FLT4

Overview

FLT4 (also known as VEGFR3) encodes vascular endothelial growth factor receptor 3, a receptor tyrosine kinase involved in VEGF/VEGFR signaling and the stress-activated MAPK cascade. FLT4 is predominantly amplified in radiation-associated angiosarcoma and is enriched compared to sporadic angiosarcoma.

Alterations observed in the corpus

  • Mostly amplification in 16% of RT-ANGS vs 8% of sporadic AS; implicated in stress-activated MAPK cascade and VEGF/VEGFR signaling PMID:37350195.
  • Co-occurs with MYC amplification, CRKL, HRAS, and KMT2D alterations in breast/chest wall RT-AS PMID:37350195.
  • Identified among significantly mutated genes in 188 primary LUAD tumours (TSP cohort); VEGFR-3 receptor tyrosine kinase. PMID:18948947
  • FLT4 (VEGFR3) mutations are among the low-frequency RTK hits identified in advanced thyroid cancers (PDTC/ATC) by MSK-IMPACT 341-gene sequencing (n=117 tumors) PMID:26878173
  • Identified as a novel recurrently mutated gene (1–4% frequency) in microsatellite-stable metastatic colorectal cancer by MSK-IMPACT sequencing of 1,134 colorectal adenocarcinomas PMID:29316426

Cancer types (linked)

  • ANGS — FLT4 amplification enriched in RT-AS (16%) vs sporadic AS (8%); participates in both VEGF/VEGFR signaling and stress-activated MAPK cascade pathways PMID:37350195.

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • FLT4 is part of both the stress-activated MAPK cascade and VEGF/VEGFR signaling pathways identified as potential molecular targets in RT-AS PMID:37350195.

Open questions

Sources

This page was processed by crosslinker on 2026-05-05. - PMID:18948947

This page was processed by crosslinker on 2026-05-05. - PMID:26878173

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