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SF3B1:SF3B1
ACMG/AMP
0%
complete
Final classification
VUS
SF3B1
This variant

A specific SF3B1 sequence change was not resolved, so this case could not be linked to variant-specific somatic observations or germline disease database entries.

Transcript
HGVS · transcript:coding
SF3B1
GRCh38
GRCh37
gene-specific framework lacked a usable explicit final combination framework, so generic ACMG/AMP 2015 final-combination rules were applied as fallback; applied criteria: none; combination = no applied criteria, which maps to VUS.
Classification rationale
VUS
SF3B1

A specific SF3B1 sequence change was not resolved, so this case could not be linked to variant-specific somatic observations or germline disease database entries. Population evidence could not be assessed because no genomic coordinates or allele frequency data were available for comparison with ACMG/AMP frequency thresholds. No variant-specific functional studies were identified, and generic PVS1 could not be applied because both the exact variant consequence and gene-level loss-of-function eligibility remained unresolved.1 In silico evidence could not be assessed because no resolvable variant was available for SpliceAI, REVEL, BayesDel, or same-residue PM5 comparison.2

1 pvs1_gene_contextpvs1_variant_assessmentpvs1_generic_framework ↗
2 pm5_candidates
LYFE Sciences is an AI system, and it can make mistakes. Criteria may be applied incorrectly, sources may be misread, and a confident-looking classification can still be wrong. Double-check every criterion and its underlying evidence before relying on any call.
Applied criteria · 0 applied · 28 assessed
MetEvidence satisfies this criterion.
Not metEvaluated against available evidence; threshold not reached.
Not assessedApplies in principle, but no evidence was found to evaluate it.
N/ADoesn't apply to this variant type.
Applied · 0

No criteria were applied for this variant.

Assessed · not applied · 0 not met · 28 not assessed
Pathogenic
PVS1 A specific sequence change, variant class, and transcript consequence were not resolved, and germline loss-of-function eligibility for this gene was not established.
PS1 No specific nucleotide change or protein consequence was resolved, so it was not possible to determine whether this variant creates the same amino acid change as a previously established pathogenic variant.
PS2 No de novo data were identified for a specific variant, and no family-based confirmation could be evaluated.
PS3 No variant-specific functional studies were identified because a specific sequence change was not resolved and no relevant PMID-backed functional literature was retrieved.
PS4 No variant-specific case enrichment or case-control data could be evaluated because a specific variant was not resolved.
PM1 No amino acid position or protein domain could be assigned, so it was not possible to determine whether this variant lies in a critical region or mutational hot spot without benign variation.
PM2 No genomic coordinates were resolved, so no gnomAD population frequency was available.
PM3 No phase or trans observations with a pathogenic variant were identified, and no specific variant was available for recessive-case review.
PM4 No in-frame protein length change was established because the variant class and protein consequence were not resolved.
PM5 Classic same-residue PM5 review could not be performed because no missense residue context was resolved, and available comparator harvesting did not confirm safe use of PM5 logic for this case.
PM6 No assumed de novo evidence was identified for a specific variant, so PM6 could not be evaluated.
PP1 No segregation data were identified for a specific variant, so cosegregation with disease could not be assessed.
PP2 No resolved variant class was available, so it was not possible to determine whether this is a missense variant in a gene with low benign missense variation and a common pathogenic missense mechanism.
PP3 No computational predictor results were available because no specific variant coordinates or consequence were resolved.
PP4 No phenotype-specific or molecularly specific disease presentation data were provided for a resolved variant, so PP4 could not be assessed.
PP5 No resolved variant was available for review of reputable-source pathogenic assertions, and this criterion is not used without variant-specific supporting evidence.
Benign
BA1 No gnomAD allele frequency was available because no genomic coordinates were resolved.
BS1 No gnomAD allele frequency was available because no genomic coordinates were resolved.
BS2 No specific variant was resolved, so observation in healthy adult individuals could not be evaluated.
BS3 No well-established functional studies showing a benign effect were identified because a specific variant was not resolved and no relevant PMID-backed functional literature was retrieved.
BS4 No family segregation data were identified for a specific variant, so lack of segregation with disease could not be assessed.
BP1 No resolved variant class was available, so it could not be determined whether this is a missense change in a gene where truncating variants are the predominant established disease mechanism.
BP2 No phase data were identified, so it was not possible to determine whether this variant is observed in trans with a pathogenic variant for a dominant disorder or in cis for any disorder.
BP3 No in-frame deletion or insertion within a repetitive region without known function was established because the variant class and location were not resolved.
BP4 No computational predictor results were available because no specific variant coordinates or consequence were resolved.
BP5 No alternate molecular explanation or resolved variant-specific clinical context was provided, so BP5 could not be assessed.
BP6 No resolved variant was available for review of reputable-source benign assertions, and this criterion is not used without variant-specific supporting evidence.
BP7 No synonymous or intronic variant context was resolved, and no splice prediction data were available, so BP7 could not be assessed.
Research & evidence
Population frequency
v4.1
This variant is absent from gnomAD v4.1.
v2.1
This variant is absent from gnomAD v2.1.
Allele frequency by ancestry
three datasets · side by side
ClinVar No data
No ClinVar submissions were recorded for this variant.
In silico No data
No in-silico prediction was recorded for this variant.
Functional No data
No calibrated functional assay or RNA evidence was identified for this variant.
Somatic evidence
COSMIC
This variant has not previously been reported in somatic cancers (COSMIC).
Hotspots
This variant does not lie in a statistically significant cancer hotspot.
Sources & reference links

No sources recorded.