Genetic Information

Gene & Transcript Details

Gene
BRCA2
Transcript
NM_000059.4 MANE Select
Total Exons
Reference Sequence
NC_000013.10
Alternative Transcripts
IDStatusDetails
NM_000059.4 MANE Select 11954 nt | 200–10456
NM_000059.2 Alternative 11386 nt | 228–10484
NM_000059.3 RefSeq Select 11386 nt | 228–10484

Variant Details

HGVS Notation
NM_000059.4:c.516+1G>A
Protein Change
Splice
Location
Exon 6 (Exon 6 of )
6
5'Exon Structure3'
Functional Consequence
Loss of Function
Alternate Identifiers

Clinical & Population Data

Population Frequency

gnomAD
Global Frequency
0.0 in 100,000
Extremely Rare
ACMG Criteria Applied PM2
This variant is absent or extremely rare in population databases (PM2 criteria applies).

ClinVar

Open
Classification
Pathogenic
1 publications
Publications List
PMID: 12759930

The c.516+1G>A intronic pathogenic mutation results from a G to A substitution one nucleotide after coding exon 5 of the BRCA2 gene. This alteration has been previously detected in multiple individuals in six unrelated Belgian families with breast cancer; RNA studies showed that this alteration led to skipping of multiple exons (Claes K et al. Genes Chromosomes Cancer. 2003 Jul;37:314-20; Claes K et al. Br. J. Cancer. 2004 Mar;90(6):1244-51; Machackova E et al. BMC Cancer. 2008 May;8:140). This alteration has also been detected in 1/313 unselected Chinese breast cancer patients (Li G. et al J. Cancer Res. Clin. Oncol. 2017 Oct;143(10):2011-2024). Of note, this alteration is also designated as IVS6+1G>A in published literature. This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). This nucleotide position is highly conserved in available vertebrate species. In silico splice site analysis predicts that this alteration will weaken the native splice donor site. In addition to the clinical data presented in the literature, alterations that disrupt the canonical splice site are expected to cause aberrant splicing, resulting in an abnormal protein or a transcript that is subject to nonsense-mediated mRNA decay. As such, this alteration is classified as a disease-causing mutation.

PMID: 12759930

This variant is not present in population databases (ExAC no frequency). This variant has been reported in the literature in individuals affected with breast cancer (PMID: 12759930, 28664449). ClinVar contains an entry for this variant (Variation ID: 51786). Experimental studies using patient lymphoblastoid cells have shown that this intronic change leads to multiple alternative transcripts, skipping exons 5, 6, and 5 and 6, resulting in truncated protein products (PMID: 12759930, 18489799). Donor and acceptor splice site variants typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in BRCA2 are known to be pathogenic (PMID: 20104584). For these reasons, this variant has been classified as Pathogenic. This sequence change affects a donor splice site in intron 6 of the BRCA2 gene. It is expected to disrupt RNA splicing and likely results in an absent or disrupted protein product.

Clinical Statement

"This variant has been reported in ClinVar as Pathogenic (5 clinical laboratories)."

COSMIC Somatic Evidence

Open
COSMIC ID
Recurrence
0 occurrences
PM1 Criteria
Not Applied
COSMIC Database Preview
COSMIC Preview
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Functional Impact & Domains

Functional Domain

Hotspot Status
Not a hotspot
Domain Summary
This variant is not located in a mutational hotspot or critical domain.
Related Variants in This Domain
No evidence of other pathogenic variants at this position in gene BRCA2.

Functional Studies & Therapeutic Relevance

Functional Summary

The variant has not been functionally characterized.

Database Previews
OncoKB
OncoKB Preview
JAX-CKB
JAX-CKB Preview

Click on previews to view full database entries. External databases may require institutional access.

Computational Analysis

Pathogenicity Predictions

SpliceAI
Predictor Consensus
Mixed/VUS
PP3 Applied
Yes
REVEL Score
0.0
Threshold: ≥0.75 = PP3 applied

SpliceAI Scores

Window: ±500bp
Effect Type Score Position
- Acceptor Loss (AL) 0.95 -41 bp
- Donor Loss (DL) 0.98 -1 bp
+ Acceptor Gain (AG) 0.02 225 bp
+ Donor Gain (DG) 0.04 330 bp
High impact (≥0.5) Medium impact (0.2-0.49) Low impact (<0.2)

VCEP Guidelines

Applied ACMG/AMP Criteria (VCEP Specific)

Filter Criteria:
PVS1

PVS1 (Very Strong)

According to VCEP guidelines, the rule for PVS1 is: 'Very Strong Null variant (splice site (donor/acceptor +/−1,2)...) in a gene where LOF is a known mechanism of disease.' The evidence for this variant shows: NM_000059.4:c.516+1G>A alters the canonical +1 splice donor site in BRCA2. Therefore, this criterion is applied at Very Strong strength because loss of function is the established mechanism and this is a canonical splice site variant.

PS1

PS1 (Not Applied)

According to standard ACMG guidelines, the rule for PS1 is: 'Strong: for predicted missense substitutions where a previously classified pathogenic variant has the same amino acid change.' The evidence for this variant shows: NM_000059.4:c.516+1G>A is a splice site variant, not a missense change. Therefore, PS1 is not applied.

PS2

PS2 (Not Applied)

According to standard ACMG guidelines, the rule for PS2 is: 'Strong: de novo (both maternity and paternity confirmed).' No de novo data are provided for this variant. Therefore, PS2 is not applied.

PS3

PS3 (Not Applied)

According to VCEP guidelines, the rule for PS3 is: 'Strong: well-established in vitro or in vivo functional studies supportive of a damaging effect.' The evidence for this variant shows: no functional studies have been reported. Therefore, PS3 is not applied.

PS4

PS4 (Not Applied)

According to VCEP guidelines, the rule for PS4 is: 'Strong: prevalence in affected individuals significantly increased compared to controls (case-control OR ≥4, p≤0.05).' No case-control data are provided. Therefore, PS4 is not applied.

PM1

PM1 (Not Applied)

According to standard ACMG guidelines, the rule for PM1 is: 'Moderate: located in a mutational hot spot or critical functional domain without benign variation.' The evidence for this variant shows: it is a splice site change, not within a defined missense hotspot or domain. Therefore, PM1 is not applied.

PM2

PM2 (Supporting)

According to VCEP guidelines, the rule for PM2 is: 'Supporting: Absent from controls in an outbred population, from gnomAD v2.1 (non-cancer) and gnomAD v3.1.' The evidence for this variant shows: MAF = 0% and it is not present in gnomAD. Therefore, PM2 is applied at Supporting strength because it is absent from population controls.

PM3

PM3 (Not Applied)

According to VCEP guidelines, the rule for PM3 is: 'Supportive to Strong: observed in trans with a pathogenic variant in patients with Fanconi anemia.' No Fanconi anemia phenotype or phase data are provided. Therefore, PM3 is not applied.

PM4

PM4 (Not Applied)

According to standard ACMG guidelines, the rule for PM4 is: 'Moderate: protein length changes due to in-frame indels or stop-loss.' The evidence for this variant shows: it is a splice site change, not an in-frame indel. Therefore, PM4 is not applied.

PM5

PM5 (Not Applied)

According to standard ACMG guidelines, the rule for PM5 is: 'Moderate: different pathogenic missense change at same residue or PTC in same exon.' The evidence for this variant shows: no data on other PTCs in the same exon. Therefore, PM5 is not applied.

PM6

PM6 (Not Applied)

According to standard ACMG guidelines, the rule for PM6 is: 'Moderate: assumed de novo without confirmation of paternity/maternity.' No de novo data are provided. Therefore, PM6 is not applied.

PP1

PP1 (Not Applied)

According to VCEP guidelines, the rule for PP1 is: 'Supporting to Strong: co-segregation in multiple affected family members.' No segregation data are provided. Therefore, PP1 is not applied.

PP2

PP2 (Not Applied)

According to standard ACMG guidelines, the rule for PP2 is: 'Supporting: missense variant in a gene with low rate of benign missense variation.' The evidence for this variant shows: it is a splice site change, not a missense. Therefore, PP2 is not applied.

PP3

PP3 (Supporting)

According to VCEP guidelines, the rule for PP3 is: 'Supporting: Apply PP3 for predicted splicing (SpliceAI ≥0.2).' The evidence for this variant shows: SpliceAI donor loss 0.98 and acceptor loss 0.95, predicting significant splice disruption. Therefore, PP3 is applied at Supporting strength because computational tools strongly predict a deleterious splicing effect.

PP4

PP4 (Not Applied)

According to VCEP guidelines, the rule for PP4 is: 'Supporting to Strong: phenotype specific to the gene based on multifactorial likelihood.' No phenotype data are provided. Therefore, PP4 is not applied.

PP5

PP5 (Supporting)

According to standard ACMG guidelines, the rule for PP5 is: 'Supporting: reputable source reports variant as pathogenic without available evidence.' The evidence for this variant shows: ClinVar lists it as Pathogenic by five clinical labs. Therefore, PP5 is applied at Supporting strength because a reputable source reports pathogenicity without detailed evidence.

BA1

BA1 (Not Applied)

According to VCEP guidelines, the rule for BA1 is: 'Stand Alone: allele frequency >0.1% in gnomAD.' The evidence for this variant shows: MAF = 0%, below threshold. Therefore, BA1 is not applied.

BS1

BS1 (Not Applied)

According to VCEP guidelines, the rule for BS1 is: 'Strong: allele frequency >0.01% in gnomAD.' The evidence for this variant shows: MAF = 0%, below threshold. Therefore, BS1 is not applied.

BS2

BS2 (Not Applied)

According to VCEP guidelines, the rule for BS2 is: 'Supporting to Strong: observed in healthy individuals without Fanconi anemia.' No data on healthy individuals are provided. Therefore, BS2 is not applied.

BS3

BS3 (Not Applied)

According to VCEP guidelines, the rule for BS3 is: 'Strong: well-established functional studies show no damaging effect.' No such studies exist for this variant. Therefore, BS3 is not applied.

BS4

BS4 (Not Applied)

According to VCEP guidelines, the rule for BS4 is: 'Strong: lack of segregation in affected family members.' No segregation data are provided. Therefore, BS4 is not applied.

BP1

BP1 (Not Applied)

According to VCEP guidelines, the rule for BP1 is: 'Supporting: silent or missense outside functional domain with no splicing impact.' The evidence for this variant shows: it is a canonical splice site change. Therefore, BP1 is not applied.

BP2

BP2 (Not Applied)

According to standard ACMG guidelines, the rule for BP2 is: 'Supporting: observed in trans with a pathogenic variant in a dominant disease without recessive phenotype.' No such data are provided. Therefore, BP2 is not applied.

BP3

BP3 (Not Applied)

According to standard ACMG guidelines, the rule for BP3 is: 'Supporting: in-frame indel in repetitive region without functional impact.' The evidence for this variant shows: it is a splice site change. Therefore, BP3 is not applied.

BP4

BP4 (Not Applied)

According to VCEP guidelines, the rule for BP4 is: 'Supporting: no predicted impact via protein or splicing (BayesDel ≤0.18 and SpliceAI ≤0.1).' The evidence for this variant shows: SpliceAI >0.9, predicting disruption. Therefore, BP4 is not applied.

BP5

BP5 (Not Applied)

According to standard ACMG guidelines, the rule for BP5 is: 'Supporting: variant found in a case with an alternate molecular basis for disease.' No such data are provided. Therefore, BP5 is not applied.

BP6

BP6 (Not Applied)

According to standard ACMG guidelines, the rule for BP6 is: 'Supporting: reputable source reports variant as benign without evidence.' No benign assertions exist. Therefore, BP6 is not applied.

BP7

BP7 (Not Applied)

According to VCEP guidelines, the rule for BP7 is: 'Supporting: silent or intronic outside consensus splice sites with no impact.' The evidence for this variant shows: it affects the canonical +1 splice site. Therefore, BP7 is not applied.