FLT1是致癌基因，编码蛋白是细胞表面受体，其是血管内皮生长因子（VEGF）途径的成员，其参与细胞存活和肿瘤血管生成的受体酪氨酸激酶。 VEGF配体VEGFA与FLT1的结合激活途径信号传导，其进而调节血管生成，细胞存活，迁移和侵袭。此外，研究表明VEGFA-FLT1复合物激活丝裂原活化蛋白激酶（MAPK）和PI3K / AKT信号传导，因此异常激活促进肿瘤存活。FLT1还可以从缺氧诱导的应激中拯救肿瘤细胞并调节与转移相关的巨噬细胞中的炎症反应基因。在多种肿瘤类型中检测到FLT1的体细胞突变，但突变产生的影响尚不明确。在结直肠癌和非小细胞肺癌等肿瘤类型中发现FLT1的点突变或移码缺失。

FLT1 (also VEGFRA) is a cell surface receptor that is a member of the vascular endothelial growth factor (VEGF) pathway. Binding of the VEGF ligand, VEGFA, to FLT1 activates pathway signaling, which in turn regulates angiogenesis, cell survival, migration and invasion hus aberrant activation promotes tumor survival. FLT1 has also been shown to rescue tumor cells from hypoxia-induced stress and to regulate inflammatory response genes in macrophages associated with metastases. Somatic mutations in FLT1 have been identified in a variety of tumor types, however, the impact of these alterations are not well-studied. FLT1 overexpression and activation have been associated with increased transformation and invasion in colorectal, pancreatic, and breast cancer models.

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