Genetic Information

Gene & Transcript Details

Gene
GATA2
Transcript
NM_032638.5 MANE Select
Total Exons
Reference Sequence
NC_000003.11
Alternative Transcripts
IDStatusDetails
NM_032638.5 MANE Select 3383 nt | 349–1791
NM_032638.3 Alternative 3383 nt | 333–1775
NM_032638.4 RefSeq Select 3383 nt | 335–1777

Variant Details

HGVS Notation
NM_032638.5:c.380_383dup
Protein Change
S129Pfs*57
Location
Exon 3 (Exon 3 of )
3
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
Unknown
0 publications
Clinical Statement

""

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 GATA2.

Functional Studies & Therapeutic Relevance

Functional Summary

The GATA2 S129Pfs*57 variant is a truncating mutation that likely results in loss of function. Truncating mutations in GATA2 are associated with loss of protein expression and have been identified in hematological malignancies, such as myelodysplastic syndromes, where they are linked to poor prognosis. In vivo studies using GATA2 knockout mouse models demonstrate that loss of GATA2 function contributes to increased leukemogenesis, indicating an inactivating effect of such mutations.

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
Unknown
PP3 Applied
No
REVEL Score
0.0
Threshold: ≥0.75 = PP3 applied

SpliceAI Scores

Window: ±500bp
Effect Type Score Position
- Acceptor Loss (AL) 0.05 -174 bp
- Donor Loss (DL) 0.01 301 bp
+ Acceptor Gain (AG) 0.01 -104 bp
+ Donor Gain (DG) 0.01 -493 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 standard ACMG guidelines, the rule for PVS1 is: "Null variant (nonsense, frameshift, canonical ±1 or 2 splice sites, initiation codon, single or multi-exon deletion) in a gene where loss of function is a known mechanism of disease". The evidence for this variant shows: c.380_383dup causes a frameshift (p.S129Pfs*57) leading to premature truncation in GATA2, and loss-of-function is a known mechanism for GATA2-related hematologic disease. Therefore, this criterion is applied at Very Strong strength because it is a null variant in a LoF gene.

PS1

PS1 (Not Applied)

According to standard ACMG guidelines, the rule for PS1 is: "Same amino acid change as a previously established pathogenic variant but different nucleotide change". The evidence for this variant shows: this is a novel frameshift, not matching any previously reported amino acid change. Therefore, this criterion is not applied because the variant does not result in the same amino acid change as a known pathogenic variant.

PS2

PS2 (Not Applied)

According to standard ACMG guidelines, the rule for PS2 is: "De novo (both maternity and paternity confirmed) in a patient with the disease and no family history". The evidence for this variant shows: no parental testing or de novo data are available. Therefore, this criterion is not applied because de novo status cannot be confirmed.

PS3

PS3 (Strong)

According to standard ACMG guidelines, the rule for PS3 is: "Well-established in vitro or in vivo functional studies supportive of a damaging effect on the gene or gene product". The evidence for this variant shows: in vitro and in vivo studies demonstrate that GATA2 truncating mutations cause loss of function and increased leukemogenesis in model systems. Therefore, this criterion is applied at Strong strength because functional studies support a damaging effect.

PS4

PS4 (Not Applied)

According to standard ACMG guidelines, the rule for PS4 is: "Prevalence in affected individuals significantly increased compared with controls". The evidence for this variant shows: no case-control or prevalence data are available. Therefore, this criterion is not applied because statistical enrichment in cases cannot be assessed.

PM1

PM1 (Not Applied)

According to standard ACMG guidelines, the rule for PM1 is: "Located in a mutational hot spot and/or critical functional domain without benign variation". The evidence for this variant shows: domain or hotspot location information is unavailable. Therefore, this criterion is not applied due to lack of domain annotation.

PM2

PM2 (Moderate)

According to standard ACMG guidelines, the rule for PM2 is: "Absent from controls (or at extremely low frequency if recessive)". The evidence for this variant shows: variant not found in gnomAD or other population databases (MAF=0%). Therefore, this criterion is applied at Moderate strength because it is absent from population controls.

PM3

PM3 (Not Applied)

According to standard ACMG guidelines, the rule for PM3 is: "Detected in trans with a pathogenic variant for recessive disorders". The evidence for this variant shows: no data on occurrence in trans with another pathogenic variant. Therefore, this criterion is not applied.

PM4

PM4 (Not Applied)

According to standard ACMG guidelines, the rule for PM4 is: "Protein length changes due to in-frame deletions/insertions or stop-loss variants". The evidence for this variant shows: this is a frameshift variant, not an in-frame indel or stop-loss. Therefore, this criterion is not applied.

PM5

PM5 (Not Applied)

According to standard ACMG guidelines, the rule for PM5 is: "Novel missense change at an amino acid residue where a different pathogenic missense change has been seen". The evidence for this variant shows: this is a frameshift, not a missense change. Therefore, this criterion is not applied.

PM6

PM6 (Not Applied)

According to standard ACMG guidelines, the rule for PM6 is: "Assumed de novo, but without confirmation of paternity and maternity". The evidence for this variant shows: no de novo data are available. Therefore, this criterion is not applied.

PP1

PP1 (Not Applied)

According to standard ACMG guidelines, the rule for PP1 is: "Cosegregation with disease in multiple affected family members". The evidence for this variant shows: no family segregation data are available. Therefore, this criterion is not applied.

PP2

PP2 (Not Applied)

According to standard ACMG guidelines, the rule for PP2 is: "Missense variant in a gene with a low rate of benign missense variation and where missense variants are a common mechanism of disease". The evidence for this variant shows: it is a frameshift, not missense. Therefore, this criterion is not applied.

PP3

PP3 (Not Applied)

According to standard ACMG guidelines, the rule for PP3 is: "Multiple lines of computational evidence support a deleterious effect on the gene/gene product". The evidence for this variant shows: SpliceAI score is low (0.05) and the variant is a clear frameshift causing truncation; computational data do not add further support. Therefore, this criterion is not applied.

PP4

PP4 (Not Applied)

According to standard ACMG guidelines, the rule for PP4 is: "Patient's phenotype or family history is highly specific for a disease with a single genetic etiology". The evidence for this variant shows: no specific phenotype or family history data are provided. Therefore, this criterion is not applied.

PP5

PP5 (Not Applied)

According to standard ACMG guidelines, the rule for PP5 is: "Reputable source reports variant as pathogenic, but without accessible evidence". The evidence for this variant shows: no such reports in ClinVar or other sources. Therefore, this criterion is not applied.

BA1

BA1 (Not Applied)

According to standard ACMG guidelines, the rule for BA1 is: "Allele frequency is too high for the disorder". The evidence for this variant shows: allele frequency is 0% in population databases. Therefore, this criterion is not applied.

BS1

BS1 (Not Applied)

According to standard ACMG guidelines, the rule for BS1 is: "Allele frequency is greater than expected for the disorder". The evidence for this variant shows: MAF=0%. Therefore, this criterion is not applied.

BS2

BS2 (Not Applied)

According to standard ACMG guidelines, the rule for BS2 is: "Observed in healthy individuals with full penetrance expected at an early age". The evidence for this variant shows: no observations in healthy individuals. Therefore, this criterion is not applied.

BS3

BS3 (Not Applied)

According to standard ACMG guidelines, the rule for BS3 is: "Well-established functional studies show no damaging effect on protein function or splicing". The evidence for this variant shows: functional studies demonstrate damaging effect. Therefore, this criterion is not applied.

BS4

BS4 (Not Applied)

According to standard ACMG guidelines, the rule for BS4 is: "Lack of segregation in affected family members". The evidence for this variant shows: no segregation data are available. Therefore, this criterion is not applied.

BP1

BP1 (Not Applied)

According to standard ACMG guidelines, the rule for BP1 is: "Missense variant in a gene where only loss of function causes disease". The evidence for this variant shows: it is a loss-of-function frameshift. Therefore, this criterion is not applied.

BP2

BP2 (Not Applied)

According to standard ACMG guidelines, the rule for BP2 is: "Observed in trans with a pathogenic variant for dominant disorders or in cis with a pathogenic variant". The evidence for this variant shows: no such observations. Therefore, this criterion is not applied.

BP3

BP3 (Not Applied)

According to standard ACMG guidelines, the rule for BP3 is: "In-frame deletions/insertions in a repetitive region without known function". The evidence for this variant shows: this is a frameshift, not an in-frame indel. Therefore, this criterion is not applied.

BP4

BP4 (Not Applied)

According to standard ACMG guidelines, the rule for BP4 is: "Multiple lines of computational evidence suggest no impact on gene or gene product". The evidence for this variant shows: computational splicing prediction is low impact but the variant causes truncation; computational data do not override. Therefore, this criterion is not applied.

BP5

BP5 (Not Applied)

According to standard ACMG guidelines, the rule for BP5 is: "Variant found in a case with an alternate molecular basis for disease". The evidence for this variant shows: no alternate molecular basis identified. Therefore, this criterion is not applied.

BP6

BP6 (Not Applied)

According to standard ACMG guidelines, the rule for BP6 is: "Reputable source reports variant as benign, but without accessible evidence". The evidence for this variant shows: no such reputably benign reports. Therefore, this criterion is not applied.

BP7

BP7 (Not Applied)

According to standard ACMG guidelines, the rule for BP7 is: "Synonymous variant with no predicted impact on splicing". The evidence for this variant shows: it is a frameshift, not synonymous. Therefore, this criterion is not applied.