Middle East (AME) (ESMO Asia 2023)
In breast cancer (n=22), relevant alterations included ERBB2 amp (22%) and mutations in PIK3CA (43%), ESR1 (4.8%), ERBB2 (4.8%) and BRCA1/2 (4.8%). Conclusions This analysis of the first tumor samples tested by a new CGP panel in AME demonstrated detection of actionable alterations at the expected frequency with only 15 days median TAT.
Real-world evidence • Clinical • Tumor mutational burden • MSi-H Biomarker • BRCA Biomarker • Next-generation sequencing • Real-world
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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) • ER (Estrogen receptor) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MSI (Microsatellite instability) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • FGFR1 (Fibroblast growth factor receptor 1) • CCNE1 (Cyclin E1)
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BRAF V600E • KRAS mutation • BRCA2 mutation • BRCA1 mutation • EGFR mutation • MSI-H/dMMR • KRAS G12C • PIK3CA mutation • BRAF V600 • NTRK1 fusion • HER-2 mutation • MET exon 14 mutation • ALK fusion • KRAS G12 • EGFR mutation + PIK3CA mutation
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Guardant360 TissueNext™
6ms
Mechanisms of osimertinib resistance using circulating tumor DNA analyses for EGFR-mutated non-small cell lung cancer, results from ELUCIDATOR: A prospective observational multicenter study (ESMO Asia 2023)
Furthermore, additional EGFR resistance mutations, such as C797S, were 1 case. Expected Conclusions MET amp and PIK3CA mutation are the common resistance mechanisms of osimertinib PD, and the rate of additional EGFR resistance mutations is lower compared with prior studies.
Clinical • Observational data • Circulating tumor DNA
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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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TP53 mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • EGFR exon 19 deletion • MET amplification • EGFR C797S • MET mutation • EGFR mutation + PIK3CA mutation
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Tagrisso (osimertinib)
7ms
Molecular heterogeneity of Primary liver carcinomas: early study (ECP 2023)
HCC CK19+/CK7+ targeted therapy might benefit from a CTNNB1, TP53, ALK, EGFR, MAP2K2, RET, PTEN, and IDH2 panel, standardized for PLC spectrum. This knowledge would allow better understanding the clinical course and PLC heterogeneity, together with improving tumor classification and treatment.
EGFR (Epidermal growth factor receptor) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • FGFR4 (Fibroblast growth factor receptor 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • MAP2K2 (Mitogen-activated protein kinase kinase 2) • KRT19 (Keratin 19)
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TP53 mutation • EGFR mutation • PIK3CA mutation • KIT mutation • ALK mutation • AR mutation • PDGFRA mutation • ERBB3 mutation • EGFR mutation + PIK3CA mutation • EGFR mutation + ALK mutation
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Oncomine Precision Assay
8ms
BYL719 reverses gefitinib-resistance induced by PI3K/AKT activation in non-small cell lung cancer cells. (PubMed, BMC Cancer)
Moreover, the combined effect and mechanism of gefitinib and BYL719 were also confirmed in the NSCLC cells and patient-derived organoids under 3D culture condition, as well as in vivo. Taken together, the data indicate that PIK3CA mutation induces more aggressive growth and gefitinib resistance in NSCLC cells, and the combination treatment with gefitinib and BYL719 is a promising therapeutic approach to overcoming EGFR-TKIs resistance induced by PI3K/AKT activation.
Journal
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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EGFR mutation • PIK3CA mutation • EGFR T790M • EGFR mutation + PIK3CA mutation
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gefitinib • Piqray (alpelisib)
8ms
Clinicopathological and molecular analyses of uterine carcinosarcomas using next-generation sequencing: A single-center experience. (PubMed, Indian J Pathol Microbiol)
Although no statistical significance was found between the detected mutation and clinicopathological data, it was concluded that PDGFRA mutation might be associated with advanced-stage disease development. This study's findings regarding different molecular types of UCS and information on oncogenesis of UCS can provide inferences for targeted therapies in the future by identifying targetable mutations representing early oncogenic events and thereby contribute toward further studies on this subject.
Journal • Next-generation sequencing
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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) • ER (Estrogen receptor) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha)
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KRAS mutation • EGFR mutation • BRAF mutation • NRAS mutation • PIK3CA mutation • KIT mutation • PDGFRA mutation • EGFR mutation + PIK3CA mutation • PIK3CA mutation + KRAS mutation
8ms
Impact of co-mutations on the prognosis of targeted therapy in EGFR-mutant advanced NSCLC: A result of real-world study (ESMO 2023)
Multifactorial analysis showed that TP53 mutation (HR 2.198, 95% CI 1.006-4.803; P = 0.048) and RB1 mutation (HR 8.798, 95% CI 1.604-48.269; P = 0.012) were independent risk factors for PFS with first-line targeted therapy. Conclusions This research added to the evidence that co-alterations such as TP53, MET, and RB1 are prospective prognostic biomarkers in NSCLC patients treated with EGFR-TKI.
Clinical • Real-world evidence • Real-world • Metastases
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • DNMT3A (DNA methyltransferase 1) • RB1 (RB Transcriptional Corepressor 1)
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TP53 mutation • KRAS mutation • EGFR mutation • PIK3CA mutation • EGFR amplification • PIK3CA H1047R • KRAS G12V • DNMT3A mutation • PIK3CA E545K • RB1 mutation • KRAS G12 • KRAS G12S • EGFR mutation + PIK3CA mutation • PIK3CA E545
8ms
Impact of Co-mutations on the Prognosis of Targeted Therapy in EGFR-Mutant Advanced NSCLC: a Result of Real-World Study (IASLC-WCLC 2023)
This research added to the evidence that co-alterations such as TP53, MET, and RB1 are prospective prognostic biomarkers in NSCLC patients treated with EGFR-TKI.
Clinical • Real-world evidence • Real-world • Metastases
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • DNMT3A (DNA methyltransferase 1) • RB1 (RB Transcriptional Corepressor 1)
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TP53 mutation • KRAS mutation • EGFR mutation • PIK3CA mutation • EGFR amplification • PIK3CA H1047R • KRAS G12V • DNMT3A mutation • PIK3CA E545K • RB1 mutation • KRAS G12 • KRAS G12S • EGFR mutation + PIK3CA mutation • PIK3CA E545
8ms
Study on the Molecular Markers of Resistance in the First-line Treatment of NSCLC with EGFR Positive by Aumolertinib (IASLC-WCLC 2023)
Based on NGS and PD-L1 IHC, gene mutation, TMB and PD-L1 expression are analyzed. Cox single factor and PFS are used to verify that these molecular markers are independent of TMB and PD-L1 for targeted therapy of lung cancer.
Clinical • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • PTEN (Phosphatase and tensin homolog) • FGFR1 (Fibroblast growth factor receptor 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A)
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PD-L1 expression • EGFR mutation • BRAF mutation • PIK3CA mutation • MET amplification • EGFR T790M • PTEN mutation • FGFR1 amplification • CDKN2A mutation • PIK3CA amplification • EGFR positive • EGFR mutation + PIK3CA mutation • PIK3CA mutation + PTEN mutation • EGFR mutation + PTEN mutation • BRAF amplification
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Ameile (aumolertinib)
8ms
The Histologic and Molecular Spectrum of Highly Differentiated HPV-independent Cervical Intraepithelial Neoplasia. (PubMed, Am J Surg Pathol)
In conclusion, highly differentiated cervical HPV-negative precursors are characteristic intraepithelial squamous lesions with somatic mutations that resemble those described in vulvar HPV-independent carcinogenesis. For optimal reproducibility, we propose a simplistic classification of these HPV-negative cervical precursors in TP53-mutated d-CIN and p53 wild-type verruciform intraepithelial neoplasia.
Journal
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • SMARCB1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily B, Member 1)
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TP53 mutation • EGFR mutation • PIK3CA mutation • TP53 wild-type • CDKN2A negative • EGFR mutation + PIK3CA mutation • SMARCB1 mutation • TP53 overexpression
10ms
FOLFOXIRI With or Without Panitumumab in Metastatic Colorectal Cancer (VOLFI) (clinicaltrials.gov)
P2, N=93, Completed, AIO-Studien-gGmbH | Active, not recruiting --> Completed
Trial completion • Metastases
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • ERCC1 (Excision repair cross-complementation group 1) • RAS (Rat Sarcoma Virus) • MTHFR (Methylenetetrahydrofolate Reductase)
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EGFR mutation • PIK3CA mutation • KRAS wild-type • RAS wild-type • EGFR exon 18 mutation • KRAS exon 2 mutation • EGFR mutation + PIK3CA mutation • KRAS exon 2 wild-type • KRAS exon 3 mutation • KRAS exon 4 mutation
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5-fluorouracil • Vectibix (panitumumab) • oxaliplatin • irinotecan • leucovorin calcium
11ms
Amivantamab and lazertinib in treatment-naïve EGFR-mutated advanced non–small-cell lung cancer (NSCLC): Long-term follow-up and ctDNA results from CHRYSALIS. (ASCO 2023)
Sponsored by Pharmaceutical/Biotech Company, Janssen R&D, LLC. At a median duration of treatment of 33.5 months, median DOR, PFS, and OS have not been reached in treatment-naïve pts receiving ami+laz, with 50% remaining progression-free and on treatment. No new safety signals were identified. The ongoing phase 3 MARIPOSA study (NCT04487080) is further investigating ami+laz vs osimertinib vs laz in previously untreated, EGFR-mutated, advanced NSCLC.
Circulating tumor DNA • Metastases
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CCNE1 (Cyclin E1)
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EGFR mutation • HER-2 amplification • PIK3CA mutation • EGFR L858R • EGFR exon 19 deletion • EGFR amplification • CCNE1 amplification • EGFR mutation + PIK3CA mutation
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Tagrisso (osimertinib) • Rybrevant (amivantamab-vmjw) • Leclaza (lazertinib)
11ms
Clinical and genomic landscape of EGFR-mutant lung cancers (LCs) with squamous and adenosquamous differentiation. (ASCO 2023)
Pts with EGFR+ sq/adenosq LCs exhibit inferior TTD and OS with 1L osimertinib compared to adenocarcinoma controls. Sq/adenosq LCs appear to be molecularly distinct with enrichment in EGFR L858R and atypical EGFR mutations. Transcriptomic profiling of a subset of samples will be presented.
Clinical
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • RB1 (RB Transcriptional Corepressor 1)
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EGFR mutation • PIK3CA mutation • EGFR L858R • EGFR mutation + PIK3CA mutation
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MSK-IMPACT
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Tagrisso (osimertinib)
11ms
Association of CDK4 amplification with duration of response to bevacizumab in glioblastoma. (ASCO 2023)
Using a large clinical genomic database with GBM subjected to comprehensive molecular profiling, we demonstrated that amplification of CDK4 and EGFR were associated with long-term and short-term responses to bevacizumab, respectively. This warrants further investigation in independent cohorts controlled for age and other prognostic factors. If confirmed, a genetic basis for treatment optimization may provide meaningful clinical outcomes.
EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDK4 (Cyclin-dependent kinase 4) • RAF1 (Raf-1 Proto-Oncogene Serine/Threonine Kinase)
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EGFR mutation • PIK3CA mutation • EGFR amplification • CDK4 amplification • EGFR mutation + PIK3CA mutation
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MI Tumor Seek™
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Avastin (bevacizumab)
11ms
ctDNA detection in patients with brain metastases arising from solid tumors. (ASCO 2023)
This study illustrates the feasibility of detecting actionable mutations from ctDNA among pts with BrMs, with and without extracranial disease. A higher frequency of actionable mutations in several targetable genes was observed in ctDNA when comparing pts with and without BrMs, thus providing therapeutic opportunities. Additional studies comparing ctDNA and alterations in BrMs tissue are needed to determine if ctDNA can be considered a surrogate to support treatment decisions.
Clinical • BRCA Biomarker • Circulating tumor DNA
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • ER (Estrogen receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA2 (Breast cancer 2, early onset)
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KRAS mutation • BRCA2 mutation • EGFR mutation • PIK3CA mutation • ER mutation • ESR1 mutation • EGFR mutation + PIK3CA mutation
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Guardant360® CDx
1year
Alterations in PIK3CA/PTEN as resistance mechanisms in lung cancer patients progressing on first-line next generation EGFR/ALK tyrosine kinase inhibitors (AACR 2023)
We identified pts with EGFR mutations or ALK rearrangements who developed PIK3CA/PTEN alterations in tissue biopsy and/or circulating tumor DNA upon progression to first-line osimertinib/alectinib. Activating PI3KCA mutations and molecular events leading to PTEN loss are frequent events at resistance to first-line EGFR/ALK TKIs, and can be detected concomitantly. Functional assays confirmed that these alterations act as resistance mechanisms. These observations are of interest as PI3KCA/mTOR inhibitors may have a role in overcoming resistance.
Clinical
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EGFR (Epidermal growth factor receptor) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog)
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EGFR mutation • PIK3CA mutation • ALK rearrangement • PIK3CA E545K • ALK fusion • EGFR mutation + PIK3CA mutation • PIK3CA E545 • PIK3CA mutation + PTEN mutation • EGFR mutation + PTEN mutation • PIK3CA N345K • ALK rearrangement + PIK3CA mutation
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Tagrisso (osimertinib) • Alecensa (alectinib)
1year
Preclinical evaluation of avutometinib (VS-6766; RAF/MEK clamp) in combination with EGFR inhibition in colorectal cancer patient-derived xenograft (PDX) models harboring KRAS mutations (AACR 2023)
Mice bearing PDX tumors were randomized into groups of 6 mice treated with avuto alone or in combination with panitumumab for 21 days with tumor volume measured twice weekly.Results In 3D proliferation assays with a panel of KRAS mt CRC cell lines (including G12D, G12V and G13D mutations), the EGFR/ErbB family inhibitor afatinib showed the strongest synergy score with avuto relative to inhibitors of SHP2, ERK1/2, mTOR or CDK4/6. The combination of avuto and panitumumab showed significant anti-tumor activity in a CRC PDX model harboring KRASG12V with less tumor regression observed in a KRASG12D PDX model or in a KRASG12V PDX model with concurrent PIK3CA mutation. These results support the ongoing clinical evaluation of avutometinib in combination with the anti-EGFR antibody cetuximab for treatment of KRAS mt CRC (NCT05200442).
Preclinical • Combination therapy
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KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CDK4 (Cyclin-dependent kinase 4)
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KRAS mutation • PIK3CA mutation • KRAS G12D • KRAS G12V • KRAS G12 • KRAS G13 • EGFR mutation + PIK3CA mutation
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Erbitux (cetuximab) • Gilotrif (afatinib) • Vectibix (panitumumab) • avutometinib (VS-6766)
1year
Metastatic models of resistance to next generation tyrosine kinase inhibitors (TKIs) in HER2-positive breast cancer (BC) (AACR 2023)
Dual GFP-Luc tagged HER2+ BT474 naïve parental cells and their acquired lapatinib (LapR), neratinib (NeraR), and tucatinib (TucaR) resistant (Res) derivatives harboring acquired HER2 L755S, HER2 L755S and a pathogenic PIK3CA mutation, or EGFR amplification, respectively were used. Additional studies to investigate the organ-specific metastatic tropism of each acquired resistant model are currently ongoing. Molecular and functional characterization of our established metastatic cultures will guide future in vivo studies, including testing the efficacy of new targeted treatment regimens to treat organ-specific metastasis, and expanding such studies to additional relevant cell and patient-derived xenograft/organoid models.
Metastases
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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HER-2 positive • EGFR mutation • HER-2 amplification • PIK3CA mutation • EGFR amplification • HER-2 L755S • EGFR mutation + PIK3CA mutation
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lapatinib • Nerlynx (neratinib) • Tukysa (tucatinib)
1year
Clinical and genomic features in patients with second primary glioblastoma following first primary renal cell carcinoma. (PubMed, BMC Cancer)
This is the first study to investigate the pathogenesis and clinical features of spGBM following spRCC. We found that spGBMs are old-age related, highly malignant, and have short survival time. Moreover, they might be misdiagnosed and treated as brain metastases from RCC. Thus, the incidence of spGBMs after fpRCC is underestimated. Further studies are needed to investigate the underlying molecular mechanisms and clinical biomarkers for the development of spGBM following fpRCC.
Journal • Tumor mutational burden
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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)
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TP53 mutation • EGFR mutation • PIK3CA mutation • TMB-L • EGFR mutation + PIK3CA mutation
over1year
UNcommon EGFR mutations: International Case series on efficacy of osimertinib in Real-life practice in first liNe setting (UNICORN). (PubMed, J Thorac Oncol)
Osimertinib demonstrated activity in ucEGFRmut with high rate of disease control systemically and intracranially. Several resistance mechanisms were identified. This report comprises, to the best of our knowledge, the largest dataset of its kind.
Journal
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EGFR (Epidermal growth factor receptor) • 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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TP53 mutation • EGFR mutation • PIK3CA mutation • MET amplification • EGFR T790M • EGFR exon 20 insertion • EGFR L861Q • EGFR C797S • EGFR G719X • MET mutation • EGFR exon 20 mutation • EGFR mutation + PIK3CA mutation • EGFR E709K
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Tagrisso (osimertinib)
over1year
A Tale of Concurrent Gene Mutations in EGFR and TP53 through a Next-Generation Sequencing Approach (AMP 2022)
In the present study, exon 5 was the most common mutation site of TP53. EGFR resistance mutation T790M was found to be predominantly associated with TP53 exon 8 mutations. This group of patients who were treated with third-generation TKI, osimertinib, had progressive disease and/or succumbed.
Next-generation sequencing
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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TP53 mutation • EGFR mutation • PIK3CA mutation • EGFR L858R • EGFR exon 19 deletion • EGFR T790M • EGFR exon 20 insertion • EGFR exon 20 mutation • EGFR mutation + PIK3CA mutation • TP53 exon 5 mutation
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Tagrisso (osimertinib)
over1year
Post-Therapy Samples Collected through Rapid Tissue Donation Confirms the Necessity of Tissue-Based NextGeneration Sequencing in Identifying Driver Mutations (AMP 2022)
These patients received various therapies including pembrolizumab, nivolumab, capmatinib, bevacizumab, osimertinib, brigatinib, erlotinib, and alectinib, as well as sotorasib. Collection and sequencing of RTD samples provides an opportunity to detect resistance mutations and to understand more about post-treatment disease progression and tumor heterogeneity. The identification of drivers by comprehensive NGS tissue testing in two cases serves as a reminder about the value of such testing when no drivers are identified by small panels or blood-based NGS testing.
Next-generation sequencing • PD(L)-1 Biomarker
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • EML4 (EMAP Like 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • AGK (Acylglycerol Kinase)
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KRAS mutation • EGFR mutation • KRAS G12C • BRAF mutation • PIK3CA mutation • EGFR exon 20 insertion • KRAS G12V • MET exon 14 mutation • EML4-ALK fusion • ALK fusion • MET mutation • KRAS G12 • NRAS Q61 • BRAF fusion • EGFR exon 20 mutation • AGK-BRAF fusion • NRAS Q61L • EGFR mutation + PIK3CA mutation • KRAS Q61L
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Keytruda (pembrolizumab) • Opdivo (nivolumab) • Avastin (bevacizumab) • Tagrisso (osimertinib) • erlotinib • Alecensa (alectinib) • Lumakras (sotorasib) • Alunbrig (brigatinib) • Tabrecta (capmatinib)
over1year
PIK3CA mutations associated with a poor postoperative prognosis in patients with pulmonary pleomorphic carcinoma: a retrospective cohort study. (PubMed, BMC Cancer)
The postoperative prognosis of PPC with PIK3CA pathogenic mutations is particularly poor. Pathogenic mutations of PIK3CA may be a postoperative prognostic marker. Inhibition of signaling pathways associated with PIK3CA mutations may also be a target for chemotherapy after relapse of PPC.
Retrospective data • Journal • IO biomarker
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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TP53 mutation • EGFR mutation • PIK3CA mutation • EGFR mutation + PIK3CA mutation
over1year
Real-world data of EGFR mutation testing in Chinese non-small cell carcinoma: Low tumor cell number and tumor cellularity can be accepted. (PubMed, Pathol Res Pract)
In clinical practice, specimen with low adequacy could attempt in gene mutation testing, including biopsy and surgical specimen. However, the amount of tumor for molecular testing should be reported and suboptimal samples with a negative EGFR mutation result should be considered for combination using of other mutation test method or repeat testing of an alternate tumor sample, especially for the surgical samples.
Retrospective data • Journal • Real-world evidence
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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) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NRAS (Neuroblastoma RAS viral oncogene homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS)
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KRAS mutation • EGFR mutation • BRAF mutation • NRAS mutation • PIK3CA mutation • EGFR negative • EGFR mutation + PIK3CA mutation
over1year
The genetic profile of primary and recurrent gliomas: A mono-institutional experience using next-generation sequencing (ESMO 2022)
High TMB in second samples is consistent with reports of treatment-induced hypermutagenesis. We showed that NGS should be performed both at diagnosis and at relapse.
Clinical • Tumor mutational burden • BRCA Biomarker • Next-generation sequencing
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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) • TMB (Tumor Mutational Burden) • BRCA2 (Breast cancer 2, early onset) • PTEN (Phosphatase and tensin homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • NF1 (Neurofibromin 1) • TERT (Telomerase Reverse Transcriptase) • MTAP (Methylthioadenosine Phosphorylase) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
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TP53 mutation • BRAF V600E • BRCA2 mutation • EGFR mutation • TMB-H • PIK3CA mutation • BRAF V600 • CDKN2A mutation • TERT mutation • EGFR mutation + PIK3CA mutation • IDH wild-type
|
FoundationOne® CDx
almost2years
Genomic Landscape of Liquid Biopsy in Advanced Lung Cancer Patients, an Indian Experience (IASLC-WCLC 2022)
A high positivity rate of detection of actionable and prognostic genomic alterations in the liquid biopsy has established the importance of blood as an important resource of detecting mutations in advanced NSCLC which directly impacts the clinical outcome in these patients. Furthermore, presence of co-positivity of mutations highlights the biologic mechanisms responsible for drug resistance in NSCLC patients.
Clinical • Liquid biopsy
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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) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • MAP2K1 (Mitogen-activated protein kinase kinase 1)
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TP53 mutation • BRAF V600E • KRAS mutation • EGFR mutation • NRAS mutation • PIK3CA mutation • BRAF V600 • EGFR L858R • EGFR T790M • ALK rearrangement • MET exon 14 mutation • ROS1 rearrangement • EGFR positive • EGFR mutation + PIK3CA mutation • ALK rearrangement + PIK3CA mutation
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Oncomine Lung Cell-Free Total Nucleic Acid Research Assay
almost2years
An Exploratory Study on Biomarkers Related to Primary Resistance Of EGFR-TKIs Therapy in Lung Cancer (IASLC-WCLC 2022)
1. Some mutations affecting the function of tumor cells and the activation of special signaling pathways may be related to the primary resistance of EGFR-TKIs. 2.
Tumor Mutational Burden • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • PTEN (Phosphatase and tensin homolog) • CDK6 (Cyclin-dependent kinase 6)
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KRAS mutation • EGFR mutation • PD-L1 overexpression • PIK3CA mutation • MET amplification • EGFR T790M • PTEN deletion • EGFR expression • PTEN mutation • MET mutation • EGFR mutation + PIK3CA mutation • PIK3CA mutation + PTEN mutation • EGFR mutation + PTEN mutation • KRAS deletion
almost2years
Acquired EGFR-resistant mutations in non–small cell lung cancer (NSCLC). (ASCO 2022)
Acquired resistance in EGFR mutant NSCLC is very heterogeneous and their frequency is still low most likely due to lack of enough sequencing of EGFR resistant tumors. While T790M and C797S mutations are well described, this report also notes a significant number of L718V mutations, primarily in osimertinib-treated pts with an original L858R. These data support the NGS evaluation of patients with resistant EGFR mutant lung cancers.
PD(L)-1 Biomarker • MSi-H 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) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • MSI (Microsatellite instability) • SMAD4 (SMAD family member 4) • CTNNB1 (Catenin (cadherin-associated protein), beta 1)
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PD-L1 expression • TP53 mutation • EGFR mutation • TMB-H • MSI-H/dMMR • HER-2 amplification • PIK3CA mutation • EGFR L858R • MET amplification • EGFR T790M • EGFR C797S • EGFR T790M + EGFR C797S • EGFR mutation + PIK3CA mutation • HER-2 amplification + PD-L1 expression
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PD-L1 IHC 22C3 pharmDx
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Tagrisso (osimertinib)
almost2years
Identification of pretreatment genomic biomarkers and mechanisms of acquired resistance to first-line osimertinib in advanced EGFR-mutant lung cancers. (ASCO 2022)
Pts with an identified mechanism of resistance did not have improved post-progression survival (12 mo HR 1.6, p = 0.09), but receiving next line of therapy based on post-progression tumor biopsy results (including platinum-etoposide for transformation) did improve post-progression survival (12 mo HR 0.4, p = 0.01). Pts with atypical EGFR drivers or concurrent TP53+/-RB1 alterations have significantly shorter rwPFS on first line osimertinib, highlighting need for additional interventions for these patients. Given the high frequency of transformation and improvement in post-progression survival by tailoring next line of therapy to the identified mechanism, pts with EGFR-mutant lung cancer on first line osimertinib may benefit from tissue biopsies at progression. For pts without an identified resistance mechanism by NGS, additional methods of interrogating tumors at progression are needed.
Preclinical • Clinical
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • RB1 (RB Transcriptional Corepressor 1) • CCND1 (Cyclin D1) • CDK4 (Cyclin-dependent kinase 4)
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KRAS mutation • EGFR mutation • HER-2 amplification • PIK3CA mutation • EGFR L858R • EGFR exon 19 deletion • MET amplification • EGFR amplification • EGFR C797S • KRAS G12A • KRAS G12 • EGFR mutation + PIK3CA mutation • EGFR G724S
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MSK-IMPACT
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Tagrisso (osimertinib) • etoposide IV
2years
Integrative molecular analysis of combined small-cell lung carcinoma reveals EGFR and KRAS mutational analysis as the theragnostic tools in whole small cells lung carcinoma landscape (ENETS 2022)
These data support the extension of routine EGFR, KRAS and PIK3CA mutational analysis to C-SCLC and their subclassification into neuroendocrine vs. non-neuroendocrine for inclusion in proper clinical trials.
EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • RB1 (RB Transcriptional Corepressor 1)
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TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12C • PIK3CA mutation • PTEN mutation • KRAS G12 • EGFR mutation + KRAS mutation • EGFR mutation + PIK3CA mutation • PIK3CA mutation + KRAS mutation
2years
Landscape of concomitant driver mutations in EGFR-mutated NSCLCs (AACR 2022)
In our large cohort study, we present the landscape of EGFR+ dual drivers and their associated clinical and genomic features and survival outcomes, which could aid in therapeutic decisions and facilitate the development of combination therapies.
Tumor Mutational Burden
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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) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • RB1 (RB Transcriptional Corepressor 1) • TSC2 (TSC complex subunit 2) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • ARID2 (AT-Rich Interaction Domain 2)
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KRAS mutation • EGFR mutation • KRAS G12C • BRAF mutation • HER-2 amplification • PIK3CA mutation • MET amplification • MET exon 14 mutation • ROS1 fusion • KRAS G12A • MET mutation • PIK3CA amplification • HER-2 S310F • KRAS G12 • KRAS G12S • KRAS G13 • EGFR mutation + PIK3CA mutation • HER-2 exon 20 mutation • KRAS A146T • KRAS A146V • HER-2 exon 23 mutation
2years
PIK3CA and PTEN mutations as drivers of osimertinib resistance in patients with NSCLC (AACR 2022)
Importantly, our in vitro experiments from multiple cell line models indicated that PIK3CA-mediated resistance to osimertinib could be partially reversed by co-treatment with AKT (capivasertib, AstraZeneca) and PI3K alpha (alpelisib, Novartis) inhibitors; PTEN-mediated resistance could be rescued by co-treatment with capivasertib and PI3K beta (AZD8186, AstraZeneca) inhibitors. Our in vivo analysis show that PIK3CA GOF CRISPR engineered cells displayed diminished response to osimertinib when implanted in mice; importantly, combination with AKT (capivasertib) or PI3K alpha (alpelisib) inhibitors enhanced response on treatment and delayed outgrowth after withdrawal treatment. In addition, we observed that combination treatment with capivasertib induced tumour stasis in a PIK3CA-E454K and two PTENloss PDX models.Altogether our in vitro and in vivo data provide evidence of PIK3CA mutants and PTEN loss-driven mechanisms of resistance to osimertinib and offer possible therapeutic combination strategies for those patients that develop resistance or experience a sub-optimal response to osimertinib through PIK3CA/PTEN mutations
Clinical
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EGFR (Epidermal growth factor receptor) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • PIK3CB (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta)
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EGFR mutation • PIK3CA mutation • PIK3CA H1047R • PTEN mutation • EGFR mutation + PIK3CA mutation • PIK3CA mutation + PTEN mutation • EGFR mutation + PTEN mutation • PIK3CA E453K
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Tagrisso (osimertinib) • Piqray (alpelisib) • Truqap (capivasertib) • AZD8186
2years
De novo molecular mechanisms of resistance to mobocertinib (AACR 2022)
These data suggest that intrinsic genetic alterations, present at baseline in patients with NSCLC harboring an EGFR exon 20 insertion mutation, might impact the response to mobocertinib treatment. The presence of PIK3CA mutations, EGFR gene amplification, or cell cycle regulator MYC-CDK4-CCND1 amplification is associated with lack of response to mobocertinib, which might guide rational combinations for future clinical investigation.
Tumor Mutational Burden
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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) • GNAQ (G Protein Subunit Alpha Q) • CCND1 (Cyclin D1) • PTCH1 (Patched 1) • MSH6 (MutS homolog 6) • CDK4 (Cyclin-dependent kinase 4) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • HNF1A (HNF1 Homeobox A)
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TP53 mutation • EGFR mutation • PIK3CA mutation • EGFR amplification • EGFR exon 20 insertion • CCND1 amplification • CDK4 amplification • PTCH1 mutation • EGFR exon 20 mutation • EGFR mutation + PIK3CA mutation • MLL3 mutation
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Exkivity (mobocertinib)
2years
Molecular characteristics of HRAS mutated non-small cell lung cancer (NSCLC) (AACR 2022)
HRAS has been indirectly targeted with tipifarnib, a farnesyltransferase inhibitor rendering HRAS inactive in head and neck tumors... HRAS mutations are detectable but uncommon events in NSCLC and significantly enriched in squamous histology. HRAS mutations often occur with PIK3CA co-mutations and trended towards higher activation of MAPK pathway and MSI-H frequency. This warrants further investigation on possible clinical applications of HRAS pathway inhibitors and utility of immune checkpoint inhibitors for this subset of NSCLC.
Tumor mutational burden • PD(L)-1 Biomarker • MSi-H Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • HRAS (Harvey rat sarcoma viral oncogene homolog)
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PD-L1 expression • KRAS mutation • EGFR mutation • TMB-H • MSI-H/dMMR • PIK3CA mutation • HRAS mutation • NRAS G12 • EGFR mutation + PIK3CA mutation • KRAS Q61
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MI Tumor Seek™
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Zarnestra (tipifarnib)
2years
A streamlined workflow for liquid biopsy extraction and highplex digital PCR analysis using the Maxwell® RSC system and 6-color Crystal Digital PCR™ (AACR 2022)
Furthermore, following the same extraction and sample testing workflow, we simultaneously detected a set of PIK3CA mutations and HER2 amplification from cfDNA samples. This proof-of-concept workflow creates the foundation for further development of streamlined sample-to-answer protocols that will better assist cancer researchers across the biomarker testing landscape.
Liquid biopsy
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha)
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EGFR mutation • HER-2 amplification • PIK3CA mutation • EGFR exon 18 mutation • EGFR mutation + PIK3CA mutation
2years
Morphological and Molecular Characteristics in Low Grade Fetal Adenocarcinoma of the Lung: Two Case Reports and Literature Review. (PubMed, Int J Surg Pathol)
This rare tumor has unique clinicopathological characteristics with specific genetic aberrations involving the Wnt pathway. These results provide a molecular basis for development of new therapies to treat these tumors.
Review • Journal
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • DICER1 (Dicer 1 Ribonuclease III)
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KRAS mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • CTNNB1 mutation • EGFR mutation + PIK3CA mutation
2years
Use of Circulating Tumour DNA (ctDNA) for Measurement of Therapy Predictive Biomarkers in Patients with Cancer. (PubMed, J Pers Med)
Despite this limitation, blood-based predictive biomarkers, such as mutant EGFR for predicting response to EGFR tyrosine kinase inhibitors in advanced non-small-cell lung cancer and mutant PIK3CA for predicting response to alpelisib in combination with fulvestrant in advanced breast cancer, may be used when tissue is unavailable. Although tissue remains the gold standard for detecting predictive biomarkers, it is likely that several further blood-based assays will soon be validated and used when tissue is unavailable or unsuitable for analysis.
Review • Journal • IO biomarker • Circulating tumor DNA
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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 mutation + PIK3CA mutation
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Piqray (alpelisib) • fulvestrant
2years
INTEGRATIVE MOLECULAR ANALYSIS OF COMBINED SMALL-CELL LUNG CANCER IDENTIFIES TWO MAJOR SUBGROUPS WITH DIFFERENT THERAPEUTICAL PERSPECTIVES (AIOM 2021)
These data support the extension of routine EGFR, KRAS and PIK3CA mutational analysis to C-SCLC and their subclassification into neuroendocrine vs. non-neuroendocrine for inclusion in proper clinical trials.
EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • RB1 (RB Transcriptional Corepressor 1)
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TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12C • PIK3CA mutation • PTEN mutation • KRAS G12 • EGFR mutation + PIK3CA mutation • PIK3CA mutation + KRAS mutation
over2years
Clinical • Enrollment change
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog)
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EGFR mutation • HER-2 overexpression • PIK3CA mutation • EGFR mutation + PIK3CA mutation
over2years
[VIRTUAL] Landscape of Tumor Genetic Testing and Targeted Therapies in a Large Real-World Population (AMP 2021)
In advanced breast cancer, 28% with PIK3CA mutations received Alpelisib. Erdafitinib was used in 60% of bladder cancer patients with FGFR3 mutation. All patients with NTRK3 fusion received Larotrectinib...Off-label use of targeted therapy was uncommon, occurring in <1% of patients; examples include Binimetinib+Encorafinib for BRAF V600E (lung), Vendatinib for RET M918T (lung), Afatinib and Neratinib for ERBB2 S310F (lung and breast), and Olaparib for BRCA1 mutated colorectal cancer... We demonstrate that automated data mining can provide insights into the genomic and therapeutic landscape of a real-world patient population. Across all tumor types, most patients are being given appropriate targeted therapies as per guidelines or, more rarely, offlabel. Early-stage patients were less likely to have been treated with targeted therapies, and genetic testing results may become actionable as their disease progresses and new drugs are approved.
Clinical • Real-world evidence • BRCA Biomarker • PARP Biomarker
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • FGFR3 (Fibroblast growth factor receptor 3) • PALB2 (Partner and localizer of BRCA2) • CDK12 (Cyclin dependent kinase 12)
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BRAF V600E • BRCA1 mutation • EGFR mutation • PIK3CA mutation • BRAF V600 • NTRK3 fusion • EGFR exon 19 deletion • RET fusion • ATM mutation • MET exon 14 mutation • PALB2 mutation • FGFR3 mutation • ROS1 fusion • CDK12 mutation • RET M918T • HER-2 S310F • FGFR3 fusion • EGFR mutation + PIK3CA mutation • BRAF amplification
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Lynparza (olaparib) • Gilotrif (afatinib) • Vitrakvi (larotrectinib) • Nerlynx (neratinib) • Piqray (alpelisib) • Balversa (erdafitinib) • Mektovi (binimetinib)