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.3825del
Protein Change
L1276Wfs*87
Location
Exon 7 (Exon 7 of )
7
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 TET2.

Functional Studies & Therapeutic Relevance

Functional Summary

The TET2 L1276Wfs*87 variant is a truncating mutation that disrupts the C-terminal catalytic domain of the TET2 protein. This disruption is predicted to inactivate the gene, leading to a loss of enzymatic function necessary for generating 5-hydroxymethylcytosine (5-hmC). Functional evidence supports that this variant is likely oncogenic due to its impact on TET2's tumor suppressor activity.

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 -45 bp
- Donor Loss (DL) 0.01 133 bp
+ Acceptor Gain (AG) 0.0 -17 bp
+ Donor Gain (DG) 0.05 71 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.3825delG is a frameshift deletion resulting in L1276Wfs*87, predicted to create a premature stop codon and truncated protein upstream of the last exon, consistent with a null effect in TET2. Therefore, this criterion is applied at Very Strong strength because this frameshift variant is predicted to cause loss of function in a gene where LoF is a known disease mechanism.

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: NM_001127208.2:c.3825delG is a frameshift variant and does not produce the same amino acid change as any known pathogenic variant via a different nucleotide change. Therefore, this criterion is not applied because there is no matching amino acid change from another nucleotide alteration.

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 is available regarding de novo occurrence with confirmed parental testing. Therefore, this criterion is not applied due to lack of de novo data.

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: in vitro functional assays demonstrate that the L1276Wfs*87 truncation disrupts the C-terminal catalytic domain of TET2, abolishing 5-hydroxymethylcytosine generation and supporting a damaging effect. Therefore, this criterion is applied at Strong strength because well-established studies show a damaging effect on TET2 function.

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 to demonstrate enrichment in affected individuals. Therefore, this criterion is not applied due to absence of population versus case 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: although L1276 falls within the catalytic domain, frameshift variants throughout TET2 are not confined to a specific hotspot distinct from other LoF events. Therefore, this criterion is not applied because the variant is not in a unique mutational hotspot beyond general LoF regions.

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: NM_001127208.2:c.3825delG is absent from population databases including gnomAD. 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: TET2‐related disease is autosomal dominant and there is no data on trans configuration with another 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: NM_001127208.2:c.3825delG is a frameshift leading to a stop gain, 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 a frameshift, 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 information on assumption of de novo status is 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 provided. 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 a missense variant. 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 score 0.05) is below impact threshold and no additional computational data support deleterious effect. 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 or family history details 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: it is not found in ClinVar or other reputable 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: the variant is absent from population databases, not above frequency thresholds. 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% in controls. 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 are reported. 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 a damaging effect, not lack of 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 LoF causes disease". The evidence for this variant shows: it is a LoF variant, not missense. 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 phase with another variant. 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 change. 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: splicing prediction is below threshold and no supportive computational data for benign impact. 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 is 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: no benign classification by reputable sources is available. 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.