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KDR
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Interpretation 2294
Tier 2
KDR
Variants
KDR K270N
Primary Sites
Colon
Tumor Types
Adenocarcinoma
Interpretation

KDR encodes the protein VEGF2, a receptor tyrosine kinase that regulates angiogenesis and vascular development. While KDR mutations are rare, amplification or protein overexpression have been reported in small proportion of a variety of solid tumors. It is unclear if KDR mutation plays a role in colorectal carcinoma pathogenesis; however, it may have a role in clinical outcome prediction and therapeutic response. For example, increased expression of VEGFA, FLT1, and KDR in colorectal carcinoma is associated with a poor prognosis and lack of response to bevacizumab therapy. Although the functional consequence of KDR K270N has not been characterized, it has been reported previously as a somatic variant in in colorectal carcinomas. These results should be interpreted in the clinical context. Most therapies blocking KDR signaling target the angiogenesis pathway in general, such as bevacizumab, an antibody that targets VEGF-A.

Citations
  1. Slattery ML, Lundgreen A, Wolff RK. VEGFA, FLT1, KDR and colorectal cancer: assessment of disease risk, tumor molecular phenotype, and survival. Mol Carcinog. 2014 Feb;53 Suppl 1:E140-50.
  2. Smith NR, et al. Vascular endothelial growth factor receptors VEGFR-2 and VEGFR-3 are localized primarily to the vasculature in human primary solid cancers. Clin Cancer Res. 2010 Jul 15;16(14):3548-61.
  3. Zhang SD, McCrudden CM, Meng C, Lin Y, Kwok HF. The significance of combining VEGFA, FLT1, and KDR expressions in colon cancer patient prognosis and predicting response to bevacizumab. Onco Targets Ther. 2015 Apr 15;8:835-43.
Last updated: 2019-01-22 18:32:41 UTC
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When using PMKB, please cite: Huang et al., JAMIA 2017


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