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Validation Study

Cohort 1: Pathogenic Variant Concordance Study

Pre-registered validation study with binary acceptance criteria. Twenty clinical cases with known pathogenic or likely pathogenic variants evaluated against an established clinical reference laboratory.

Study specification

DocumentHEL-VAL-C1-2026-001 v1.0
Study typePre-registered validation study
PeriodFebruary - March 2026
Classifier versionv3.6.4 (final)
Reference comparatorEstablished clinical reference laboratory
Sample size20 cases
Clinical domains11 (rare disease, oncology, cardiology, neurology, metabolic, ophthalmology, nephrology, neuromuscular, hearing, syndromic, reproductive)
Variant types6 (missense, nonsense, frameshift, splice, compound heterozygous, multi-gene carrier)
Zygosity coverage3 (heterozygous, homozygous, compound heterozygous)
Acceptance thresholdat least 18/20 (90%) for all primary criteria
Standards appliedISO 15189:2022, EU IVDR (2017/746), AMP/CAP 2018, ACMG/AMP 2015

Results against pre-registered acceptance criteria

MetricResult
P1 - Variant detection20/20 (100%)
P2 - Gene assignment20/20 (100%)
P3 - ACMG concordance (FULL)14/20 (70%)
P3 - ACMG concordance (CLINICAL, one-tier P/LP)6/20 (30%)
P3 - PARTIAL or DISCORDANT0/20 (0%)
P3 - Overall (FULL + CLINICAL)20/20 (100%)
S1 - HGVS notation match20/20 (100%)
S2 - Consequence match20/20 (100%)
S3 - Zygosity match20/20 (100%)
All primary criteria met20/20 (100%)

Validation decision: GO

All 20 cases (100%) met all three primary concordance criteria (variant detection, gene assignment, ACMG concordance), exceeding the pre-defined GO threshold of 90% (>= 18/20). No PARTIAL or DISCORDANT results were observed. The six CLINICAL (one-tier P/LP) differences are within the expected range of inter-laboratory ACMG classification variability as documented in the peer-reviewed literature (Amendola 2016, Harrison 2017). The six CLINICAL differences fall in two patterns: cases where Helena applied more conservative ClinGen SVI 2023 thresholds (SpliceAI < 0.2 for PP3_splice), and cases where Helena applied ClinVar 2-star+ override or VCEP gene-specific rules to elevate Likely Pathogenic to Pathogenic.

The validation process additionally identified and resolved four classifier defects through iterative improvement (v3.6.0 to v3.6.4). The most significant was the systematic autosomal recessive loss-of-function gene curation expansion (approximately 150 genes with Definitive or Strong ClinGen Gene-Disease Validity for biallelic LoF disease mechanism), which prevents PVS1 misclassification of loss-of-function variants in autosomal recessive disease genes whose population constraint metrics are statistically underpowered.