Genetic Information

Gene & Transcript Details

Gene
TET2
Transcript
NM_001127208.2 MANE Select
Total Exons
Reference Sequence
NC_000004.11
Alternative Transcripts
IDStatusDetails
NM_001127208.3 MANE Select 9589 nt | 297–6305
NM_001127208.1 Alternative 9677 nt | 387–6395
NM_001127208.2 RefSeq Select 9796 nt | 488–6496

Variant Details

HGVS Notation
NM_001127208.2:c.4227del
Protein Change
K1409Nfs*39
Location
Exon 10 (Exon 10 of )
10
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: 36066697

This sequence change creates a premature translational stop signal (p.Lys1409Asnfs*39) in the TET2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TET2 are known to be pathogenic (PMID: 36066697). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with TET2-related conditions. For these reasons, this variant has been classified as Pathogenic.

Clinical Statement

"This variant has been reported in ClinVar as Pathogenic (1 clinical laboratories)."

COSMIC Somatic Evidence

Open
COSMIC ID
COSM6918250
Recurrence
1 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 TET2.

Functional Studies & Therapeutic Relevance

Functional Summary

The TET2 K1409Nfs*39 variant is a truncating mutation that disrupts the C-terminal catalytic domain of the TET2 protein, a tumor suppressor and DNA demethylase. This disruption is predicted to cause gene inactivation, leading to a loss of enzymatic function necessary for generating 5-hydroxymethylcytosine (5-hmC). Functional evidence supports that this variant results in a loss-of-function effect, contributing to oncogenic processes in hematologic malignancies.

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) 0.0 -40 bp
- Donor Loss (DL) 0.11 112 bp
+ Acceptor Gain (AG) 0.0 -18 bp
+ Donor Gain (DG) 0.0 314 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: NM_001127208.2:c.4227delA causes a frameshift leading to a premature stop (K1409Nfs*39) in TET2, a gene where LoF is a known mechanism. Therefore, this criterion is applied at Very Strong strength because it is a null variant in a LoF‐sensitive gene.

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 other variant producing the exact same amino acid change by a different nucleotide change. Therefore, this criterion is not applied.

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 information on de novo status or parental testing. Therefore, this criterion is not applied.

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 demonstrate that K1409Nfs*39 truncates the catalytic domain of TET2, abolishing 5-hmC production and causing loss of enzymatic function. Therefore, this criterion is applied at Strong strength because in vitro/in vivo data 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 cohort data available. Therefore, this criterion is not applied.

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: although within the catalytic region, truncating variants are assessed under PVS1 rather than PM1, and no specific hotspot annotation is provided. Therefore, this criterion is not applied.

PM2

PM2 (Moderate)

According to standard ACMG guidelines, the rule for PM2 is: "Absent from controls (or at extremely low frequency if recessive disorders)". The evidence for this variant shows: c.4227delA is not observed in gnomAD or other population databases (MAF 0%). Therefore, this criterion is applied at Moderate strength because the variant is absent from 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 phase or second allele in a recessive context. 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: the change is a frameshift, which is addressed by PVS1 rather than PM4. 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: it is not a missense variant. 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 or family data. 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 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 is a common mechanism". 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: in silico prediction (SpliceAI max 0.11) does not support significant impact, and no other computational tools indicate deleteriousness. 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 phenotype data provided. Therefore, this criterion is not applied.

PP5

PP5 (Supporting)

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: ClinVar lists this variant as Pathogenic from one clinical laboratory without accessible primary data. Therefore, this criterion is applied at Supporting strength.

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: MAF is 0%. 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". The evidence for this variant shows: MAF is 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 such observations. 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". The evidence for this variant shows: functional studies show a 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. 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 LoF 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 phase data. 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 in-frame. 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: only one computational tool (SpliceAI) with low impact score; insufficient for multiple lines. 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 data on alternate molecular basis. 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 benign assertions. 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.