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BIOMARKER:

FGFR3 amplification

i
Entrez ID:
11d
Genomic correlates of response and resistance to the irreversible FGFR1-4 inhibitor futibatinib based on biopsy and circulating tumor DNA profiling. (PubMed, Ann Oncol)
In this largest and most systematic analysis of acquired resistance to an FGFR inhibitor from prospective clinical trials, emergence of secondary FGFR2 kinase domain mutations was observed in most patients receiving clinical benefit to futibatinib. ctDNA analysis shows clinically relevant potential as a noninvasive method for assessing genomic profiles, identifying patients who may benefit from FGFR inhibitor treatment, and exploring acquired resistance mechanisms.
Journal • Circulating tumor DNA • Biopsy
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TP53 (Tumor protein P53) • FGFR2 (Fibroblast growth factor receptor 2) • FGFR3 (Fibroblast growth factor receptor 3) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
|
FGFR1 amplification • FGFR2 mutation • FGFR2 fusion • FGFR2 amplification • FGFR1 rearrangement • FGFR3 amplification • FGFR2 N550K
|
Lytgobi (futibatinib)
1m
Fulvestrant, Palbociclib and Erdafitinib in ER+/HER2-/FGFR-amplified Metastatic Breast Cancer (clinicaltrials.gov)
P1, N=35, Completed, Vanderbilt-Ingram Cancer Center | Active, not recruiting --> Completed | Trial completion date: Sep 2024 --> Mar 2024
Trial completion • Trial completion date
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HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • FGFR2 (Fibroblast growth factor receptor 2) • FGFR1 (Fibroblast growth factor receptor 1) • FGFR4 (Fibroblast growth factor receptor 4) • FGF23 (Fibroblast Growth Factor 23)
|
HER-2 negative • FGFR1 amplification • FGFR3 amplification • FGFR4 amplification • FGFR amplification
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Ibrance (palbociclib) • Balversa (erdafitinib) • fulvestrant
3ms
Genomic mutational profile of breast cancer patients from India through comprehensive next-generation sequencing analysis of circulating tumor DNA (ESMO Asia 2024)
Uncovering uncommon PIK3CA and ESR1 alterations beyond hotspot testing. These findings emphasize the clinical utility of ctDNA based comprehensive genomic profiling for treatment guidance.
Clinical • Next-generation sequencing • Tumor mutational burden • BRCA Biomarker • MSi-H Biomarker • Circulating tumor DNA
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MSI (Microsatellite instability) • FGFR2 (Fibroblast growth factor receptor 2) • PTEN (Phosphatase and tensin homolog) • EML4 (EMAP Like 4) • FGFR1 (Fibroblast growth factor receptor 1) • RB1 (RB Transcriptional Corepressor 1) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CDK12 (Cyclin dependent kinase 12)
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BRCA1 mutation • MSI-H/dMMR • HER-2 amplification • PIK3CA mutation • ATM mutation • FGFR1 amplification • FGFR2 fusion • ALK fusion • FGFR3 amplification
|
Guardant360® CDx
3ms
KRAS mutations in pulmonary adenocarcinomas (ECP 2024)
KRAS is an attractive therapeutic strategy due to its high prevalence and its role in initiating and sustaining tumour growth. Approval of KRAS G12C inhibitors in locally advanced or metastatic NSCLC has brought hope to many patients. Studies show that non G12C KRAS mutation are found in 53% of adenocarcinomas.
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) • MET (MET proto-oncogene, receptor tyrosine kinase) • PTEN (Phosphatase and tensin homolog) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • MAP2K1 (Mitogen-activated protein kinase kinase 1) • GNAS (GNAS Complex Locus)
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TP53 mutation • KRAS mutation • BRAF mutation • HER-2 amplification • KRAS G12D • PTEN mutation • KRAS G12V • MET exon 14 mutation • ALK mutation • KRAS G12A • FGFR3 amplification • KRAS G13C
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Oncomine Precision Assay
5ms
Molecular characterization of adult non-glioblastoma central nervous system (CNS) tumors to identify potential targettable alterations (ESMO 2024)
4 pts received TT at recurrence, within clinical trials: one with grade 3 meningioma and ALK rearrangement treated with alectinib, one with PTCH1 mutant medulloblastoma treated with vismodegib, and two with high TMB treated with nivolumab/ipilumumab. The incidence of targettable molecular alterations in adult CNS tumor pts was lower than in GBM. Nevertheless, in a few selected cases TT have the potential to increase treatment options at recurrence and improve outcomes.
Clinical • Tumor mutational burden • PD(L)-1 Biomarker • BRCA Biomarker • IO biomarker
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BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • 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) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • FGFR1 (Fibroblast growth factor receptor 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • NF1 (Neurofibromin 1) • MDM2 (E3 ubiquitin protein ligase) • PTCH1 (Patched 1) • BRCA (Breast cancer early onset) • NTRK (Neurotrophic receptor tyrosine kinase)
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BRAF V600E • TMB-H • MET amplification • ALK rearrangement • FGFR1 amplification • MDM2 amplification • PTCH1 mutation • BRCA mutation • FGFR3 amplification • PTCH1 rearrangement • NTRK fusion
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FoundationOne® CDx
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Opdivo (nivolumab) • Yervoy (ipilimumab) • Alecensa (alectinib) • Erivedge (vismodegib)
10ms
Fulvestrant, Palbociclib and Erdafitinib in ER+/HER2-/FGFR-amplified Metastatic Breast Cancer (clinicaltrials.gov)
P1, N=35, Active, not recruiting, Vanderbilt-Ingram Cancer Center | Trial completion date: Dec 2023 --> Sep 2024
Trial completion date • Metastases
|
HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • FGFR2 (Fibroblast growth factor receptor 2) • FGFR1 (Fibroblast growth factor receptor 1) • FGFR4 (Fibroblast growth factor receptor 4) • FGF23 (Fibroblast Growth Factor 23)
|
HER-2 negative • FGFR1 amplification • FGFR3 amplification • FGFR4 amplification • FGFR amplification
|
Ibrance (palbociclib) • Balversa (erdafitinib) • fulvestrant
12ms
Exploring the Clinical Utility of Molecular Profiling of Intrahepatic Cholangiocarcinoma in a Comprehensive Multidisciplinary Clinic. (PubMed, J Am Coll Surg)
Actionable molecular alterations were frequently observed in patients with ICC. Detection of actionable alterations was associated with improved OS. The role of targeted therapy needs further exploration in prospective multi-center studies.
Journal • Tumor mutational burden • BRCA Biomarker
|
HER-2 (Human epidermal growth factor receptor 2) • 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) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MSI (Microsatellite instability) • FGFR2 (Fibroblast growth factor receptor 2) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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BRAF V600E • BRCA2 mutation • BRCA1 mutation • TMB-H • HER-2 overexpression • HER-2 amplification • PIK3CA mutation • BRAF V600 • MET amplification • FGFR2 mutation • FGFR2 fusion • ROS1 fusion • MET mutation • FGFR3 amplification
1year
Non-Small Cell Lung Carcinoma with Clear Cell Features and FGFR3::TACC3 Gene Rearrangement: Clinicopathologic and Next Generation Sequencing Study of 7 Cases. (PubMed, Am J Surg Pathol)
Non-small cell lung carcinoma harboring FGFR3::TACC3 gene rearrangements is extremely rare, and this rearrangement may potentially be enriched in tumors that demonstrate clear cell histology. Identification of FGFR3::TACC3 in patients with lung carcinomas with clear cell features may be of importance as they could potentially be candidates for therapy with tyrosine kinase inhibitors.
Journal • Next-generation sequencing
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FGFR3 (Fibroblast growth factor receptor 3) • TACC3 (Transforming acidic coiled-coil containing protein 3)
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TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12D • FGFR3 mutation • KRAS G12 • EGFR mutation + KRAS mutation • FGFR3 amplification
1year
FGFR alterations in gliomas; clinical, radiographic and molecular characterization (SNO 2023)
FGFR3-TACC3 fusions (F3T3) gliomas represent a unique entity among IDH WT gliomas. In our cohort, 100% of the patients with F3T3-positive glioblastomas also had an associated TERT promoter mutation. To our knowledge, this is one of the larger cohorts showing the association between FGFR3 and TERT promoter alterations in glioblastomas.
Clinical
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FGFR3 (Fibroblast growth factor receptor 3) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • FGFR (Fibroblast Growth Factor Receptor) • TERT (Telomerase Reverse Transcriptase) • TACC3 (Transforming acidic coiled-coil containing protein 3) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • LMNB2 (Lamin B2)
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FGFR3-TACC3 fusion • FGFR mutation • CDKN2A mutation • FGFR fusion • FGFR3 fusion • TERT mutation • IDH wild-type • TERT promoter mutation • FGFR3 amplification
1year
FGFR alterations in gliomas; clinical, radiographic and molecular characterization (SNO 2023)
FGFR3-TACC3 fusions (F3T3) gliomas represent a unique entity among IDH WT gliomas. In our cohort, 100% of the patients with F3T3-positive glioblastomas also had an associated TERT promoter mutation. To our knowledge, this is one of the larger cohorts showing the association between FGFR3 and TERT promoter alterations in glioblastomas.
Clinical
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FGFR3 (Fibroblast growth factor receptor 3) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • FGFR (Fibroblast Growth Factor Receptor) • TERT (Telomerase Reverse Transcriptase) • TACC3 (Transforming acidic coiled-coil containing protein 3) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • LMNB2 (Lamin B2)
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FGFR3-TACC3 fusion • FGFR mutation • CDKN2A mutation • FGFR fusion • FGFR3 fusion • TERT mutation • IDH wild-type • TERT promoter mutation • FGFR3 amplification
over1year
Are fibroblast growth factor receptor 3 (FGFR3) alterations a possible predictive factor for platinum-based chemotherapy and immunotherapy in metastatic urothelial carcinoma (MUC)? (ESMO 2023)
Conclusions In our cohort, FGFR3 alterations are neither predictive nor prognostic for 1st-line platinum or 2nd-line IO. Further investigation is needed.
IO biomarker • Metastases
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FGFR3 (Fibroblast growth factor receptor 3)
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FGFR3 fusion • FGFR3 amplification • FGFR wild-type
over1year
A Phase II Trial of Anlotinib Plus Osimertinib in Advanced NSCLC with EGFR T790M Mutation After Failure of Prior EGFR TKIs (IASLC-WCLC 2023)
The combination of anlotinib and osimertinib might be an efficacy and safety treatment option for patients with EGFR T790M mutation who have failed prior EGFR-TKI. Dynamic changes of ctDNA could be used to monitor treatment response and to explore mechanisms of acquired resistance to therapy.
P2 data • Metastases
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TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • FGFR3 (Fibroblast growth factor receptor 3)
|
TP53 mutation • EGFR mutation • MET amplification • EGFR T790M • EGFR C797S • PIK3CA amplification • FGFR3 fusion • FGFR3 amplification
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Tagrisso (osimertinib) • Focus V (anlotinib)
over1year
Copy Number Variants and Late Somatic Mutations Underlying Tumor Progression in NADIM Clinical Trials (IASLC-WCLC 2023)
In this study, we report preliminary results of potential molecular mechanisms underlying disease progression in patients treated with neoadjuvant nivolumab plus chemotherapy using plasma samples from NADIM and NADIM II cohorts. A total of 10 plasma samples collected upon disease progression from patients included in NADIM or NADIM II trials were analyzed... Acquisition of somatic-copy number alterations in RET, EGFR and FGFR was found in the plasma samples collected upon disease progression in patients treated with neoadjuvant chemoimmunotherapy (NADIM I and II cohorts) which may have important implications for subsequent treatment selection.
Clinical • Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • RET (Ret Proto-Oncogene) • FGFR3 (Fibroblast growth factor receptor 3) • STK11 (Serine/threonine kinase 11) • DNMT3A (DNA methyltransferase 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • RNF43 (Ring Finger Protein 43) • SETBP1 (SET Binding Protein 1) • GRIN2A (Glutamate Ionotropic Receptor NMDA Type Subunit 2A)
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TP53 mutation • EGFR amplification • STK11 mutation • DNMT3A mutation • TET2 mutation • CBL mutation • RNF43 mutation • FGFR3 amplification • RET amplification
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TruSight Oncology 500 Assay • Oncomine Tumor Mutation Load Assay
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Opdivo (nivolumab)
over1year
Establishment And Comparison Of Three Subtypes From A Human Uterine Carcinosarcoma Cell Line (ESCA) (ESGO 2023)
Whole exome sequence showed ESCA and its subtypes, tissue block shared similar single nucleotide variants, such as TP53, ARHGAP35, CDH3 mutations, while relatively large difference in copy number variations on the basis of some common variants, such as amplification of FGFR3 (chr.4) and BCL9L (chr.11) genes.Conclusion ESCA cell line is the very first cell line of UCS until now, which showed infinite multiplication and tumorigenicity in vivo. ESCA harbored TP53, ARHGAP35, CDH3 mutations and amplification of FGFR3 and BCL9L genes, which would probably be a good model for exploring the molecular mechanism of UCS.
Preclinical
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TP53 (Tumor protein P53) • FGFR3 (Fibroblast growth factor receptor 3) • CDH3 (Cadherin 3) • BCL9L (BCL9 Like)
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TP53 mutation • FGFR3 amplification
over1year
Accuracy of genome-wide mutational analysis for tumor-informed ctDNA-guided MRD monitoring in bladder cancer. (ASCO 2023)
Our results highlight the clinical potential of personalized genome-wide mutation integration as an ultra-sensitive, non-invasive method for MRD detection and treatment response monitoring.
Circulating tumor DNA
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TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR3 (Fibroblast growth factor receptor 3) • RB1 (RB Transcriptional Corepressor 1) • KMT2D (Lysine Methyltransferase 2D) • KDM6A (Lysine Demethylase 6A)
|
TP53 mutation • PIK3CA mutation • FGFR3 amplification
|
C2inform test
over1year
Genomic characterization of FGFR-altered solid tumors using a clinically annotated pan-cancer repository. (ASCO 2023)
Activating FGFR fusions, which occur across tumor types with marked diversity in fusion partners, present opportunities for future drug development. Non-target FGFR alterations in iCCA and UC, particularly those that cluster with target FGFR alterations, may be candidates for future FGFR-targeted strategies.
Clinical • Pan tumor
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TP53 (Tumor protein P53) • FGFR2 (Fibroblast growth factor receptor 2) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • ARID1A (AT-rich interaction domain 1A) • FGFR (Fibroblast Growth Factor Receptor) • TACC3 (Transforming acidic coiled-coil containing protein 3) • BAP1 (BRCA1 Associated Protein 1)
|
FGFR1 amplification • FGFR2 mutation • FGFR2 fusion • FGFR3 mutation • FGFR fusion • FGFR1 fusion • FGFR3 amplification
|
MSK-IMPACT
over1year
Targeting FGFR Pathway Is Not an Effective Therapeutic Strategy in Patients with Unselected Metastatic Esophagogastric Cancer Resistant to Trastuzumab. (PubMed, J Pers Med)
In this Simon's two-stage phase 2, single arm study, patients with advanced EG cancer refractory to trastuzumab-containing therapies received pemigatinib, an inhibitor of FGFR. Three patients had an high Tumor Mutational Burden, and two of them are significantly long-term survivors. These results do not support the therapeutic efficacy of targeting FGFR in unselected patients with advanced EG cancer, who are refractory to trastuzumab-containing therapies.
Journal • Tumor mutational burden • Metastases
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HER-2 (Human epidermal growth factor receptor 2) • TMB (Tumor Mutational Burden) • FGFR3 (Fibroblast growth factor receptor 3)
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TMB-H • HER-2 amplification • FGFR3 amplification • FGFR3 expression
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Herceptin (trastuzumab) • Pemazyre (pemigatinib)
almost2years
AMB302/GR1017, an antibody-drug conjugate (ADC) with topoisomerase 1 inhibitor shows therapeutic potency in orthotopic glioblastoma PDX and bladder cancer models with FGFR3-TACC3 fusion (AACR 2023)
AMB302/GR1017 showed robust anti-tumor efficacies in F3-T3 fusion and FGFR3 overexpression models derived from GBM and BC in vitro and in vivo. In addition, AMB302/GR1017 was well tolerated with no adverse effects in rodent model. Our data suggest AMB302/GR1017 has a potential therapeutic option as a first-in-class FGFR3 targeting ADC for GBM, BC, and other solid tumors with FGFR3 overexpression or alterations.
Preclinical
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FGFR3 (Fibroblast growth factor receptor 3) • TACC3 (Transforming acidic coiled-coil containing protein 3)
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FGFR3-TACC3 fusion • FGFR3 overexpression • FGFR3 fusion • FGFR3 amplification • FGF3 overexpression
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AMB302
almost2years
Non-small Cell Lung Carcinoma with Clear Cell Features and FGFR3::TACC3 Gene Rearrangements: Clinicopathologic and Molecular Genetic Analysis of 7 Cases (USCAP 2023)
FGFR3 :: TACC3 fusions may occur de-novo or as a secondary treatment resistance mechanism in NSCLC. These fusions appear to be enriched in smokers or former smokers and more frequently occur with squamous cell carcinoma histology and may demonstrate clear cell morphology by light microscopy. Identification of FGFR alterations is of particular importance given the lack of targeted therapeutic options for patients with squamous cell carcinoma.
Clinical
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EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FGFR3 (Fibroblast growth factor receptor 3) • TACC3 (Transforming acidic coiled-coil containing protein 3) • NKX2-1 (NK2 Homeobox 1)
|
TP53 mutation • KRAS mutation • EGFR mutation • KRAS G12D • FGFR3 mutation • KRAS G12 • FGFR3 fusion • EGFR mutation + KRAS mutation • FGFR3 R248C • FGFR3 amplification • TP53 R273C
2years
Infiltrating gliomas with FGFR alterations: Histologic features, genetic alterations, and potential clinical implications. (PubMed, Cancer Biomark)
Histologic features correlate with FGFR alterations in IGs. FGFR3-TACC3 fusion and FGFR3 amplification are the most common FGFR alterations in IGs. FGFR alterations are a rare, but potentially viable, therapeutic target in asubset of IGs.
Journal
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • PTEN (Phosphatase and tensin homolog) • FGFR3 (Fibroblast growth factor receptor 3) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • FGFR (Fibroblast Growth Factor Receptor) • TACC3 (Transforming acidic coiled-coil containing protein 3) • CDK4 (Cyclin-dependent kinase 4) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
|
TP53 mutation • PTEN mutation • FGFR3-TACC3 fusion • FGFR mutation • FGFR3 fusion • IDH wild-type • FGFR3 amplification
2years
FGFR Mutations and Associated Variant Histology in Urothelial Carcinoma (AMP 2022)
Variant histology was appreciated in 76% of FGFR mutated cases, with the micropapillary pattern being the most prevalent (n=12 | 32%). The FGFR pathway is classically associated with low-grade papillary tumors, which, through additional mutations, can cause invasive, high-grade disease. It is speculated that the initial papillary architecture present in FGFR mutated lesions may be preserved, manifesting as the micropapillary pattern appreciated in some invasive lesions.
FGFR3 (Fibroblast growth factor receptor 3) • FGFR (Fibroblast Growth Factor Receptor)
|
FGFR3 mutation • FGFR mutation • FGFR3 S249C • FGFR3 Y373C • FGFR3 fusion • FGFR3 G370C • FGFR3 R248C • FGFR3 amplification
|
therascreen® FGFR RGQ RT-PCR Kit
2years
Genetic alterations during the neoplastic cascade towards cholangiocarcinoma in primary sclerosing cholangitis. (PubMed, J Pathol)
In conclusion, PSC-CCA exhibit a variety of genetic alterations during progression of the neoplastic cascade, with mainly CNVs being present early whereas mutations in ERBB2, TP53, and KRAS appear later in the development of CCA. These findings are promising for the development of NGS-guided diagnostic strategies in PSC-CCA.
Journal
|
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) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • MCL1 (Myeloid cell leukemia 1) • SMAD4 (SMAD family member 4) • GNAS (GNAS Complex Locus)
|
TP53 mutation • KRAS mutation • EGFR mutation • HER-2 amplification • PIK3CA mutation • HER-2 mutation • FGFR1 amplification • MYC amplification • SMAD4 mutation • FGFR3 amplification
2years
FGFR1-4 RNA-Based Gene Alteration and Expression Analysis in Squamous Non-Small Cell Lung Cancer. (PubMed, Int J Mol Sci)
NGS revealed known pathogenic FGFR2,3 variants, an FGFR3::TACC3 fusion, and a novel TACC1::FGFR1 fusion together with FGFR1,2 variants of uncertain significance not previously reported in Sq-NSCLC. These findings expand our knowledge of the Sq-NSCLC molecular background and show that combining different methods increases the rate of FGFR aberrations detection, which may improve patient selection for FGFRi treatment.
Journal
|
FGFR2 (Fibroblast growth factor receptor 2) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • TACC3 (Transforming acidic coiled-coil containing protein 3) • FGFR4 (Fibroblast growth factor receptor 4) • TACC1 (Transforming Acidic Coiled-Coil Containing Protein 1)
|
FGFR1 amplification • FGFR fusion • FGFR1 fusion • FGFR3 fusion • FGFR1 expression • FGFR4 expression • FGFR expression • FGFR3 amplification • FGFR3 expression
2years
Therapeutic Targeting of FGFR Signaling in Head and Neck Cancer. (PubMed, Cancer J)
Nonetheless, FGF/FGFR has been a promising target for HNSCC treatment, and recent preclinical studies demonstrate the potential of the combination treatment regimens involving FGFR inhibitors on HNSCC. Therefore, there are a number of FGFR inhibitors currently in clinical trials for the treatment of head and neck cancers.
Journal
|
FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1)
|
FGFR1 amplification • FGFR3 mutation • FGFR expression • FGFR3 amplification • FGF amplification
over2years
Simultaneous Detection of FGFR Gene Aberrations in Squamous Non-small Cell Lung Cancer Using Targeted DNA- and RNA-based NGS (IASLC-WCLC 2022)
Our data provide insight into the presence of various molecular aberrations simultaneously on DNA and RNA level alongside with the FGFR1 amplification and protein expression. TP53 mutations approved to be most common in analysed Sq-NSCLC tumors, while the FGFR fusions and pathogenic variants were rare. Our results highlight the necessity of detailed and extended molecular analysis (i.e.
Next-generation sequencing
|
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) • NRAS (Neuroblastoma RAS viral oncogene homolog) • RET (Ret Proto-Oncogene) • FGFR2 (Fibroblast growth factor receptor 2) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • FGFR (Fibroblast Growth Factor Receptor) • NRG1 (Neuregulin 1) • GNAQ (G Protein Subunit Alpha Q) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • GNA11 (G Protein Subunit Alpha 11) • FOXL2 (Forkhead Box L2)
|
TP53 mutation • KRAS mutation • EGFR mutation • BRAF mutation • PIK3CA mutation • FGFR1 amplification • ALK fusion • ROS1 fusion • FGFR fusion • FGFR1 fusion • FGFR1 expression • TP53 expression • FGFR3 amplification • FGFR3 expression
|
Archer® FusionPlex® Lung Kit
over2years
PD-L1 expression and FGFR-mutations among Danish patients diagnosed with metastatic urothelial carcinoma - a retrospective and descriptive study. (PubMed, APMIS)
We found no association between FGFR1-3 aberrations and PT PD-L1 expression (p=0.379). Our data emphasize the need for further studies in predictive biomarkers.
Journal • Retrospective data • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • FGFR (Fibroblast Growth Factor Receptor)
|
PD-L1 expression • FGFR1 amplification • FGFR mutation • FGFR1 expression • FGFR3 amplification
|
PD-L1 IHC 22C3 pharmDx • Oncomine™ Comprehensive Assay v3M
over2years
Natural distribution of genomic alterations correlated with the resistance to KRASG12C inhibitor in Chinese colorectal cancer. (ASCO 2022)
Novel acquired secondary KRAS mutations within the adagrasib-binding pocket such as Y96C, H95D/Q/R, R68S, 2... Our analysis results indicate about 15% KRAS G12C-mutant Chinese CRC were probable resistant to KRASG12C inhibitor. One-third of these patients had co-existed oncogenic fusions and higher TMB levels, suggesting possibilities for other therapeutic choices.
Tumor Mutational Burden
|
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) • NRAS (Neuroblastoma RAS viral oncogene homolog) • FGFR3 (Fibroblast growth factor receptor 3) • MAP2K1 (Mitogen-activated protein kinase kinase 1) • NRG1 (Neuregulin 1) • TACC3 (Transforming acidic coiled-coil containing protein 3) • ETV6 (ETS Variant Transcription Factor 6) • EWSR1 (EWS RNA Binding Protein 1) • IKZF3 (IKAROS Family Zinc Finger 3) • TGFBR2 (Transforming Growth Factor Beta Receptor 2) • GRB7 (Growth Factor Receptor Bound Protein 7) • TCF7L2 (Transcription Factor 7 Like 2) • TPM4 (Tropomyosin 4) • PAX7 (Paired Box 7)
|
TP53 mutation • BRAF V600E • KRAS mutation • TMB-H • PIK3CA mutation • BRAF V600 • MET amplification • KRAS G12D • ALK fusion • NRAS Q61K • NRAS Q61 • KRAS Q61H • NRAS G12D • FGFR3 fusion • NRAS G13 • MAP2K1 K57T • FGFR3 amplification • KRAS Q61K
|
Krazati (adagrasib)
over2years
Application of Bladder Cancer Patient-Derived Organoids as Pre-Clinical Model for Personalized Medicine (AUA 2022)
Surprisingly, a significant response to SOC (cisplatin alone or in combination with gemcitabine) was observed in 8 out of 17 analyzed samples and the non-SOC drugs were effective in few samples...For example, Docetaxel sensitivity was associated to copy number gain in TUBB1 and MIBC organoids were significantly more sensitive to a low dose of cisplatin than NMIBC organoids...Conclusions : To conclude, the genetic and phenotypic profiles of PDOs and parental tumor were very similar, supporting that PDOs are preserving tumor heterogeneity and are therefore a good model of BLCa. This indicates that PDOs can represent a tool to predict drug sensitivity in a personalized manner.
Preclinical • Tumor Mutational Burden
|
TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • FGFR3 (Fibroblast growth factor receptor 3) • TUBB1 (Tubulin Beta 1 Class VI)
|
TP53 mutation • FGFR3 amplification • TP53 amplification
|
cisplatin • gemcitabine • docetaxel
almost3years
Targeted therapies: Expanding the role of FGFR3 inhibition in urothelial carcinoma. (PubMed, Urol Oncol)
At current, erdafitinib, an inhibitor of FGFR1-4, is the only approved targeted therapy in metastatic UC following the BLC2001 study, which demonstrated a 49% overall response rate in patients with UC harboring an FGFR3 mutation. Additional FGFR-directed agents also continue to be investigated across multiple disease stages in FGFR-mutated UC including infigratinib, rogaratinib, and AZD4547, among others. Ongoing trials are combining these agents with immune checkpoint inhibitors and chemotherapy regimens. The precision medicine revolution has begun in UC, and FGFR3 inhibitors are leading the charge toward a more personalized, biomarker-driven treatment paradigm.
Review • Journal • IO biomarker
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FGFR3 (Fibroblast growth factor receptor 3)
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FGFR3 mutation • FGFR3 amplification
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Balversa (erdafitinib) • Truseltiq (infigratinib) • fexagratinib (ABSK091) • rogaratinib (BAY 1163877)
3years
Genomic characterization of non-schistosomiasis-related squamous cell carcinoma of the urinary bladder: A retrospective exploratory study. (PubMed, PLoS One)
NSR-SCCUB has potentially actionable genomic alterations with anticancer agents and many of these aberrations are also seen in UC. The recruitment of NSR-SCCUB patients harboring such mutations should be considered in biomarker driven urinary bladder cancer studies.
Journal • Retrospective data
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • PTEN (Phosphatase and tensin homolog) • FGFR3 (Fibroblast growth factor receptor 3) • CCND1 (Cyclin D1) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • CREBBP (CREB binding protein)
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CCND1 amplification • FGFR3 amplification
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Oncomine™ Comprehensive Assay v3M
3years
Oncocytic renal neoplasms with diffuse keratin 7 immunohistochemistry harbor frequent alterations in the mammalian target of rapamycin pathway. (PubMed, Mod Pathol)
At a median follow-up of 68 months (2-147 months) for 15 patients, all were alive without disease. Oncocytic renal tumors with diffuse keratin 7 labeling show frequent alterations in the TSC/MTOR pathway, despite more oncocytoma-like morphology than initially described in LOT, likely expanding the morphologic spectrum of the latter.
Journal
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MET (MET proto-oncogene, receptor tyrosine kinase) • PTEN (Phosphatase and tensin homolog) • FGFR3 (Fibroblast growth factor receptor 3) • STK11 (Serine/threonine kinase 11) • CDH1 (Cadherin 1) • TSC2 (TSC complex subunit 2) • TSC1 (TSC complex subunit 1) • EPCAM (Epithelial cell adhesion molecule) • KRT7 (Keratin-7) • FOXP1 (Forkhead Box P1) • MME (Membrane Metalloendopeptidase) • PAX8 (Paired box 8)
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MET amplification • STK11 mutation • TSC1 mutation • TSC2 mutation • MTOR mutation • FGFR3 amplification • TSC1 deletion • PAX8 positive • TSC1 deletion
3years
High FGFR1-4 mRNA expression levels correlate with response to selective FGFR inhibitors in breast cancer. (PubMed, Clin Cancer Res)
Tailored therapy with FGFRi in molecularly-selected metastatic BC based on high FGFR1-4 mRNA levels warrants prospective validation in luminal BC CDK4/6i-resistant patients and in TNBC patients without targeted therapeutic options.
Journal
|
FGFR1 (Fibroblast growth factor receptor 1) • CD31 (Platelet and endothelial cell adhesion molecule 1)
|
FGFR1 amplification • FGFR1 expression • FGFR3 amplification
3years
Molecular Alterations in Pediatric Low-Grade Gliomas That Led to Death. (PubMed, J Neuropathol Exp Neurol)
This study demonstrates that PLGG that led to death have diverse molecular characteristics. Location and co-occurring molecular alterations with malignant potential can predict poor outcomes.
Clinical • Journal
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EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • PTEN (Phosphatase and tensin homolog) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • NF1 (Neurofibromin 1) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • KIAA1549 • CDKN2C (Cyclin Dependent Kinase Inhibitor 2C) • TACC1 (Transforming Acidic Coiled-Coil Containing Protein 1)
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BRAF V600E • EGFR mutation • BRAF V600 • FGFR1 amplification • NF1 mutation • IDH1 R132H • FGFR1 fusion • FGFR3 fusion • FGFR3 amplification • FGFR1-TACC1 fusion
over3years
[VIRTUAL] The Characteristics of FGFR Genetic Aberrations in Chinese Lung Cancer Patients (IASLC-WCLC 2021)
Frequency of FGFR fusions Fusions Fusion region N (%) FGFR3-TACC3 EX18E:EX11 3(7.14%) EX17:EX8 3(7.14%) EX17:EX10 2(4.76%) EX18E:EX13 1(2.38%) EX8:EX9 1(2.38%) FGFR3-LETM1 EX8:Promoter 1(2.38%) FGFR3-SZT2 EX7:EX61 1(2.38%) FGFR3-PCDH7(intergenic) EX8:intergenic 1(2.38%) FAM53A(intergenic)-FGFR3 intergenic:EX18E,intergenic:EX8 2(4.76%) FGFR3-chr20 55284041 EX18E:chr20 55284041 1(2.38%) FGFR2-FAM184B EX17:EX8 1(2.38%) FGFR2-GRK5 EX17:EX1 1(2.38%) FGFR2-SORBS1 EX17:EX24 1(2.38%) FGFR2-PROM1 EX18:EX11 1(2.38%) FGFR2-chr10 122732846 EX17:chr10 122732846 1(2.38%) FGFR2-NPVF(intergenic) EX14:intergenic 1(2.38%) OPALIN-FGFR2 EX6E:EX2 1(2.38%) ATE1-FGFR2 EX11:EX2,EX5:EX17 2(4.76%) chr10 123156582-FGFR2 chr10 123156582:EX18 1(2.38%) DEC1(intergenic)-FGFR2 intergenic:EX6 1(2.38%) FGFR1-TACC1 EX1:EX2 1(2.38%) FGFR1-STAU1 EX1:EX7 1(2.38%) FGFR1-LETM2 EX12:EX8 1(2.38%) FGFR1-KCNU1(intergenic) EX3:intergenic 1(2.38%) FGFR1-SLC22A23 EX13:EX10 1(2.38%) FGFR1-ISL1(intergenic) EX8:intergenic,EX4:intergenic 2(4.76%) DDHD2-FGFR1 EX5:EX2 1(2.38%) ZMAT4-FGFR1 EX2:EX2 1(2.38%) HELZ-FGFR1 EX33E:EX6 1(2.38%) chr8 76149982-FGFR1 EX0:EX2 1(2.38%) chr8 138590655-FGFR1 EX0:EX2 1(2.38%) UNC5D(intergenic)-FGFR1 intergenic:EX2 1(2.38%) LOC100996508-FGFR1 EX1:EX2 1(2.38%) TACC1(intergenic)-FGFR1 intergenic:EX2 1(2.38%) Total 42(100%) Conclusion We report the prevalence of FGFR aberrations in a large lung cancer pts, including mutations, gene amplifications, gene deletion and one novel FGFR fusion. Our results revealed the potential therapeutic strategies with FGFR inhibitors for Chinese patients with lung cancer.
Clinical
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ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • FGFR2 (Fibroblast growth factor receptor 2) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • FGFR (Fibroblast Growth Factor Receptor) • TACC3 (Transforming acidic coiled-coil containing protein 3) • FGFR4 (Fibroblast growth factor receptor 4) • SORBS1 (Sorbin And SH3 Domain Containing 1)
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MET amplification • EGFR overexpression • FGFR1 amplification • FGFR2 mutation • FGFR2 fusion • ALK fusion • FGFR mutation • ALK mutation • RET mutation • ROS1 fusion • FGFR fusion • MET mutation • FGFR2 overexpression • FGFR1 fusion • FGFR2 expression • FGFR3 amplification • ALK-ROS1 fusion
over3years
[VIRTUAL] Bladder Cancer: Patient-Derived Organoids as a Tool for Precision Medicine (AUA 2021)
Interestingly, we observed a significant response to SOC (cisplatin in combination with gemcitabine) only in 4 out of 14 cases. In conclusion, our data support that PDOs are a reliable in vitro model of BLCa heterogeneity. The general low sensitivity to SOC observed in our PDOs highlights the need for novel therapies and the high genomic concordance between PT and derived organoids supports the use of organoids as a tool for this purpose.
Clinical • Tumor Mutational Burden
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HER-2 (Human epidermal growth factor receptor 2) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • FGFR3 (Fibroblast growth factor receptor 3) • RB1 (RB Transcriptional Corepressor 1) • CD44 (CD44 Molecule) • TP63 (Tumor protein 63) • GATA3 (GATA binding protein 3)
|
TP53 mutation • HER-2 amplification • FGFR3 amplification
|
cisplatin • gemcitabine
over3years
[VIRTUAL] Final results of APOLLO study: Overall survival (OS) of aumolertinib in patients with pretreated EGFR T790M-positive locally advanced or metastatic non-small cell lung cancer (NSCLC) (ESMO 2021)
Clinical benefit in OS was observed in pts with pretreated EGFR T790M-positive advanced NSCLC receiving aumolertinib. The common mechanisms of resistance to aumolertinib were EGFR C797S mutation and aberrations in bypass tracks.
Clinical
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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) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • FGFR3 (Fibroblast growth factor receptor 3) • JAK2 (Janus kinase 2) • TACC3 (Transforming acidic coiled-coil containing protein 3)
|
KRAS mutation • EGFR mutation • BRAF mutation • HER-2 amplification • PIK3CA mutation • EGFR T790M • FGFR3-TACC3 fusion • EGFR C797S • FGFR3 fusion • EGFR L718Q • FGFR3 amplification
|
Ameile (aumolertinib)
over3years
FGFR3 overexpression is a useful detection tool for FGFR3 fusions and sequence variations in glioma. (PubMed, Neurooncol Pract)
FGFR3 IHC is a useful screening tool for the detection of FGFR3 alterations and could be included in the workflow for isocitrate dehydrogenase (IDH) wild-type glioma diagnostics. Samples with positive FGFR3 staining could then be selected for NGS-based diagnostic tools.
Journal
|
FGFR3 (Fibroblast growth factor receptor 3) • TACC3 (Transforming acidic coiled-coil containing protein 3)
|
FGFR3-TACC3 fusion • FGFR3 mutation • FGFR3 overexpression • FGFR3 fusion • FGFR3 amplification • FGF3 overexpression • FGFR3 positive
almost4years
Fibroblast growth factor receptor (FGFR) gene: pathogenesis and treatment implications in urothelial carcinoma of the bladder. (PubMed, J Clin Pathol)
In April 2020, the Food and Drug Administration (FDA) approved the first targeted FGFR therapy, erdafitinib, in patients with locally advanced or metastatic bladder cancer who have progressed on platinum-based chemotherapy. Herein, we reviewed the normal structure and function of FGFR We also explored its role in the development of urothelial carcinoma and major developments in the FGFR-targeted therapy.
Journal
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FGFR3 (Fibroblast growth factor receptor 3) • HRAS (Harvey rat sarcoma viral oncogene homolog) • FGFR (Fibroblast Growth Factor Receptor)
|
FGFR3 mutation • FGFR mutation • HRAS mutation • FGFR3 fusion • FGFR3 amplification
|
Balversa (erdafitinib)
almost4years
[VIRTUAL] Impact of FGFR2/3 activating genomic alterations on response to enfortumab vedotin in metastatic urothelial carcinoma (mUC). (ASCO-GU 2021)
Background: Enfortumab Vedotin (EV), an antibody-drug conjugate that targets nectin-4, is approved for metastatic urothelial carcinoma (mUC) progressing post-platinum and PD1/L1 inhibitor therapy. In this multi-center retrospective cohort, FGFR2/3 activating genomic alterations did not appear to compromise response to EV in mUC. Larger studies are required to confirm our findings and optimal sequencing of EV and erdafitinib in mUC pts with FGFR2/3 genomic alterations requires further assessment.
PD(L)-1 Biomarker • IO biomarker
|
FGFR2 (Fibroblast growth factor receptor 2) • FGFR3 (Fibroblast growth factor receptor 3)
|
FGFR2 mutation • FGFR3 mutation • FGFR3 S249C • FGFR3 Y373C • FGFR3 amplification
|
Balversa (erdafitinib) • Padcev (enfortumab vedotin-ejfv)
almost4years
Role of Fibroblast Growth Factors Receptors (FGFRs) in Brain Tumors, Focus on Astrocytoma and Glioblastoma. (PubMed, Cancers (Basel))
Furthermore, the discovery of FGFR inhibitors revealed how these biological compounds improve the neoplastic condition by demonstrating efficacy and safety. On this basis, this review focuses on the role and involvement of FGFRs in brain tumors such as astrocytoma and glioblastoma.
Review • Journal
|
FGFR2 (Fibroblast growth factor receptor 2) • FGFR3 (Fibroblast growth factor receptor 3) • FGFR1 (Fibroblast growth factor receptor 1) • FGFR4 (Fibroblast growth factor receptor 4)
|
FGFR2 mutation • FGFR1 mutation • FGFR3 amplification
|
Lytgobi (futibatinib) • fisogatinib (BLU-554)