A thyroid nodule. Elevated calcium. A family pattern that keeps recurring across generations. The specific RET or MEN1 variant determines not just the diagnosis — but the clinical timeline.
Whole genome sequencing identifies MEN1 and RET variants that enable codon-specific risk stratification and direct surgical timing — turning genetic information into lifesaving clinical decisions.
Multiple Endocrine Neoplasia (MEN1/MEN2)
Multiple Endocrine Neoplasia comprises two genetically and clinically distinct syndromes. MEN1 is caused by pathogenic variants in MEN1, encoding menin — a nuclear scaffold protein involved in transcriptional regulation, DNA repair, and chromatin remodeling. MEN1 functions as a tumor suppressor with no identifiable mutation hotspots; over 1,300 pathogenic variants are distributed across the entire coding region. MEN2 is caused by gain-of-function pathogenic variants in RET, a receptor tyrosine kinase involved in cell growth signaling. Unlike MEN1, RET variants constitutively activate kinase function, driving uncontrolled cell proliferation. MEN2 variants cluster in specific exons (10, 11, 13–16), with strong genotype-phenotype correlation.
MEN1 affects approximately 1 in 30,000 individuals and is characterized by tumors of the parathyroid (~95% of carriers by age 50), anterior pituitary (~40%), and pancreatic islets/duodenum (~40%), plus carcinoid tumors, adrenocortical tumors, and non-endocrine features including facial angiofibromas and meningiomas. MEN2 affects 1 in 30,000–50,000 individuals and includes three subtypes: MEN2A (medullary thyroid carcinoma, pheochromocytoma, parathyroid adenoma), FMTC (familial medullary thyroid carcinoma only), and MEN2B (medullary thyroid carcinoma, pheochromocytoma, mucosal neuromas, marfanoid habitus — the most aggressive form). Penetrance is >90% for both syndromes.
A MEN2/RET diagnosis directly determines surgical decision-making in a way few genetic conditions do. The specific RET codon mutation predicts the aggressiveness of medullary thyroid carcinoma and the earliest age at which prophylactic thyroidectomy should occur: M918T (MEN2B) requires surgery within the first 6 months of life; C634R and other high-risk codons by age 5; moderate-risk mutations may allow delayed surgery with calcitonin surveillance. MEN1 diagnosis triggers lifelong biochemical and imaging surveillance for parathyroid, pituitary, and pancreatic tumors. Both syndromes benefit from cascade testing identifying relatives before tumor development.
MEN1 and MEN2 are distinct syndromes: MEN2 has strong RET codon-phenotype correlation guiding surgical timing; MEN1 has no reliable genotype-phenotype correlation, requiring uniform surveillance across all carriers. This distinction is clinically critical.
MEN1 testing is challenging because pathogenic variants lack mutation hotspots. Standard MEN1-only panels may miss ~10% of clinical cases.
MEN1 and MEN2 require comprehensive gene coverage
MEN1 is particularly challenging to test because pathogenic variants are distributed throughout the entire 20-kb coding region with no identifiable hotspots. Approximately 10% of patients meeting clinical MEN1 criteria have no detectable MEN1 variant — suggesting deep intronic, regulatory, or alternative gene involvement not captured by standard sequencing. Large MEN1 deletions require separate copy number analysis. RET testing is more straightforward due to hotspot clustering, but a panel testing only RET would miss MEN1 entirely — and vice versa. Whole genome sequencing captures complete information for both genes simultaneously.
RET codon determines thyroidectomy timing; MEN1 finding triggers lifelong surveillance
For MEN2/RET carriers, the specific codon mutation directly determines the timing of prophylactic thyroidectomy — the most direct genotype-to-surgical-decision relationship in medicine. M918T (MEN2B) requires thyroidectomy by 6 months of age; high-risk codons like C634R by age 5; moderate-risk mutations by early childhood with calcitonin surveillance. For MEN1 carriers, genetic confirmation triggers lifelong surveillance for parathyroid, pituitary, and pancreatic tumors. Both syndromes benefit from cascade testing — identifying relatives at risk before the first clinical manifestation.
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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.
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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.
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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.
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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 Multiple Endocrine Neoplasia (MEN1/MEN2) 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.
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Ships within 48 hours · Results in 6–8 weeks
