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BIOMARKER:

ERBB4 mutation

i
Other names: ERBB4, ALS19, V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 4
Entrez ID:
Related biomarkers:
6ms
Pre-Transplant Somatic Co-Occurring Mutations (by next generation sequencing) in Acute Myeloid Leukemia: Frequency and Impact on Clinical Outcomes after Allogeneic Hematopoietic Cell Transplantation - a Large Study on Behalf of the EBMT Acute Leukemia Working Party (ASH 2023)
NGS at diagnosis can be extremely useful in risk stratification of AML patients undergoing allo-HSCT, potentially allowing adequate post-transplant interventions. Notably, the 2-year LFS of 70% for patients harboring RUNX1 and/or ASXL1 and/or SRSF2 mutation indicates that allo-HSCT can overcome the adverse risk associated with these somatic mutations at diagnosis.
Clinical • Clinical data • Next-generation sequencing • Pre-transplantation
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • PTPN11 (Protein Tyrosine Phosphatase Non-Receptor Type 11) • SRSF2 (Serine and arginine rich splicing factor 2) • WT1 (WT1 Transcription Factor) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • STAG2 (Stromal Antigen 2) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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TP53 mutation • FLT3-ITD mutation • NPM1 mutation • DNMT3A mutation • ASXL1 mutation • SRSF2 mutation • U2AF1 mutation • CEBPA mutation • STAG2 mutation • FLT3 wild-type • ERBB4 mutation • ZRSR2 mutation
11ms
Enrollment change • Trial withdrawal • Metastases
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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HER-2 positive • EGFR mutation • HER-2 overexpression • HER-2 amplification • HER-2 negative • ERBB3 mutation • ERBB4 mutation
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Keytruda (pembrolizumab) • paclitaxel • Nerlynx (neratinib)
11ms
NCI-2018-01218: Neratinib and Everolimus, Palbociclib, or Trametinib in Treating Participants With Refractory and Advanced or Metastatic Solid Tumors With EGFR Mutation/Amplification, HER2 Mutation/Amplification, or HER3/4 Mutation or KRAS Mutation (clinicaltrials.gov)
P1, N=93, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting | Trial completion date: Oct 2023 --> Oct 2025 | Trial primary completion date: Oct 2023 --> Oct 2025
Enrollment closed • Trial completion date • Trial primary completion date • Combination therapy • Metastases
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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KRAS mutation • EGFR mutation • HER-2 amplification • EGFR amplification • ERBB3 mutation • ERBB4 mutation
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Mekinist (trametinib) • Ibrance (palbociclib) • everolimus • Nerlynx (neratinib)
11ms
Oncogenicity of recurrent ERBB4 mutations and potential as predictive markers (EACR 2023)
Patients with oncogenic ERBB4 mutations (n=3) harbored also TP53 alterations, which may contribute to the lack of response to neratinib, as has been suggested for ERBB2-mutant patients.ConclusionMany of the recurrent ERBB4 mutations are oncogenic. Further investigation into potential utility of clinically used pan-ERBB inhibitors, such as neratinib, for patients whose tumors harbor these ERBB4 mutations is warranted.
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • TP53 (Tumor protein P53) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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TP53 mutation • EGFR mutation • HER-2 mutation • HER-2 S310F • ERBB3 mutation • ERBB4 mutation
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Nerlynx (neratinib)
1year
Development of selection-free HER4-mutated CRISPR/Cas9 knock-ins in cutaneous melanoma cell lines (AACR 2023)
We then developed CRISPR/Cas9-modified selection-free melanoma cell lines for interrogating the role of these mutations as biomarkers of response to the oral, irreversible pan-HER (EGFR, HER2, HER4) tyrosine kinase inhibitor (TKI) neratinib (NER). Two melanoma cell lines (WM115, SKMEL24) were genome-edited by using a selection-free CRISPR/Cas9 approach... CRISPR/Cas9 technology can be utilised to introduce single-point mutations in HER4 to melanoma cell lines. In vitro functional characterisation of the isolated HER4 CRISPR/Cas9-edited melanoma cell lines will be performed in order to understand the activating potential of HER4 R106C and R711C and their sensitivity to NER.
Preclinical
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HER-2 (Human epidermal growth factor receptor 2) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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ERBB4 mutation
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Nerlynx (neratinib)
1year
Different treatment response in several head and neck squamous cell carcinoma (HNSCC) cell lines reflecting underlying genomic and molecular signatures (AACR 2023)
PI3K/mTOR dual inhibition, PI3Kalpha inhibitor, AKT inhibitor, FGFR inhibitor, ALK/IGF1R inhibitor, CDK4/6 inhibitor, BCl2 inhibitor, WEE1 inhibitor, ATR inhibitor, DNA-PK inhibitor, AT2AR inhibitor, Mcl-1 inhibitor, MEK1/2 inhibitor, EZH2 inhibitor, HDAC inhibitor, CDK9 inhibitor, DNMT3 inhibitor, BRD4/BET inhibitor, JAK2 inhibitor, CXCR4 inhibitor, FAK inhibitor, BTK inhibitor, eribulin, & VEGFR2/ PDGFR/FGFR or VEGFR2/c-MET/Axl triple blockage might be effective on TW2.6 and reverse treatment refractoriness, maybe through the inhibition of mesenchymal transformation, pRB, & PI3K/AKT /mTOR signaling and the modulation of stemness & PD1/PDL1 pathway...All cell lines will be tried to be categorized as TCGA subtypes for the reference of future drug combinations.Cell linesSCC25KBSASCAL27FaDuSCC15SCC9SCC4TW2.6Differ- entiationWellPoorPoorPoorPoorWellWellWellWell, but rapidly replicated, with high hyper-diploidy & complex rearrangementsHPV statusHPV 16/18HPV18--HPV 16/18--HPV 6/11-EGFR statusMediumLowHighHighMediumHighLowMedium to highUnknownDocetaxel sensitivity+++++++++++++ to +++++-+Cisplatin sensitivity+++++++++++++- to +-- to +5-FU sensitivity+++++++++++-+ to ++-- to +Afatinib sensitivity+++- to +-+++++ to +++++++++-Polo-like kinase Inhibitor sensitivity+++++++++++++ to +++- to +-- to +VEGFR2 Inhibitor sensitivity----+++++--++PI3K/ mTOR inhibitorAll cell lines sensitiveCDK4/6 Inhibitor response+++- to ++++++ to +++++++++++++ to +++Western blotsWeak p-AKT & VEGF-A, mild PDL1 and BMI-1, Gli-1(+)Weak p-AKT, mild PDL1 and strong VEGF-A & BMI-1, p16(+)Moderate p-AKT & BMI-1, high PDL1, mild VEGF-AHigh p-AKT & VEGF-A, mild PDL1 & BMI-1High VEGF-A, moderate p-AKT & PDL1, weak BMI-1, Gli-1(+)Weak p-AKT & VEGF-A, mild PDL1 & BMI-1Weak p-AKT, VEGF-A, & BMI-1, moderate PDL1Moderate p-AKT & VEGF-A, strong BMI-1, mild PDL1, Gli-1(+)High p-AKT, PDL1, & VEGF-A and moderate BMI-1NGSCCND1 gain, CDKN2A deletion, FRG1 mutation, HGF mutation, p53 mutation, ATR mutation, SMO mutation, RUNX1T1 mutationSTK11 mutation, PDGFRA mutation, IGF1 mutation, BCOR mutation, EGFR mutation, NOTCH1 mutation, MET mutation, IKZF1 mutation, NFKB1 mutation, DPYD mutation, FGFR4 mutation, BRCA1 mutation, MSH2 mutation, DNMT3A mutationKRAS mutation, MDM2 mutation, TMB-H, AXIN1 loss, RAD51D mutation, NOTCH1/2 mutation, ERBB4 mutation, PALB2 mutation, p53 mutation, POLE mutation, CASP8 mutation, BRCA2 mutation, RNF43 mutation, LRP1B mutation, MET mutationCDKN2A deletion, EGFR amplification, SMAD4 mutation, TMB-H, LRP1B mutation, APC mutation, CASP8 mutation, CREBBP mutation, PIK3CG mutation, NRAS mutation, ABL1 mutation, FGF23 mutation, HGF mutation, ATRX mutation, p53 mutation, ERBB2 mutation, ROS1 mutation, EP300 mutation, NRAS mutation, CDKN1A mutation, KDM6A mutation, FLT4 mutationCCND1 gain, CDKN2A deletion, FLCN mutation, TMB-H, LRP1B mutation, SMAD4 loss, SF3B1 mutation, FAT1 mutation, VHL mutation, NOTCH3 mutation, EPHA5 mutation, p53 mutation, ERCC2 mutationCCND1 gain, EGFR amplification, SMO mutation, ATR mutation, FAT1 loss, NTRK1 mutation, KMT2D mutation, p53 mutation, NOTCH3 mutationCDKN2A deletion, AXIN2 amplification, SMAD3 loss, HRAS mutation, ATR mutation, NF1 mutation. IGF1R mutation, FLCN mutation, KEAP1 mutation, ASXL1 mutation, PMS2 mutationCCND1 gain, NF1 loss, LRP1B mutation, NSD1 mutation, KMT2D mutation, p53 mutation, EPHA2 mutationFAT1 loss, CCND3/FGF10 amplification, PIK3CA H1047R mutation, STK11 mutation, RICTOR/FLCN amplification, VEGF-A amplification , TSC2 mutation, EPHB1 mutation, MAP2K4 mutation, KDM5A mutation, PDGFRB mutation, SETD2 mutation, RPTOR mutation, APC mutation, DDR2 mutation, ATM mutation, MDM2 mutation, p53 mutation, CDK12 mutation, HRAS mutation, MYC mutation, CDK8 mutation, ARID1B lossOutcomesBest; like TCGA CL (HPV+) subtypeLike TCGA basal subtype, but responded to particular treatments eachBasalBasalLike TCGA mesen-chymal subtype (HPV+)Like TCGA CL(HPV-) subtype, different characters between these 3 cell linesCL(HPV-) subtypeCL(HPV-) subtypeWorse; like TCGA EMT subtype (HPV-)Potential treatmentsAll sensitive maybe; Hedgehog inhibitor , HGF/c-MET inhibitor, and I/O could be tried(1) Taxane, cisplatin, PLKi (2) mTORi (3) IGF1Ri, METi, PDGFRi, FGFRi (4) Epigenetics (5) I/O(1) Taxane, cisplatin, 5-FU, PLKi (2) CDK4/6i (3) I/O (4) DDRi (5) KRASi, METi, HERi (6) p53 reactivator and MDM2/Mcl-1 inhibitor(1) Taxane, cisplatin, 5-FU, PLKi (2) CDK4/6i (3) Mild EGFRi response (4) I/O (5) NRASi, FGFRi, HGF/c-METi/ROS1i/HERi (6) p53 reactivator/DDRi/Epigenetics(1) Cisplatin, 5-FU (2) EGFRi and VEGFR2i (3) Weak to PLKi & CDK4/6i (4) I/O (5) mTORi (6) Ephi (7) DDR/Epigenetics (8) p53 reactivator (9) HIFi(1) Taxane and PLKi (2) EGFRi, VEGFR2i, CDK4/6i (3) NTRKi (4) Hedgehog inhibitor (5) DDRi, epigenetics,& p53 reactivator(1) Taxane &5-FU (2) EGFRi (3) HRASi (4) DDRi/Epigenetics (5) I/O (6) IGF1Ri (7) mTORi(1) EGFRi (2) CDK4/6i (3) I/O (4) Epigenetics (5) Ephi (6) p53 reactivator(1) CDK4/6 inhibitor (2) Multi-targeted VEGFR TKI (3) PI3K/AKT/mTOR inhibitor (4) ICIs combination (5) p53 reactivator/ DDR interventions/Epigenetics (6) Dasatinib, HRASi, EphB1/B4 interventions Further NGS analysis may translate these HNSCC cell lines to represent TCGA subtypes for the reference of future drug combinations, esp... Further NGS analysis may translate these HNSCC cell lines to represent TCGA subtypes for the reference of future drug combinations, esp. immunotherapy, basic/translational research, and animal models. LRP1B will be a potential ICIs efficacy biomarker in HNSCC.
Preclinical • Tumor mutational burden • BRCA Biomarker • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • ABL1 (ABL proto-oncogene 1) • NRAS (Neuroblastoma RAS viral oncogene homolog) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • ATM (ATM serine/threonine kinase) • STK11 (Serine/threonine kinase 11) • HRAS (Harvey rat sarcoma viral oncogene homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • DNMT3A (DNA methyltransferase 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • NOTCH1 (Notch 1) • NF1 (Neurofibromin 1) • KEAP1 (Kelch Like ECH Associated Protein 1) • POLE (DNA Polymerase Epsilon) • AXL (AXL Receptor Tyrosine Kinase) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • CCND1 (Cyclin D1) • MDM2 (E3 ubiquitin protein ligase) • PALB2 (Partner and localizer of BRCA2) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • PDGFRB (Platelet Derived Growth Factor Receptor Beta) • KMT2D (Lysine Methyltransferase 2D) • LRP1B (LDL Receptor Related Protein 1B) • FGFR4 (Fibroblast growth factor receptor 4) • MSH2 (MutS Homolog 2) • RNF43 (Ring Finger Protein 43) • CDK12 (Cyclin dependent kinase 12) • SMAD4 (SMAD family member 4) • IKZF1 (IKAROS Family Zinc Finger 1) • ERCC2 (Excision repair cross-complementation group 2) • PMS2 (PMS1 protein homolog 2) • VHL (von Hippel-Lindau tumor suppressor) • APC (APC Regulator Of WNT Signaling Pathway) • ATRX (ATRX Chromatin Remodeler) • TSC2 (TSC complex subunit 2) • IGF1R (Insulin-like growth factor 1 receptor) • NOTCH2 (Notch 2) • CREBBP (CREB binding protein) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • SMO (Smoothened Frizzled Class Receptor) • BCOR (BCL6 Corepressor) • ERBB4 (erb-b2 receptor tyrosine kinase 4) • FAT1 (FAT atypical cadherin 1) • KDM6A (Lysine Demethylase 6A) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • PIK3CG (Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Gamma) • NOTCH3 (Notch Receptor 3) • ARID1B (AT-Rich Interaction Domain 1B) • EP300 (E1A binding protein p300) • FLT4 (Fms-related tyrosine kinase 4) • IGF1 (Insulin-like growth factor 1) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • RAD51D (RAD51 paralog D) • RICTOR (RPTOR Independent Companion Of MTOR Complex 2) • EPHA2 (EPH receptor A2) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • CASP8 (Caspase 8) • CCND3 (Cyclin D3) • BRD4 (Bromodomain Containing 4) • DDR2 (Discoidin domain receptor 2) • FLCN (Folliculin) • KDM5A (Lysine Demethylase 5A) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • DPYD (Dihydropyrimidine Dehydrogenase) • EPHA5 (EPH Receptor A5) • EPHB1 (EPH Receptor B1) • FGF10 (Fibroblast Growth Factor 10) • FGF23 (Fibroblast Growth Factor 23) • MAP2K4 (Mitogen-Activated Protein Kinase Kinase 4) • SMAD3 (SMAD Family Member 3)
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TP53 mutation • KRAS mutation • BRCA2 mutation • BRCA1 mutation • EGFR mutation • TMB-H • NRAS mutation • PIK3CA mutation • EGFR amplification • ATM mutation • PIK3CA H1047R • STK11 mutation • DNMT3A mutation • PALB2 mutation • POLE mutation • NF1 mutation • NOTCH1 mutation • ASXL1 mutation • CDKN2A deletion • BCL2 overexpression • KEAP1 mutation • SF3B1 mutation • CDKN2A mutation • KMT2D mutation • CDK12 mutation • LRP1B mutation • VHL mutation • PIK3CA amplification • HRAS mutation • APC mutation • ATR mutation • ATRX mutation • CCND1 amplification • PDGFRA mutation • CREBBP mutation • MSH2 mutation • RNF43 mutation • ROS1 mutation • SMAD4 mutation • BCOR mutation • FGFR4 mutation • KDM6A mutation • RAD51D mutation • TSC2 mutation • FAT1 mutation • MYC mutation • ARID1B mutation • NOTCH3 mutation • PMS2 mutation • SMO mutation • IKZF1 mutation • MDM2 mutation • NTRK1 mutation • EP300 mutation • ERBB4 mutation • NSD1 mutation • PIK3CA H1047R + PIK3C2B amplification • PIK3CG mutation • SETD2 mutation • EPHA5 mutation • EPHB1 mutation • ERCC2 mutation • FGF10 amplification • FGF23 mutation • FLCN mutation • HGF mutation • PDGFRB mutation • RAD51 mutation
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cisplatin • Gilotrif (afatinib) • dasatinib • 5-fluorouracil • Halaven (eribulin mesylate)
over1year
Trial primary completion date • Combination therapy • Metastases
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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KRAS mutation • EGFR mutation • HER-2 amplification • EGFR amplification • ERBB3 mutation • ERBB4 mutation
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Mekinist (trametinib) • Ibrance (palbociclib) • everolimus • Nerlynx (neratinib)
over1year
Genomic Landscape Alterations in Primary Tumor and Matched Lymph Node Metastasis in Hormone-Naïve Prostate Cancer Patients. (PubMed, Cancers (Basel))
In the present study we found mostly concordance concerning the ERBB4 mutation between both primary PCa samples and matched lymph node metastasis, underlining that the identification of alterations in the primary tumor is extremely important for cancer prognosis prediction.
Journal
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FGFR2 (Fibroblast growth factor receptor 2) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • MLH1 (MutL homolog 1) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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FGFR2 mutation • AKT1 mutation • MLH1 mutation • ERBB4 mutation
over1year
New P2 trial
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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HER-2 positive • EGFR mutation • HER-2 overexpression • HER-2 amplification • HER-2 negative • ERBB3 mutation • ERBB4 mutation
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Keytruda (pembrolizumab) • paclitaxel • Nerlynx (neratinib)
2years
ErbB4-mediated regulation of vasculogenic mimicry capability in breast cancer cells. (PubMed, Cancer Sci)
In E872K ErbB4-overexpressing cells, but not in wild-type ErbB4-overexpressing cells, the number of VM tubes was significantly decreased by low-dose treatment with the ErbB inhibitor afatinib. Taken together, our findings demonstrated the significance of ErbB4-mediated VM formation, and suggested the possibility of ErbB4 mutations as effective targets in breast cancer.
Journal
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NRG1 (Neuregulin 1) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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ERBB4 mutation
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Gilotrif (afatinib)
2years
ERBB4 is sufficient and necessary for proliferation of BRAF WT melanoma cell lines (AACR 2022)
Furthermore, we are determining whether prioritized ERBB4 mutants found in BRAF-WT melanomas exhibit greater signaling and oncogenic activities than WT ERBB4. Consequently, these experiments will establish a functional role for ERBB4 mutations and expression in BRAF-WT melanomas and will identify potential strategies for disrupting oncogenic ERBB4 signaling in these tumors.
Preclinical
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • NF1 (Neurofibromin 1) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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BRAF mutation • HER-2 expression • EGFR expression • BRAF wild-type • NF1 mutation • ERBB4 mutation
2years
Identification of HER4 mutations with potential as biomarkers of response to neratinib (AACR 2022)
These data suggest that melanoma and EG cancers are the cancer types with the highest rate of HER4 mutations. In vitro functional characterization of the identified HER4 mutations is now required to further explore their value as biomarkers of response to NER.
HER-2 (Human epidermal growth factor receptor 2) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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HER-2 amplification • ERBB4 mutation • ERBB4 expression
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Nerlynx (neratinib)
over2years
POTENTIAL EMERGING ROLE OF LIQUID BIOPSY IN CLINICAL PRACTICE IN METASTATIC COLORECTAL CANCER (MCRC) TREATMENT (AIOM 2021)
In a prospective cohort of mCRC pts, we have shown how exosome-based liquid biopsy and some cytokines analysis might provide relevant clinical information to therapeutic stratification that must be investigated in wide studies.
Clinical • Liquid biopsy
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KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • IL6 (Interleukin 6) • CEACAM5 (CEA Cell Adhesion Molecule 5) • CXCL8 (Chemokine (C-X-C motif) ligand 8) • CD44 (CD44 Molecule) • BSG (Basigin (Ok Blood Group))
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KRAS mutation • BRAF mutation • CEACAM5 expression • CD44 expression • ERBB4 mutation • CXCL8 expression • IL6 expression
over2years
The role of ERBB4 mutations in the prognosis of advanced non-small cell lung cancer treated with immune checkpoint inhibitors. (PubMed, Mol Med)
ERBB4 mutations could serve as a predictive biomarker for the prognosis of ICIs treatment. The systematic nomogram was proven to have the great potential for evaluating the efficacy of ICIs therapy for advanced NSCLC patients.
Journal • Checkpoint inhibition • Tumor Mutational Burden • MSi-H Biomarker • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • MSI (Microsatellite instability) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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PD-L1 expression • TP53 mutation • MSI-H/dMMR • ERBB4 mutation
3years
Dynamic cfDNA Analysis by NGS in EGFR T790M-Positive Advanced NSCLC Patients Failed to the First-Generation EGFR-TKIs. (PubMed, Front Oncol)
CDK6 CNV, GRIN2A, BRCA2, EGFR D761N, EGFR Q791H, EGFR V843I, and ERBB4 mutation genes may possibly be new resistant mechanisms. Patients with undetectable cfDNA during the third-generation EGFR TKI treatment have superior clinical outcomes, and dynamic cfDNA analysis by NGS is valuable to explore potential resistant mechanisms.
Clinical • Journal • Next-generation sequencing • BRCA Biomarker
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EGFR (Epidermal growth factor receptor) • BRCA2 (Breast cancer 2, early onset) • ERBB4 (erb-b2 receptor tyrosine kinase 4) • CDK6 (Cyclin-dependent kinase 6)
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EGFR mutation • EGFR T790M • EGFR C797S • EGFR positive • ERBB4 mutation
over3years
[VIRTUAL] Molecular Characterization of AKT1 Gene in East Asian Non-Small Cell Lung Cancer Patients (IASLC-WCLC 2020)
Conclusion TP53, ERBB4, EZH2, KEAP1 gene accompanied may have less correlation with AKT1 mutation in NSCLC patients. We report different mutations than those previously reported, which emphasizes the importance of personalized medicine that could be empowered by the use of bioinformatics tools in the diagnostic process and therapeutic approaches.
Clinical
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TP53 (Tumor protein P53) • KEAP1 (Kelch Like ECH Associated Protein 1) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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TP53 mutation • KEAP1 mutation • EZH2 mutation • AKT1 mutation • ERBB4 mutation
over3years
ERBB4 high expression and mutations in gastric cancer present opportunities for clinical landscape and therapeutic development (IDDF 2020)
Conclusions This finding broadened the clinical application of TKIs targeted to ERBB2 or pan-ERBB, suggesting that they may provide therapeutic benefits to GC patients with ERBB4 overexpression or mutations. Moreover, ERBB4 is supposed to be a significant biomarker for GC treatment.
Clinical
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HER-2 (Human epidermal growth factor receptor 2) • TOP2A (DNA topoisomerase 2-alpha) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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ERBB4 mutation
over3years
[VIRTUAL] Targeting BRAF WT metastatic melanomas: Identifying ERBB4 mutant alleles as biomarkers for novel combinatorial treatment strategies (AACR-NCI-EORTC 2020)
In silico analyses of the TCGA-SKCM dataset indicate that ERBB4 mutant alleles function as drivers of BRAF WT MM. We will present our progress in developing and validating in vitro positive selection strategies to identify which of the 76 ERBB4 mutant alleles found in the TCGA-SKCM dataset function as bona fide drivers of BRAF WT MMs.
EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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BRAF mutation • ERBB4 mutation
over3years
[VIRTUAL] Targeting BRAF WT metastatic melanomas: Identifying ERBB4 mutant alleles as biomarkers for novel combinatorial treatment strategies (AACR-NCI-EORTC 2020)
In silico analyses of the TCGA-SKCM dataset indicate that ERBB4 mutant alleles function as drivers of BRAF WT MM. We will present our progress in developing and validating in vitro positive selection strategies to identify which of the 76 ERBB4 mutant alleles found in the TCGA-SKCM dataset function as bona fide drivers of BRAF WT MMs.
EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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BRAF mutation • ERBB4 mutation
almost4years
Negative feedback regulation of ErbB4 tyrosine kinase activity by ERK-mediated non-canonical phosphorylation. (PubMed, Biochem Biophys Res Commun)
Given the fact that ErbB4 mutation is one of the most common genetic alterations in melanoma cells, we demonstrated that a typical oncogenic ErbB4 mutant was resistant to the negative feedback regulation to maintain a highly active status of tyrosine kinase activity. Together, these findings indicate that feedback mechanisms are key switches determining oncogenic potentials of ErbB receptor kinases.
Journal
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ERBB4 (erb-b2 receptor tyrosine kinase 4)
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ERBB4 mutation
almost4years
[VIRTUAL] Targeting BRAF WT metastatic melanomas: Identifying ERBB4 mutations as biomarkers for novel combinatorial treatment strategies (AACR-II 2020)
In silico analyses of the TCGA-SKCM dataset indicate that ERBB4 mutant alleles function as drivers of BRAF WT MM. We will present our progress in developing and validating positive selection strategies to identify which of the 76 ERBB4 mutant alleles found in the TCGA-SKCM dataset function as bona fide drivers of BRAF WT MMs.
EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • ERBB4 (erb-b2 receptor tyrosine kinase 4)
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BRAF mutation • ERBB4 mutation