chr13-32333283-G-GA
Variant summary
The NM_000059.4(BRCA2):c.1813dupA (p.Ile605AsnfsTer11) variant causes a frameshift change. The variant is predicted to lead to nonsense-mediated mRNA decay (NMD). The variant allele was found at a cumulative frequency of 0.0000137 (AC=22) in the gnomAD database across 1,601,314 control chromosomes (no homozygotes observed). The grpmax filtering allele frequency (95% CI) is 0.0000197. Splicing prediction tools (SpliceAI) predict no significant impact on normal splicing. Variant has been reported in ClinVar as Pathogenic/Likely Pathogenic (★★★). ClinVar reports functional evidence for this variant: "SCV000918819: Functional study showed variant with diminished DNA double strand break repair capacity (Becker_2012)." and additional evidence is available in ClinVar.
Frequency
Consequence
NM_000059.4 frameshift
Scores
Clinical Significance
Conservation
Publications
- BRCA2-related cancer predispositionInheritance: AD Classification: DEFINITIVE Submitted by: ClinGen
- breast-ovarian cancer, familial, susceptibility to, 2Inheritance: AD Classification: DEFINITIVE, STRONG Submitted by: Labcorp Genetics (formerly Invitae), Genomics England PanelApp, Ambry Genetics
- Fanconi anemia complementation group D1Inheritance: AR Classification: DEFINITIVE, STRONG Submitted by: G2P, Labcorp Genetics (formerly Invitae), ClinGen, Ambry Genetics
- pancreatic cancer, susceptibility to, 2Inheritance: AD Classification: STRONG Submitted by: Genomics England PanelApp
- sarcomaInheritance: AD Classification: MODERATE Submitted by: Genomics England PanelApp
- hereditary breast ovarian cancer syndromeInheritance: AD Classification: SUPPORTIVE Submitted by: Orphanet
- Fanconi anemiaInheritance: AR Classification: SUPPORTIVE Submitted by: Orphanet
- medulloblastomaInheritance: AD Classification: LIMITED Submitted by: Ambry Genetics
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Classification according to ACMG Germline Pathogenicity v2019
Our verdict: Pathogenic. The variant received 21 points.
| Apply | Criterion Code & Title / Strength | Rationale / Clinical Context | |
|---|---|---|---|
| PVS1Null variant in LOF gene | Frameshift/stop-gained, NMD predicted, LoF disease mechanism — very strong (PVS1); Frameshift (exon 10 of 27) at amino acid 605 of 3418, predicted to trigger nonsense-mediated mRNA decay. Loss of function is a known disease mechanism for this gene. A new stop codon is introduced in the shifted frame, truncating the protein to ~614 amino acids (2804 amino acids lost). | ||
| PS3Functional studies show damaging effect | Well-established functional study supports damaging effect (PS3); SCV000918819: Functional study showed variant with diminished DNA double strand break repair capacity (Becker_2012).; SCV000186437: This alteration, in compound heterozygosity with another BRCA2 mutation, was also reported in an individual with Fanconi anemia (Myers, 2012). The c.1813dupA pathogenic mutation was reported in two unrelated probands with a personal and/or family history of breast/ovarian cancers and was shown to diminish DNA double strand break repair capacity in response to irradiation (Becker , 2012).; SCV004562779: Functional data indicate that cell lines derived from patients harboring the c.1813dup variant are more susceptible than wild-type to radiation induced chromosomal abnormalities (Becker 2012). PMID: 22729890.; SCV000805657: A functional in vitro study using blood lymphocytes on this variant has demonstrated significantly higher radiation-induced chromosomal aberrations (Becker et al. 2012. PubMed ID: 22729890). | ||
| PM2Absent/extremely low in population databases | Rare in gnomAD for AD/XL gene (popmax AF below threshold) — PM2 Supporting; GnomAD popmax AF = 0.0000197 — borderline rare for AD+AR gene (base 0.0001, raised to 0.000139 by highest known P/LP ClinVar AF 0.000139) — PM2 supporting. | ||
| PP5Reputable source reports pathogenic | ClinVar ≥3 stars pathogenic — very strong (PP5); ClinVar germline classification: Pathogenic/Likely Pathogenic, 3 star(s). |
Variant Effect in Transcripts
Automated classification analysis was done for transcript: NM_000059.4. You can select a different transcript below to see updated classification assignments.
RefSeq Transcripts
| Sel. | Gene / Transcript | Tags | HGVSc / HGVSp | Effect | Exon rank | Protein / UniProt |
|---|---|---|---|---|---|---|
BRCA2 | MANE Select | c.1813dupA p.Ile605AsnfsTer11 | frameshift | Exon 10 of 27 | Prot: NP_000050.3 UniProt: | |
BRCA2 | c.1813dupA p.Ile605AsnfsTer11 | frameshift | Exon 10 of 27 | Prot: NP_001419006.1 UniProt: | ||
BRCA2 | c.1813dupA p.Ile605AsnfsTer11 | frameshift | Exon 10 of 27 | Prot: NP_001393649.1 UniProt: |
Ensembl Transcripts
| Sel. | Gene / Transcript | Tags | HGVSc / HGVSp | Effect | Exon rank | Protein / UniProt |
|---|---|---|---|---|---|---|
BRCA2 | TSL:5MANE Select | c.1813dupA p.Ile605AsnfsTer11 | frameshift | Exon 10 of 27 | Prot: ENSP00000369497.3 UniProt: | |
BRCA2 | TSL:1 | c.1813dupA p.Ile605AsnfsTer11 | frameshift | Exon 10 of 27 | Prot: ENSP00000439902.1 UniProt: | |
BRCA2 | TSL:1 | c.1444dupA p.Ile482AsnfsTer11 | frameshift | Exon 10 of 27 | Prot: ENSP00000499438.2 UniProt: |
Frequencies
Allele frequencies (AF), counts (AC/AN), homozygotes and coverage
| Source / population | AF | AC | Hom | AN | Coverage |
|---|---|---|---|---|---|
Global population databases 6 sources | |||||
GnomAD3 genomes | AF: 0.0000264 | AC:4 | Hom:0 | AN:151588 | Cov:32 |
GnomAD2 exomes | AF: 0.0000129 | AC:3 | AN:232106 | ||
GnomAD4 exome | AF: 0.0000124 | AC:18 | Hom:0 | AN:1449726 | Cov:35 |
GnomAD4 genome | AF: 0.0000264 | AC:4 | Hom:0 | AN:151588 | Cov:32 |
TOPMed (Bravo) | AF: 0.00000756 | AC:2 | Hom:0 | AN:264690 | |
ALFA (dbGaP/dbSNP Allele Frequency Aggregator) | AF: 0.0000891 | AC:2 | Hom:0 | AN:22458 | |
Case/control cohorts
| Cohort | Cases | Controls | ||||
|---|---|---|---|---|---|---|
| AF | AC | AN | AF | AC | AN | |
Epi25 | 0.0000239 | 1 | 41926 | 0.00 | 0 | 66740 |
SCHEMA | 0.0000195 | 2 | 102430 | 0.0000164 | 3 | 182546 |
ClinVar
Computational Scores
| Algorithm | Calibrated pred. | Score | Prediction |
|---|---|---|---|
Mutation Taster | N/A | 0/200 | disease causing (ClinVar) |
PhyloP100 | Benign | 0.51 |
Splicing Scores
| Algorithm | Calibrated pred. | Score | Prediction |
|---|---|---|---|
SpliceAI score (max) | Benign | 0.0 | Details are displayed if max score is > 0.2 |
Find out detailed SpliceAI scores and Pangolin per-transcript scores at
MaxEntScan Visualizer can be used to analyze the impact of this mutation on the neighboring sequence.