What you carry at this position in your DNA and what research says about it.
Blood Vessel Growth: 6/10 evidence, 20 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): T/T
Typical Blood Vessel Growth and Lower Tumor Risk
This genotype is associated with standard receptor activity and typical blood vessel growth. It helps maintain a lower baseline risk for aggressive tumor progression.
What this genotype means: Standard blood vessel growth; Lower risk of aggressive tumor progression; Standard response to anti-angiogenic therapies.
Sample genotype (not yours): A/A
Highest Tumor Angiogenesis and Strongest Drug Response
This genotype is associated with the most active blood vessel growth, presenting a higher risk for tumor progression alongside a highly favorable response to specific cancer drugs.
What this genotype means: Most active blood vessel growth; Highest risk of aggressive tumor progression; Maximum survival benefit from anti-angiogenic therapies.
Sample genotype (not yours): T/A
Elevated Tumor Angiogenesis and Enhanced Drug Response
This genotype is linked to more active blood vessel growth, which can promote tumor progression but also enhances the effectiveness of certain cancer therapies.
What this genotype means: Increased blood vessel growth; Higher risk of aggressive tumor progression; Enhanced survival on anti-angiogenic therapies.
Gene function and biological role
Gene Function: The KDR gene encodes vascular endothelial growth factor receptor 2, a key protein that sits on the surface of endothelial cells lining blood vessels. When vascular endothelial growth factor binds to this receptor, it triggers a cascade of signals that promote the growth of new blood vessels [1]. This process, known as angiogenesis, is vital for wound healing, tissue repair, and cardiovascular health. However, abnormal or excessive angiogenesis can also fuel the growth and spread of tumors by supplying them with oxygen and nutrients [2]. Because of its central role in vessel formation, this receptor is a primary target for anti-angiogenic cancer therapies.
Variant Impact: The rs1870377 variant, also known as Q472H, is a missense mutation in the KDR gene that changes the amino acid glutamine to histidine at position 472 of the receptor protein. This structural change alters the binding efficiency of vascular endothelial growth factor to the receptor, directly influencing downstream signaling and blood vessel growth [3]. The reference T allele is associated with standard receptor activity and typical vessel formation. In contrast, the variant A allele increases receptor activity and promotes more aggressive blood vessel growth, which can influence both tumor progression and cardiovascular risk [2].
Key Insight: The same genetic variant that increases the risk of aggressive tumor growth also makes those tumors significantly more sensitive to modern anti-angiogenic cancer drugs, leading to better survival outcomes during treatment.
Location: KDR. Chromosome 4 · 4q12 · 55.1 Mb
Estimated prevalence by population
Global 64.1%; European 57.5%; African 79.8%; East Asian 28.4%; South Asian 69.0%; Americas 72.4%; Ashkenazi 63.8%; Finnish 48.7%; Middle Eastern 68.9%; Amish 57.0%.
Estimated TT genotype frequency.
Global 31.1%; European 36.7%; African 19.0%; East Asian 49.8%; South Asian 28.1%; Americas 25.4%; Ashkenazi 32.2%; Finnish 42.2%; Middle Eastern 28.2%; Amish 37.0%.
Estimated TA genotype frequency.
Global 4.8%; European 5.9%; African 1.1%; East Asian 21.8%; South Asian 2.9%; Americas 2.2%; Ashkenazi 4.1%; Finnish 9.2%; Middle Eastern 2.9%; Amish 6.0%.
Estimated AA genotype frequency.
Showing effects for T/T genotype
Cancer & Oncology
Cancer Prognosis & Treatment Outcome
Tumor Angiogenesis. Evidence: 3/10. Source: PMID 26081139. Typical Growth.
Pharmacogenomics
Chemotherapy Response
Cancer Drug Response. Evidence: 6/10. Source: PMID 39864574. Typical Response.
Cardiovascular & Metabolic
Lipids & Cholesterol
Blood Lipid Response. Evidence: 3/10. Source: PMID 22507619. Typical Lipids.
Immunity & Inflammation
Autoimmune Diseases
Lupus. Evidence: 3/10. Source: PMID 23111153. Typical Risk.
Showing effects for A/A genotype
Tumor Angiogenesis. Evidence: 3/10. Source: PMID 26081139. Increased Growth.
Cancer Drug Response. Evidence: 6/10. Source: PMID 39864574. Enhanced Response.
Blood Lipid Response. Evidence: 3/10. Source: PMID 22507619. Altered Lipids.
Lupus. Evidence: 3/10. Source: PMID 23111153. Altered Risk.
Showing effects for T/A genotype
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Carrying two copies of the reference T allele results in standard functioning of the vascular endothelial growth factor receptor 2. This typical receptor activity supports balanced blood vessel growth throughout the body, which is protective against abnormal neovascularization. Clinical studies indicate that individuals with this genotype have a lower risk of aggressive tumor behaviors, such as those seen in astrocytomas, because their blood vessels do not over-proliferate to feed abnormal growths [1]. However, if cancer does develop, this standard activity means there is no extra sensitivity to anti-angiogenic therapies like sorafenib or sunitinib, resulting in standard survival rates on these medications [2]. Additionally, this genotype maintains a typical baseline for cardiovascular health and blood lipid levels under normal dietary conditions [3].
Standard blood vessel growth; Lower risk of aggressive tumor progression; Standard response to anti-angiogenic therapies.
Sample genotype: AA (Homozygous)
Carrying two copies of the variant A allele maximizes the signaling activity of the vascular endothelial growth factor receptor 2, driving highly active blood vessel growth. This state of hyper-angiogenesis can support rapid tumor growth and is associated with more aggressive clinical courses in malignancies such as astrocytomas [1]. Despite this risk, the genotype offers a major therapeutic advantage if anti-angiogenic cancer treatment is ever required. Because the tumors are highly reliant on these active receptors, drugs like sorafenib, sunitinib, and bevacizumab are exceptionally effective, leading to significantly prolonged survival times [2]. However, this strong response is accompanied by a higher incidence of cardiovascular side effects, including treatment-induced high blood pressure [3].
Most active blood vessel growth; Highest risk of aggressive tumor progression; Maximum survival benefit from anti-angiogenic therapies.
Sample genotype: TA (Heterozygous)
Carrying one copy of the variant A allele increases the activity of the vascular endothelial growth factor receptor 2, leading to more rapid blood vessel growth. This enhanced angiogenesis can facilitate tumor progression by increasing microvessel density, which has been linked to more aggressive behavior in certain cancers like astrocytomas [1]. On the positive side, this increased receptor activity makes tumors highly dependent on angiogenesis, rendering them significantly more sensitive to anti-angiogenic drugs [2]. Patients with this genotype who undergo treatment with therapies like sorafenib, sunitinib, or bevacizumab often show a higher likelihood of survival [2]. However, this increased sensitivity also elevates the risk of therapy-related side effects, such as high blood pressure and hand-foot syndrome [3].
Increased blood vessel growth; Higher risk of aggressive tumor progression; Enhanced survival on anti-angiogenic therapies.
Variants with shared genetic architecture
rs2071559 · KDR Gene · Chr 4 · Cardiovascular and Eye Health
rs2305948 · KDR Gene · Chr 4 · Stroke and Heart Risk
rs2010963 · VEGFA Gene · Chr 6 · Heart and Eye Health
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com