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BIOMARKER:

KDR amplification

i
Other names: KDR, CD309, FLK1, VEGFR, VEGFR2, Kinase insert domain receptor (a type III receptor tyrosine kinase)
Entrez ID:
Related biomarkers:
Associations
Trials
11ms
Druggable genomic landscapes of high-grade gliomas. (PubMed, Front Med (Lausanne))
Among the JH MTB cohort of patients with IDH1 wild-type high-grade gliomas who received targeted therapies, trametinib monotherapy or in combination with dabrafenib conferred radiographic partial response in 75% of patients harboring BRAF or NF1 actionable mutations...While multiple host, tumor and drug-related features may limit the delivery and efficacy of targeted therapies for patients with high-grade gliomas, genotype-matched targeted therapies confer favorable clinical outcomes. Further studies are needed to generate more data on the impact of biochemical features of targeted therapies on their clinical efficacy for high-grade gliomas.
Journal
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BRAF (B-raf proto-oncogene) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • NF1 (Neurofibromin 1) • KDR (Kinase insert domain receptor)
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BRAF mutation • NF1 mutation • IDH wild-type • KDR amplification • KDR amplification
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Mekinist (trametinib) • Tafinlar (dabrafenib) • Cabometyx (cabozantinib tablet)
1year
PDGFRA, KIT, and KDR Gene Amplification in Glioblastoma: Heterogeneity and Clinical Significance. (PubMed, Neuromolecular Med)
FISH proved effective for detailed interpretation of molecular heterogeneity. The study uncovered an even more diverse range of amplification patterns involving the 4q12 oncogenes in GBM than previously described, thus highlighting a complex tumoral heterogeneity to be considered when devising more effective therapies.
Journal
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PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • KDR (Kinase insert domain receptor)
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KDR amplification
1year
PRIMARY CARDIAC ANGIOSARCOMA- GENOMIC AND MOLECULAR LANDSCAPE (CTOS 2023)
Our results highlight the presence of KDR mutations in primary CAS that have been reported predominantly in primary breast AS in previous studies. Primary CAS is characterized by POT1 mutations, which have previously been reported only in CAS in Li-Fraumeni like families. We are limited by the small number of samples with RNAseq data to derive inferences about the immune profile of CAS, which is also confounded by chemotherapy administered to the patients prior to surgical resection.
Tumor mutational burden
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TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • NOTCH1 (Notch 1) • KDR (Kinase insert domain receptor) • POT1 (Protection of telomeres 1) • RECQL (RecQ Like Helicase) • ZFHX4 (Zinc Finger Homeobox 4)
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POT1 mutation • KDR mutation • KDR amplification
over1year
Association between hepatic angiosarcoma and end-stage renal disease: nationwide population-based evidence and enriched mutational signature of aristolochic acid exposure. (PubMed, J Pathol)
In summary, a significant proportion of HAS in Taiwan is associated with ESRD and harbors a distinctive mutational signature, which concomitantly links nephrotoxicity and mutagenesis resulting from the exposure to aristolochic acid or related compounds. High TMB may support the eligibility for immunotherapy in treating ESRD-associated HAS.
Journal • Tumor mutational burden • IO biomarker
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TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • KDR (Kinase insert domain receptor) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • ATRX (ATRX Chromatin Remodeler)
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TMB-H • CDKN2A deletion • ATRX mutation • KDR mutation • KDR amplification • KDR amplification
over3years
The role of RB1 alteration and 4q12 amplification in IDH-WT glioblastoma. (PubMed, Neurooncol Adv)
Meanwhile, 4q12 amplification (KDR/PDGFRA/KIT) denoted patients with worse OS. Identifying subgroups of GBM IDH-WT with distinct survival is important for optimal clinical trial design, incorporation of targeted therapies, and personalized neuro-oncological care.
Journal
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • RB1 (RB Transcriptional Corepressor 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • KDR (Kinase insert domain receptor) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase)
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TP53 mutation • EGFR mutation • RB1 mutation • SETD2 mutation • KDR amplification • KDR amplification
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MSK-IMPACT