Genetic Information

Gene & Transcript Details

Gene
PTEN
Transcript
NM_000314.8 MANE Select
Total Exons
Reference Sequence
NC_000010.10
Alternative Transcripts
IDStatusDetails
NM_000314.7 RefSeq Select 8514 nt | 845–2056
NM_000314.5 Alternative 8719 nt | 1032–2243
NM_000314.4 Alternative 5572 nt | 1032–2243
NM_000314.3 Alternative 3416 nt | 1032–2243
NM_000314.6 Alternative 8718 nt | 1032–2243
NM_000314.8 MANE Select 8515 nt | 846–2057

Variant Details

HGVS Notation
NM_000314.8:c.722T>C
Protein Change
F241S
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
COSM5126
Recurrence
5 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 PTEN.

Functional Studies & Therapeutic Relevance

Functional Summary

The PTEN F241S variant has been functionally characterized and demonstrates a damaging effect. It is located in the phosphatase domain of the PTEN protein and results in loss of phosphatase activity, decreased protein stability, and reduced nuclear localization. Functional assays in yeast, glioblastoma cell lines, and Drosophila models show that this variant leads to loss of PTEN function, acts as a dominant negative regulator of the PI3-AKT signaling pathway, and delays developmental growth.

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
Mixed/VUS
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 -87 bp
- Donor Loss (DL) 0.0 -6 bp
+ Acceptor Gain (AG) 0.01 -33 bp
+ Donor Gain (DG) 0.0 -108 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 (Not Applied)

According to VCEP guidelines, the rule for PVS1 is: "Use PTEN PVS1 decision tree." The evidence for this variant shows: c.722T>C (p.F241S) is a missense change, not a null variant. Therefore, this criterion is not applied because PVS1 applies only to predicted loss‐of‐function variants as per the PTEN PVS1 decision tree.

PS1

PS1 (Not Applied)

According to VCEP guidelines, the rule for PS1 is: "Same amino acid change as a previously established pathogenic variant regardless of nucleotide change..." The evidence for this variant shows: no other PTEN variant at p.Phe241 has been reported as pathogenic. Therefore, PS1 is not applied.

PS2

PS2 (Not Applied)

According to VCEP guidelines, the rule for PS2 is: "De novo (both maternity and paternity confirmed) observation in a patient with the disease and no family history." The evidence for this variant shows: no de novo data are available. Therefore, PS2 is not applied.

PS3

PS3 (Moderate)

According to PTEN Pre-processing, the finding for PS3 is: "Applied PS3_Moderate evidence based on high-confidence functional score (-2.3994) < threshold (-1.11)." The evidence for this variant shows: multiple well-established functional assays demonstrate loss of PTEN phosphatase activity, decreased stability, and dominant-negative effect. Therefore, PS3 is applied at Moderate strength because the variant meets the PTEN-specific phosphatase activity threshold.

PS4

PS4 (Not Applied)

According to VCEP guidelines, the rule for PS4 is: "Probands with specificity score ≥4 or significantly increased prevalence in affected versus controls." The evidence for this variant shows: no case‐level or cohort data are available. Therefore, PS4 is not applied.

PM1

PM1 (Not Applied)

According to VCEP guidelines, the rule for PM1 is: "Located in a mutational hot spot and/or critical functional domain: residues 90-94, 123-130, 166-168." The evidence for this variant shows: p.Phe241 lies outside these defined catalytic motifs. Therefore, PM1 is not applied.

PM2

PM2 (Supporting)

According to VCEP guidelines, the rule for PM2 is: "Absent in population databases present at <0.00001 allele frequency in gnomAD." The evidence for this variant shows: not observed in gnomAD or other large controls. Therefore, PM2 is applied at Supporting strength.

PM3

PM3 (Not Applied)

According to standard ACMG guidelines, the rule for PM3 is: "For recessive disorders, detected in trans with a pathogenic variant." The evidence for this variant shows: no evidence of recessive biallelic occurrence. Therefore, PM3 is not applied.

PM4

PM4 (Not Applied)

According to VCEP guidelines, the rule for PM4 is: "Protein length changes due to in-frame indels or stop-loss variants." The evidence for this variant shows: it is a missense change without protein length alteration. Therefore, PM4 is not applied.

PM5

PM5 (Not Applied)

According to VCEP guidelines, the rule for PM5 is: "Missense change at a residue where a different missense change is pathogenic." The evidence for this variant shows: no other pathogenic missense reported at p.Phe241. Therefore, PM5 is not applied.

PM6

PM6 (Not Applied)

According to VCEP guidelines, the rule for PM6 is: "Assumed de novo without confirmation." The evidence for this variant shows: no de novo assumption data. Therefore, PM6 is not applied.

PP1

PP1 (Not Applied)

According to VCEP guidelines, the rule for PP1 is: "Co-segregation with disease in family members." The evidence for this variant shows: no segregation data. Therefore, PP1 is not applied.

PP2

PP2 (Not Applied)

According to standard ACMG guidelines, the rule for PP2 is: "Missense in a gene with low rate of benign missense and where missense is common disease mechanism." The evidence for this variant shows: insufficient data on benign missense rate in PTEN. Therefore, PP2 is not applied.

PP3

PP3 (Not Applied)

According to VCEP guidelines, the rule for PP3 is: "Multiple lines of computational evidence support deleterious effect; REVEL >0.7." The evidence for this variant shows: mixed in silico predictions and no consensus REVEL >0.7. Therefore, PP3 is not applied.

PP4

PP4 (Not Applied)

According to standard ACMG guidelines, the rule for PP4 is: "Patient phenotype highly specific for gene." The evidence for this variant shows: no phenotype data. Therefore, PP4 is not applied.

PP5

PP5 (Not Applied)

According to standard ACMG guidelines, the rule for PP5 is: "Reputable source reports variant as pathogenic." The evidence for this variant shows: not found in ClinVar or other databases. Therefore, PP5 is not applied.

BA1

BA1 (Not Applied)

According to VCEP guidelines, the rule for BA1 is: "gnomAD allele frequency >0.00056." The evidence for this variant shows: allele frequency = 0%. Therefore, BA1 is not applied.

BS1

BS1 (Not Applied)

According to VCEP guidelines, the rule for BS1 is: "gnomAD allele frequency from 0.0043% to 0.056%." The evidence for this variant shows: allele frequency = 0%. Therefore, BS1 is not applied.

BS2

BS2 (Not Applied)

According to VCEP guidelines, the rule for BS2 is: "Observed homozygous in healthy individual." The evidence for this variant shows: no homozygous observations. Therefore, BS2 is not applied.

BS3

BS3 (Not Applied)

According to VCEP guidelines, the rule for BS3 is: "Well-established functional studies show no damaging effect." The evidence for this variant shows: functional studies demonstrate damaging effect. Therefore, BS3 is not applied.

BS4

BS4 (Not Applied)

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

BP1

BP1 (Not Applied)

According to standard ACMG guidelines, the rule for BP1 is: "Missense in gene where only truncating variants cause disease." The evidence for this variant shows: PTEN missense variants are known to be disease-causing. Therefore, BP1 is not applied.

BP2

BP2 (Not Applied)

According to VCEP guidelines, the rule for BP2 is: "Observed in trans with a pathogenic PTEN variant." The evidence for this variant shows: no trans observations. Therefore, BP2 is not applied.

BP3

BP3 (Not Applied)

According to standard ACMG guidelines, the rule for BP3 is: "In-frame indel in repetitive region without functional impact." The evidence for this variant shows: not an indel. Therefore, BP3 is not applied.

BP4

BP4 (Not Applied)

According to VCEP guidelines, the rule for BP4 is: "Multiple lines of computational evidence suggest no impact; REVEL <0.5." The evidence for this variant shows: in silico predictions are mixed with some pathogenic scores. Therefore, BP4 is not applied.

BP5

BP5 (Not Applied)

According to VCEP guidelines, the rule for BP5 is: "Variant found with alternate molecular basis." The evidence for this variant shows: no alternate molecular diagnosis. Therefore, BP5 is not applied.

BP6

BP6 (Not Applied)

According to standard ACMG guidelines, the rule for BP6 is: "Reputable source reports variant as benign." The evidence for this variant shows: no such reports. Therefore, BP6 is not applied.

BP7

BP7 (Not Applied)

According to VCEP guidelines, the rule for BP7 is: "Synonymous variant with no splicing impact." The evidence for this variant shows: it is missense. Therefore, BP7 is not applied.