MUTYH-Associated Polyposis — an autosomal recessive hereditary colorectal cancer syndrome that mimics attenuated FAP but requires both parents to be carriers, meaning families with 'no family history' of cancer can still produce affected children.
Whole genome sequencing reads the complete MUTYH gene, identifying both alleles simultaneously — the only way to establish the biallelic genotype that defines MAP and distinguishes it from APC-negative attenuated FAP.
MUTYH-Associated Polyposis
MUTYH-associated polyposis (MAP) is an autosomal recessive hereditary colorectal cancer predisposition syndrome caused by biallelic pathogenic variants in the MUTYH gene on chromosome 1p34.1, which encodes the MutY DNA glycosylase — a base excision repair enzyme that corrects oxidative DNA damage. Unlike FAP and Lynch syndrome, MAP follows recessive inheritance: both copies of MUTYH must be inactivated for full expression of the syndrome. MAP is characterized by adenomatous polyposis (typically 10-100 polyps, occasionally more), colorectal cancer risk approaching 50-80% by age 70 without surveillance, and a lower but elevated risk of duodenal adenomas and cancer, similar to attenuated FAP.
Two common MUTYH missense variants — c.536A>G (p.Tyr179Cys, formerly Y165C) and c.1187G>A (p.Gly396Asp, formerly G382D) — account for approximately 80% of MAP alleles in individuals of Northern European ancestry. These two variants are so prevalent in European populations that MUTYH heterozygosity (single-allele carrier status) is found in approximately 1-2% of the population — a fact that has practical implications for cancer risk counseling. Biallelic carriers (MAP patients) are most commonly compound heterozygotes of these two common variants. However, in non-European populations, a broader and less characterized spectrum of MUTYH variants contributes to MAP, and fixed two-variant panels have substantially reduced sensitivity.
The autosomal recessive inheritance of MAP has critical clinical implications that differ from dominant hereditary cancer syndromes. A parent with MAP is an obligate MUTYH heterozygote who, if partnered with another carrier (prevalence ~1-2%), has a 25% chance of an affected child. Many MAP patients have no family history of colorectal cancer because parents are unaffected heterozygous carriers. This means MAP should be considered in any patient with 10-100 colorectal adenomas even without a family history. Distinguishing MAP from APC-negative attenuated FAP requires detecting both MUTYH alleles — a task that requires complete MUTYH gene sequencing.
Two-variant MUTYH panels miss 20% of disease alleles in Europeans and have poor coverage in non-European populations. Identifying biallelic status requires complete gene sequencing — detecting a single allele is never sufficient to diagnose MAP.
A single MUTYH variant on a panel result tells you almost nothing about MAP risk
Standard polyposis panels test for the two common MUTYH p.Tyr179Cys and p.Gly396Asp variants. A report identifying one of these variants describes a heterozygous carrier — a person with no elevated colorectal cancer risk from MAP alone, unless a second MUTYH allele is also present. The clinical action depends entirely on knowing both alleles. If a patient is compound heterozygous for a common MUTYH variant plus a rare variant not tested on a limited panel, they have MAP and require intensive surveillance or prophylactic colectomy. Whole genome sequencing identifies all MUTYH variants across the entire gene simultaneously, enabling definitive biallelic genotyping in a single test.
Non-European MAP patients carry rare MUTYH variants that two-variant panels systematically miss
The p.Tyr179Cys and p.Gly396Asp variants are common in Northern Europeans but are found at much lower frequencies in other populations. MAP in South Asian, East Asian, Middle Eastern, and African ancestry patients is caused by a diverse range of rare MUTYH variants, many of which are population-specific. A patient of South Asian ancestry with attenuated polyposis who tests negative on a two-variant MUTYH panel may have MAP caused by a rare MUTYH allele not represented on the panel. Only complete MUTYH gene sequencing — as provided by whole genome sequencing — has equivalent sensitivity across all ancestry backgrounds.
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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.
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