Your immune system can't hear its bacterial warning system properly. Understanding why opens pathways to stop the inflammation before it damages your gut.
Whole genome sequencing reveals the full landscape of genetic susceptibility to inflammatory bowel disease, identifying NOD2 and IL23R variants that predict disease severity and therapeutic response.
Inflammatory Bowel Disease (Crohn's Disease)
Inflammatory bowel disease (IBD) including Crohn's disease (CD) and ulcerative colitis is characterized by chronic intestinal inflammation leading to abdominal pain, diarrhea, blood in stool, weight loss, and potential complications including strictures, fistulas, and colorectal cancer. Prevalence of Crohn's disease is approximately 1 in 1,000 in developed countries, with higher incidence in younger patients (peak onset 15–35 years). Genetic contribution is substantial: heritability is estimated at 50–80%, and the field has identified more than 200 GWAS loci associated with IBD. The first Crohn's disease susceptibility gene identified was NOD2/CARD15 in 2001, a landmark discovery that opened the field to understanding innate immune dysfunction in CD. NOD2 encodes an intracellular pattern recognition receptor that detects bacterial muramyl dipeptide (MDP), triggering NF-κB signaling and inflammatory response. Three common NOD2 variants (R702W, G908R, 1007fs) account for approximately 15–20% of population attributable risk in European ancestry CD patients.
Homozygous or compound heterozygous NOD2 variants confer approximately 20–40-fold increased Crohn's disease risk compared to non-carriers. NOD2 loss-of-function variants impair MDP sensing and reduce inflammatory responses to bacteria, paradoxically increasing disease risk through failure of appropriate bacterial containment and dysbiotic expansion of pathogenic flora. This counterintuitive mechanism—why would reduced immune response cause inflammation?—is now understood in the context of dysbiosis and barrier dysfunction. IL23R encodes interleukin-23 receptor, involved in Th17 lineage differentiation; the protective variant rs11209026 (R381Q) actually reduces Th17 polarization, suggesting IL-23/Th17 axis hyperactivation drives IBD. This discovery led directly to therapeutic development: IL-23 pathway inhibitors (ustekinumab, risankizumab, guselkumab) are now approved for CD and UC, producing dramatic clinical responses in subgroups of patients.
NOD2 genotyping provides prognostic insight into disease course: homozygous NOD2 carriers typically develop earlier-onset disease, more extensive colonic involvement, and higher rates of complications including strictures and fistulas. IL23R protective variant carriers predict better response to IL-23 inhibitors, suggesting that future pharmacogenomic prediction could guide therapy selection. Genetic understanding of IBD has principally driven drug development rather than altering individual patient management; the landmark discovery that IL23R variants were protective led directly to ustekinumab, risankizumab, and guselkumab—now approved therapies that benefit the broader IBD population. Understanding the genetic basis of IBD is shifting clinical perspective from viewing it as primarily a gastrointestinal disorder to recognizing its deep immunological underpinnings.
Genetic testing is not standard for IBD diagnosis. Genome Test captures all 200+ GWAS loci for comprehensive genetic risk profiling.
IBD involves 200+ genetic loci, each with small individual effect
Genetic contribution to IBD is distributed across more than 200 GWAS loci, each with small individual effect sizes. Standard genetic panels do not test for this polygenic architecture. NOD2 genotyping is sometimes performed for prognostic assessment but is not routine in IBD diagnosis, which relies on endoscopy, histology, and radiography. Genetic testing does not replace clinical diagnosis. However, whole genome sequencing provides the comprehensive GWAS variant data necessary for future polygenic risk score calculation—enabling individualized genetic risk assessment that may eventually guide therapy intensity, predict disease severity, and inform family screening.
NOD2 variants predict disease course and therapeutic opportunity
NOD2 genotyping identifies high-risk patients destined for early-onset, extensive disease with complications. These patients benefit from more aggressive upfront therapy and closer surveillance for stricture and fistula formation. IL23R genetic variants identify patients likely to respond to IL-23 inhibitors—ustekinumab, risankizumab, and guselkumab are now approved for CD and produce dramatic responses in genetically susceptible subgroups. A comprehensive genetic assessment through Genome Test establishes a baseline for future clinical utility: as polygenic risk models mature and are clinically validated, patients with genetic data on file can benefit from new therapeutic recommendations based on their individual genetic profile.
Your full DNA (not just a part of it)
Traditional genetic testing looks at narrow sets of genes, missing most parts of your genome. We sequence your full genome — every gene and every region between genes.
Comprehensive insights and specialized reports
Easy to read and with answers you and your doctor can act on. Not a file to interpret — 200+ clinical reports, organized by category.
Your test becomes more valuable every year
Your DNA does not change, but genome science is accelerating. Every month, new variant-disease associations are discovered. We validate these findings and update your reports automatically. Your test becomes more valuable every year.
The results doctors bring to their hardest cases.
Forty years of uncertainty. One test.
A patient had spent decades in the UK healthcare system without a diagnosis. Dante data, accepted by NHS clinical teams at Queen Elizabeth University Hospital Glasgow, identified Noonan Syndrome and a RUNX1 leukemia-associated variant that had gone undetected. After 40 years, they finally had an answer.
A complete read delivers a complete picture.
A patient came to Dante to investigate periodic paralysis. Reading the complete genome identified a concurrent hereditary cardiac finding — Brugada syndrome — that their doctor confirmed with an ECG. The result also explained a family member's unresolved cardiac history. One test. Every answer in it.
Sequenced in 2019. The data worked in 2021.
Jennifer sequenced her genome with Dante two years before her breast cancer diagnosis. When treatment began, Dante's pharmacogenomics data showed her prescribed chemotherapy would cause serious adverse effects. Her doctor selected an alternative — and she started effective treatment from day one.
Every genetic question deserves a complete answer.
Whether you are searching for answers today or protecting your health for tomorrow, a complete read of your entire genome is the only place to start.
It runs in your family. Now you can know if it runs in your genes.
Your genome contains inherited variants associated with medical conditions like cardiac, cancer, and neurological. We read all of them — with the clinical depth to give the result meaning.
Learn more →When traditional lab tests say you're fine. And you know you're not.
Standard diagnostic tests check for a pre-selected set of answers. We sequence your full DNA — including parts that no test was designed to check. If the answer is in your genome, we will help you find it.
Learn more →Your diagnosis may be right. Your treatment plan may be incomplete.
Your genes determine which treatments are most likely to work — and which are not. We give your doctor the tools and insights to inform your treatment plan.
Learn more →You want to know before something forces the question.
Some people don't wait for a diagnosis or a family history to act. Whole genome sequencing gives you the complete genetic picture now — so you and your doctor can make informed decisions before anything becomes urgent.
Learn more →You already took a DNA test. Here's what it couldn't tell you.
Most consumer DNA tests read less than 0.1% of your genome. We read all of it.
Learn more →Clinical-grade results. Chosen by individuals, trusted by doctors for their most complex cases.
Dante Genome Test helped specialists at a UK national acute hospital in the identification of Noonan Syndrome and a rare leukemia-associated genetic variant that had gone undetected. That result changed the medical care of the patient.
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Common questions about whole genome sequencing.
What is the difference between whole genome sequencing and a targeted genetic test?
Targeted genetic tests — including standard hereditary cancer panels — read a pre-defined list of known variants in a specific set of genes. They are designed to find what they already know to look for. Whole genome sequencing reads your entire genome: all 6 billion base pairs, every gene, every region between genes. A Mayo Clinic study published in JAMA Oncology found that standard testing guidelines missed more than half of patients with inherited cancer mutations. Genome Test does not have a fixed list.
What will I receive when my results are ready?
Your Dante Genome delivers 200+ physician-ready reports organized by clinical category — hereditary cancer, cardiac conditions, rare diseases, pharmacogenomics, carrier status, and more. Reports are delivered to your secure Genome Manager and are formatted for direct clinical use. Your genome data is permanently retained and re-analyzed automatically as science advances.
What happens if a clinically significant variant is found?
If a pathogenic or likely-pathogenic variant is identified, it will be clearly flagged in your physician-ready report with clinical context, published evidence, and recommended next steps. We recommend sharing any clinically significant finding with your physician or a genetic counselor, who can guide decisions about surveillance, risk reduction, or cascade testing for family members.
How is this different from a consumer DNA test like 23andMe or AncestryDNA?
Consumer DNA tests use genotyping chips that read less than 0.1% of your genome — a tiny pre-selected set of common variants. They are optimized for ancestry and population-level traits, not clinical genetic findings. The Dante Genome Test sequences 100% of your genome at 30X coverage, the same standard used in clinical diagnostic settings. The two tests are not comparable in scope, methodology, or clinical utility.
How long does it take to get results, and how are they delivered?
Your collection kit ships within 48 hours of ordering. Once your sample arrives at our CLIA-certified laboratory, sequencing and analysis takes 6–8 weeks. Results are delivered securely to your Genome Manager, where you can access your reports, share them with your physician, and receive automatic updates as new findings are validated against your genome.
We work with patient advocacy groups worldwide.
Dante Labs works with patient advocacy groups of any size — for Inflammatory Bowel Disease (Crohn's Disease) and other conditions, rare and common. We support groups in any country, including virtual patient advocacy groups.
We can provide customized reports, group discounts, and packages tailored for your members. Please reach out using the form and we'll be in touch within two business days.
- Custom genomic reports for your members
- Group discounts and tailored packages
- Any country — including virtual groups
- Rare and common conditions covered
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We’ll be in touch within 2 business days. To follow up directly: hello@dantelabs.com
One test.
A lifetime of answers.
One kit, sent to your home. Your entire genome sequenced at the clinical standard used for diagnostic decisions. 200+ physician-ready reports delivered to your Genome Manager in 6–8 weeks — permanent and updated as science advances.
Ships within 48 hours · Results in 6–8 weeks
