Genetic Information

Gene & Transcript Details

Gene
KMT2A
Transcript
NM_005933.3 MANE Select
Total Exons
Reference Sequence
NC_000011.9
Alternative Transcripts
IDStatusDetails
NM_005933.4 Alternative 16591 nt | 22–11931
NM_005933.2 Alternative 14982 nt | 24–11933
NM_005933.3 Alternative 16599 nt | 24–11933

Variant Details

HGVS Notation
NM_005933.3:c.3086del
Protein Change
K1029Rfs*65
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
COSM6697145
Recurrence
4 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 KMT2A.

Functional Studies & Therapeutic Relevance

Functional Summary

The KMT2A K1029Rfs*65 variant is a truncating mutation in the KMT2A gene, which is a tumor suppressor. Functional evidence indicates that truncating mutations in KMT2A typically result in proteins lacking methyltransferase activity. Although these mutations alone do not spontaneously induce tumor formation in mice, they may contribute to the dysregulation of genes involved in tumorigenesis.

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) 0.07 -60 bp
- Donor Loss (DL) 0.02 76 bp
+ Acceptor Gain (AG) 0.0 -285 bp
+ Donor Gain (DG) 0.0 468 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 in a gene where loss of function (LoF) is a known mechanism of disease (e.g., nonsense, frameshift, canonical ±1 or 2 splice sites, initiation codon, single exon deletion in a LoF gene)". The evidence for this variant shows: c.3086delA results in a frameshift leading to a premature stop codon (K1029Rfs*65) in KMT2A, a gene where LoF is established as a disease mechanism. Therefore, this criterion is applied at Very Strong strength because this is a truncating variant expected to result in loss of function.

PS1

PS1 (Not Applied)

According to standard ACMG guidelines, the rule for PS1 is: "Same amino acid change as a known pathogenic variant but different nucleotide change". The evidence for this variant shows: there is no report of a different nucleotide change resulting in the same amino acid alteration. Therefore, this criterion is not applied because the variant does not match a known pathogenic amino acid change.

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: parental testing data are not available. Therefore, this criterion is not applied due to lack of de novo confirmation.

PS3

PS3 (Strong)

According to standard ACMG guidelines, the rule for PS3 is: "Well-established functional studies supportive of a damaging effect on the gene or gene product". The evidence for this variant shows: functional studies indicate that truncating mutations in KMT2A abolish methyltransferase activity and contribute to dysregulation of genes involved in tumorigenesis. Therefore, this criterion is applied at Strong strength because well-established in vitro/in vivo 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 prevalence data are available. Therefore, this criterion is not applied due to absence of statistical association data.

PM1

PM1 (Not Applied)

According to standard ACMG guidelines, the rule for PM1 is: "Located in a mutational hot spot or well-established functional domain without benign variation". The evidence for this variant shows: exon/domain structure and hotspot data are not defined. Therefore, this criterion is not applied due to lack of localization information.

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: absent from population databases including gnomAD (MAF=0%). Therefore, this criterion is applied at Moderate strength because the variant is not observed in 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: phasing and zygosity information relative to another pathogenic variant are not available. Therefore, this criterion is not applied due to lack of trans configuration data.

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 leading to truncation rather than an in-frame change. Therefore, this criterion is not applied because the variant is not an in-frame indel or stop-loss.

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: it is 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 data on de novo status are available. Therefore, this criterion is not applied.

PP1

PP1 (Not Applied)

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

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 variant, 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 (e.g., conservation, splicing impact)". The evidence for this variant shows: in silico splicing prediction (SpliceAI max 0.07) indicates minimal impact and no other deleterious computational evidence. 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 highly specific for a disease with a single genetic etiology". The evidence for this variant shows: no detailed phenotype/family history 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: not found in ClinVar or other databases. 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 (based on population data)". The evidence for this variant shows: allele frequency is 0% in gnomAD, not high. 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: allele frequency is 0%, below disease threshold. 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 observation 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: segregation data are not 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 LoF causes disease". The evidence for this variant shows: it is a frameshift variant. 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 data on cis/trans configuration. 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: it is a frameshift, not an in-frame event in a repetitive region. 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". The evidence for this variant shows: computational evidence is insufficient to suggest no impact because the variant truncates the protein. 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 reported. 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: not reported as benign. 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 not synonymous. Therefore, this criterion is not applied.