PTEN is a tumor suppressor gene that encodes a phosphatase converting the lipid messenger PIP3 back to PIP2 at the cell membrane, thereby restraining the AKT/mTOR signaling pathway that drives cell growth, proliferation, and survival. It is one of the most frequently mutated genes across many types of human cancer, and its loss promotes unchecked cell growth, survival, and genomic instability, partly through impaired DNA repair. Germline loss-of-function variants in PTEN cause Cowden syndrome, an inherited cancer predisposition disorder associated with elevated risk of breast and thyroid cancer.
This variant
By disrupting PTEN before the phosphatase domain's later coding sequence, this germline frameshift is expected to reduce the tumor-suppressor function that restrains AKT/mTOR signaling and underlies PTEN hamartoma tumor syndrome.
Transcript
NM_000314.8
HGVS · transcript:coding
NM_000314.8:c.722_723dup
GRCh38
chr10:87957938 C>CTT
GRCh37
chr10:89717695 C>CTT
Likely Pathogenic: PVS1 (very strong) plus PM2 (supporting) satisfy the PTEN Expert Panel's Rule20 combination.
Classification rationale
PVS1PM2Likely Pathogenic
PTEN c.722_723dupframeshift · exon 7
PVS1 very strong: the p.E242Lfs*15 frameshift is 5' of the PTEN VCEP p.D375 NMD threshold and is predicted to undergo nonsense-mediated decay. PM2 supporting: the variant is absent from gnomAD v2.1 and v4.1, satisfying the PTEN VCEP population-frequency rule.
PVS1 + PM2→Likely Pathogenic
LYFE Sciences is an AI system, and it can make mistakes. Criteria
may be applied incorrectly, sources may be misread, and a confident-looking
classification can still be wrong. Double-check every criterion and
its underlying evidence before relying on any call.
Gene diagram
· NM_000314.8 · variants mapped to exon structure
PTENNM_000314.8
Fetching transcript structure from UCSC…
Exons
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Transcript span
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Strand
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Variants mapped
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Source
UCSC ncbiRefSeqCurated
All variants in PTEN—click a row to locate it on the plot · use the link column to open its page
Protein
Location
Classification
Link
Applied criteria · 2 applied · 14 assessed
MetEvidence satisfies this criterion.
Not metEvaluated against available evidence; threshold not reached.
Not assessedApplies in principle, but no evidence was found to evaluate it.
N/ADoesn't apply to this variant type.
Applied · 2
Strength Supporting Moderate Strong Very strong
✓
PVS1very strongPathogenic
Met: the p.E242Lfs*15 frameshift is 5' of the PTEN VCEP p.D375 NMD threshold, so the decision tree assigns full-strength PVS1.
The case normalization identifies NM_000314.8:c.722_723dup as a frameshift producing NP_000305.3:p.(Glu242LeufsTer15), also represented as p.(E242Lfs*15).The PTEN VCEP decision tree states that a nonsense or frameshift variant with a stop codon or disruption at or 5' to p.D375 (c.1121), in biologically relevant transcript NM_000314.8 and predicted to undergo NMD, receives PVS1.The PTEN VCEP specification explicitly directs reviewers to use the PTEN PVS1 decision tree for PVS1 strength assignment.
Met at supporting: the variant is absent from gnomAD v2.1 and v4.1, satisfying the PTEN PM2 absence criterion below 0.00001 allele frequency.
The governing ClinGen PTEN Expert Panel Version 3.2 defines PM2 supporting as absent from gnomAD or another large sequenced population, with allele frequency <0.00001 (0.001%); if multiple alleles occur in a subpopulation, that subpopulation frequency must be <0.00002 (0.002%).The variant is reported absent from gnomAD v2.1 and gnomAD v4.1.The variant is also reported absent from GNOMAD_V2_1_NON_CANCER and GNOMAD_V3_1_NON_CANCER, including the specified non-cancer cohort views.
Assessed · not applied
· 4 not met · 10 not assessed
Pathogenic
PS2Not assessed: no documented proband-level parental testing, confirmed maternity and paternity, or absence of family history for c.722_723dup.
PS3Not assessed: the governing PTEN assay table covers missense variants and contains no entry for this frameshift, c.722_723dup / p.E242Lfs*15.
PS4Not assessed: no variant-specific specificity score or qualifying case-control odds ratio, p value, and confidence interval are available for c.722_723dup.
PM1Not met: residue 242 is outside PTEN VCEP critical motifs 90-94, 123-130, and 166-168, and no E242 hotspot was identified.
PM4Not met: p.E242Lfs*15 is a frameshift with premature termination, whereas the PTEN PM4 rule requires an in-frame length change or stop-loss extension.
PM6Not assessed: no documented presumed de novo proband observation, parental testing status, or family-history assessment for c.722_723dup.
PP1Not assessed: zero informative meioses or exact-variant affected-relative segregation data are documented, below the PTEN VCEP minimum of 3 meioses.
Benign
BA1Not met: the variant is absent from gnomAD v2.1 and v4.1, rather than exceeding the PTEN BA1 threshold of 0.00056 allele frequency.
BS1Not met: the variant is absent from gnomAD v2.1 and v4.1, below both PTEN BS1 intervals beginning at 0.0000043 allele frequency.
BS2Not assessed: no homozygous observation in a healthy or PHTS-unaffected individual is available to satisfy the PTEN BS2 rule.
BS3Not assessed: no variant-specific benign functional result was found for the frameshift c.722_723dup / p.E242Lfs*15 in the governing PTEN assay material.
BS4Not assessed: no tested affected relatives or family-level non-segregation observations are documented for c.722_723dup.
BP2Not assessed: no paired pathogenic PTEN variant or documented cis/trans/phase observation is available to satisfy the BP2 rule.
BP5Not assessed: no two qualifying cases with a highly penetrant alternate diagnosis and non-overlapping PTEN histories are documented.
This variant does not lie in a statistically significant hotspot. This variant has previously been reported in somatic cancers (COSMIC; COSV64290304, n = 9 times).
Hotspots
This variant does not lie in a statistically significant hotspot.
17218262 ↗Essential role for nuclear PTEN in maintaining chromosomal integrity.ONCOKB
25741868 ↗Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology.CLINVAR
9467011 ↗Mutation spectrum and genotype-phenotype analyses in Cowden disease and Bannayan-Zonana syndrome, two hamartoma syndromes with germline PTEN mutation.CLINVAR
21194675 ↗A clinical scoring system for selection of patients for PTEN mutation testing is proposed on the basis of a prospective study of 3042 probands.CLINVAR
23788249 ↗ACMG recommendations for reporting of incidental findings in clinical exome and genome sequencing.CLINVAR
25356965 ↗ACMG policy statement: updated recommendations regarding analysis and reporting of secondary findings in clinical genome-scale sequencing.CLINVAR
26389258 ↗Cancer Genetics Risk Assessment and Counseling (PDQ®): Health Professional VersiCLINVAR