The PTEN NM_000314.8:c.392C>T (NP_000305.3:p.(Thr131Ile)) missense variant has previously been reported in somatic cancers (COSMIC; COSV64300549, n = 2 times). Experimental evidence: High-confidence T131I phosphatase assay Cum_score -1.91132903 meets the VCEP PS3 threshold of ≤ -1.11. Based on available guidelines, this variant is considered to be Likely Pathogenic. This variant is considered to be Pathogenic by the VCEP (Clingen PTEN Variant Curation Expert Panel, Clingen; ClinVar ID 39669).
Five-step scale from benign to pathogenic. This variant is likely pathogenic. Select a step to read what it means.
This variantScenario
BenignPathogenic
Likely pathogenic.A likely pathogenic classification under the recorded framework.
In plain language
Gene-level background from the recorded interpretation.
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About PTEN
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.
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01The reasoning
How it was classified
The recorded framework is ClinGen PTEN VCEP v3.2. The criteria and strengths shown below come from the saved assessment; this page does not recalculate the classification.
Recorded applied criteria
The applied criteria and their strengths are shown as assessed under the stated framework.
ACMG/AMP criteria under ClinGen PTEN VCEP v3.2, with the data and sources behind each one.
28 criteria with recorded statuses: 5 met · 5 not met · 10 not assessed · 8 not applicable. Open any row for the full reasoning, the rule and the evidence behind it.
For the requested consequence/LoF criteria, the variant is a PTEN missense substitution; PVS1 and PM4 do not apply to this consequence, and the VCEP marks BP3 Not Applicable.
Only PM6 is met, at Strong strength, based on the VCEP-described count of two presumed de novo probands.
PS2, PP1, and BS4 cannot be independently evaluated from the available confirmed parentage, segregation, and non-segregation data.
Only PS4, PP4, PP5, BP5, and BP6 were adjudicated.
PS4 requires variant-specific case-control enrichment or qualifying phenotype-specificity scores; neither is available.
PP4, PP5, and BP6 are not applicable under the PTEN VCEP specification.
BP5 remains not assessed because the required alternate molecular basis evidence and two qualifying cases are not documented.
The PTEN VCEP v3.2 rules govern all three criteria and distinguish predictor use by variant situation: REVEL for missense variants and SpliceAI/VarSeak concordance for splicing variants.
This variant is missense, p.(Thr131Ile), with REVEL 0.965; therefore PP3 is met and BP4 is not met, while the splice-prediction result is not counted for either criterion.
BP7 is not applicable because the variant is neither synonymous nor intronic.
No criteria match.
Met · 5
PS3ModerateVCEPMet at moderate strength: high-confidence T131I phosphatase assay Cum_score -1.91132903 meets the VCEP PS3 threshold of ≤ -1.11.
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Reasoning
PS3_Moderate is met under the PTEN VCEP specification. In mmc2.xlsx, Table S2, the exact variant row T131I / Thr131Ile has High_conf=True and Cum_score=-1.91132903. The VCEP requires a high-confidence Table S2 result and applies PS3_Moderate when phosphatase activity is ≤ -1.11; -1.91132903 meets that threshold. The independently extracted PMID:21828076 functional study also reports that T131I fully abrogated PTEN PIP3 phosphatase activity in yeast, consistent with a damaging effect, but the assigned strength here is determined by the VCEP Table S2 rule.
VCEP rule
Well-established _in vitro_ or _in vivo_ functional studies supportive of a damaging effect on the gene or gene product.
* Phosphatase activity ≤ -1.11 per Mighell et al. 2018, PMID: 29706350.
ClinGen PTEN VCEP specification v3.2: Table S2 variants must be high confidence, and PS3_Moderate applies for phosphatase activity ≤ -1.11.
Rodríguez-Escudero et al. 2011, PMID:21828076: the exact p.T131I mutant fully abrogated PTEN PIP3 phosphatase activity in a heterologous S. cerevisiae assay.
PM2SupportingVCEPMet, Supporting: the variant is absent from gnomAD v2.1 and v4.1, consistent with allele frequency 0 below the VCEP PM2 threshold of 0.00001.
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Reasoning
The PTEN VCEP permits PM2 at Supporting strength when a variant is present at less than 0.00001 (0.001%) allele frequency in gnomAD or another large sequenced population; if multiple alleles occur in a subpopulation, that subpopulation frequency must be less than 0.00002 (0.002%). NM_000314.8:c.392C>T (p.Thr131Ile) is absent from the default all-comers gnomAD v2.1 and v4.1 datasets, satisfying an allele frequency of zero and therefore both thresholds. The VCEP rule does not specify a non-cancer or exome-only source, and the non-cancer searches are also absent.
VCEP rule
Absent in population
* Databases present at \<0.00001 (0.001%) allele frequency in gnomAD or another large sequenced population. If multiple alleles are present within any subpopulation, allele frequency in that subpopulation must be \<0.00002 (0.002%).
Evidence considered
ClinGen PTEN VCEP specification v3.2, PM2 Supporting rule: databases present at <0.00001 (0.001%) allele frequency in gnomAD or another large sequenced population; if multiple alleles are present within any subpopulation, the allele frequency in that subpopulation must be <0.00002 (0.002%).
gnomAD v2.1: NM_000314.8:c.392C>T is absent, corresponding to no observed allele and an allele frequency of 0 in the reported dataset.
gnomAD v4.1: NM_000314.8:c.392C>T is absent, corresponding to no observed allele and an allele frequency of 0 in the reported dataset.
gnomAD v2.1 non-cancer and gnomAD v3.1 non-cancer searches also report the variant absent; these datasets are not separately registered source keys.
PM6StrongVCEPMet, strong: two probands are reported with presumed de novo occurrence, unconfirmed parentage, disease, and no family history.
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Reasoning
The ClinGen PTEN Expert Panel submission audit records two probands with presumed de novo occurrence, unconfirmed maternity/paternity, disease, and no family history. This matches the VCEP PM6 Strong rule for two presumed de novo probands. The underlying case-level pedigree and parental-test records are not provided, so human review is warranted.
VCEP rule
Two probands with presumed _de novo_ occurrence (maternity/ paternity not confirmed) with the disease and no family history.
Evidence considered
The ClinGen PTEN Expert Panel submission audit states: two probands with presumed de novo occurrence, maternity/paternity not confirmed, in a patient with the disease and no family history.
This evidence meets the VCEP PM6 Strong threshold of two probands with presumed de novo occurrence when maternity and paternity are not confirmed.
Still missing
Primary case reports or laboratory records confirming the two individual observations, phenotypes, family histories, and parental testing are not available.
PP3SupportingVCEPMet: REVEL score 0.965 exceeds the PTEN VCEP PP3 missense threshold of >0.7.
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Reasoning
NM_000314.8:c.392C>T, NP_000305.3:p.(Thr131Ile), is a missense variant. The PTEN VCEP PP3 rule names REVEL for missense variants and requires a REVEL score > 0.7. The exact-variant REVEL score is 0.965, which exceeds the VCEP threshold; the available SpliceAI result was not used because SpliceAI is named by this rule only for splicing variants, not for this missense situation. PP3 is met at supporting strength.
VCEP rule
Multiple lines of computational evidence support a deleterious effect on the gene or gene product.
* Splicing variants: Concordance of SpliceAl and VarSeak
* Missense variants: REVEL score > 0.7
Evidence considered
ClinGen PTEN VCEP v3.2 PP3 rule: for missense variants, the named predictor is REVEL and the cutoff is >0.7.
Local REVEL predictor lookup for NM_000314.8:c.392C>T / NP_000305.3:p.(Thr131Ile): REVEL score = 0.965; this exceeds the VCEP PP3 missense cutoff.
SpliceAI max delta score = 0.004 was not used for PP3 because the VCEP rule assigns SpliceAI to its splicing-variant path, whereas this variant is missense.
PP5SupportingVCEPNot applicable: the PTEN VCEP explicitly prohibits use of PP5 regardless of the variant's external pathogenic classifications.
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PM1VCEPNot met: residue 131 lies outside the VCEP catalytic intervals 90–94, 123–130, and 166–168, with no significant hotspot reported.
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Reasoning
The variant affects residue 131. The VCEP defines PM1 to include catalytic-motif residues 90-94, 123-130, and 166-168 of NP_000305.3; residue 131 is outside all three specified intervals. The case hotspot search found no statistically significant hotspot, and vcep_materials.json contains no PTEN domain_tables entry requiring an additional authoritative domain interval check. Thus the VCEP PM1 location requirement is not met.
VCEP rule
Located in a mutational hot spot and/or critical and well-established functional domain. Defined to include residues in catalytic motifs: 90-94, 123-130, 166-168 (NP_ 000305.3)
Evidence considered
The variant is NP_000305.3:p.(Thr131Ile), so the affected residue is 131.
The VCEP PM1 rule defines catalytic-motif residues 90-94, 123-130, and 166-168 in NP_000305.3; residue 131 is not in any interval.
The case hotspot result reports no statistically significant hotspot for PTEN T131.
The vcep_materials.json domain_tables object is empty, so there is no gene-specific authoritative domain-table entry to extend the listed VCEP intervals.
BA1VCEPNot met: the variant is absent from gnomAD v2.1 and v4.1, rather than exceeding the VCEP BA1 threshold of 0.00056.
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Reasoning
The PTEN VCEP defines BA1 as a gnomAD Filtering allele frequency greater than 0.00056 (0.056%). NM_000314.8:c.392C>T (p.Thr131Ile) is reported absent from the default all-comers gnomAD v2.1 and v4.1 datasets, so no allele frequency exceeding the BA1 threshold is present. The VCEP rule does not specify a non-cancer or exome-only source for BA1, and the available non-cancer searches are also absent.
VCEP rule
gnomAD Filtering allele frequency >0.00056 (0.056%)
BS1VCEPNot met: the variant is absent from gnomAD v2.1 and v4.1, with no allele frequency in either VCEP BS1 interval.
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Reasoning
The PTEN VCEP defines BS1 Strong as a gnomAD Filtering allele frequency from 0.000043 (0.0043%) up to 0.00056 (0.056%), and BS1 Supporting as 0.0000043 (0.00043%) up to 0.000043 (0.0043%). NM_000314.8:c.392C>T (p.Thr131Ile) is absent from gnomAD v2.1 and v4.1, so the available data do not show an allele frequency in either BS1 interval. The VCEP rule does not specify a non-cancer or exome-only source for BS1, and the available non-cancer searches are also absent.
VCEP rule
gnomAD Filtering allele frequency from 0.000043 (0.0043%) up to 0.00056 (0.056%)...Allele frequency from 0.0000043 (0.00043%) up to 0.000043 (0.0043%).
Evidence considered
ClinGen PTEN VCEP specification v3.2, BS1 Strong rule: gnomAD Filtering allele frequency from 0.000043 (0.0043%) up to 0.00056 (0.056%).
ClinGen PTEN VCEP specification v3.2, BS1 Supporting rule: allele frequency from 0.0000043 (0.00043%) up to 0.000043 (0.0043%).
gnomAD v2.1: NM_000314.8:c.392C>T is absent; no allele frequency or allele count is reported.
gnomAD v4.1: NM_000314.8:c.392C>T is absent; no allele frequency or allele count is reported.
gnomAD v2.1 non-cancer and gnomAD v3.1 non-cancer searches also report the variant absent; these datasets are not separately registered source keys.
BS3VCEPNot met: high-confidence T131I phosphatase Cum_score -1.91132903 is not >0, and an independent assay reports complete activity loss.
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Reasoning
BS3 is not met. The governing PTEN VCEP BS3_Supporting rule requires phosphatase activity >0 in the Mighell et al. 2018 Table S2 assay, whereas the exact high-confidence T131I / Thr131Ile row has Cum_score=-1.91132903. The independently extracted PMID:21828076 study likewise reports complete loss of PIP3 phosphatase activity for T131I rather than absence of a damaging effect.
VCEP rule
_In vitro_ or _in vivo_ functional study or studies showing no damaging effect on protein function.
* Phosphatase activity >0 per Mighell et al. 2018, PMID: 29706350.
Evidence considered
Mighell et al. 2018 supplementary mmc2.xlsx, Table S2, row T131I / Thr131Ile: High_conf=True; Cum_score=-1.91132903, which does not satisfy the VCEP BS3 threshold >0.
ClinGen PTEN VCEP specification v3.2: BS3_Supporting applies to phosphatase activity >0 per Mighell et al. 2018; no BS3 strength is assigned because this variant's measured activity is damaging.
Rodríguez-Escudero et al. 2011, PMID:21828076: the exact p.T131I mutant fully abrogated PTEN PIP3 phosphatase activity in yeast, not a no-damage result.
BP4VCEPNot met: REVEL score 0.965 is above, rather than below, the PTEN VCEP BP4 missense threshold of <0.5.
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Reasoning
NM_000314.8:c.392C>T, NP_000305.3:p.(Thr131Ile), is a missense variant. The PTEN VCEP BP4 rule names REVEL for missense variants and requires a REVEL score < 0.5. The exact-variant REVEL score is 0.965, so the VCEP BP4 missense condition is not met. The available SpliceAI result was not used because SpliceAI is named by this rule only for splicing variants, not for this missense situation.
VCEP rule
Multiple lines of computational evidence suggest no impact on gene or gene product.
* Splicing variants: Concordance of SpliceAl and VarSeak
* Missense variants: REVEL scores < 0.5
Evidence considered
ClinGen PTEN VCEP v3.2 BP4 rule: for missense variants, the named predictor is REVEL and the cutoff is <0.5.
Local REVEL predictor lookup for NM_000314.8:c.392C>T / NP_000305.3:p.(Thr131Ile): REVEL score = 0.965; this does not satisfy the VCEP BP4 missense cutoff.
SpliceAI max delta score = 0.004 was not used for BP4 because the VCEP rule assigns SpliceAI to its splicing-variant path, whereas this variant is missense.
PS1VCEPNot assessed: no alternate p.Thr131 missense change is established as pathogenic, and no qualifying pathogenic-splicing comparator at c.392 is available.
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Reasoning
The variant is NP_000305.3:p.(Thr131Ile). The governing rule requires the same amino acid change as a previously established pathogenic variant, regardless of nucleotide change, or an alternative variant at the same nucleotide position as a pathogenic splicing variant with equivalent or greater predicted impact. The available evidence includes a functional study mentioning T131L and T131I, but it does not establish an alternate T131 missense change as pathogenic, and no pathogenic splicing comparator at c.392 was provided. Therefore PS1 cannot be assessed from the available VCEP-governed evidence.
VCEP rule
Same amino acid change as a previously established pathogenic variant regardless of nucleotide change OR different variant at same nucleotide position as a pathogenic splicing variant, where in silico models predict impact equal to or greater than the known pathogenic variant.
Evidence considered
The variant is NP_000305.3:p.(Thr131Ile).
ClinGen PTEN VCEP PS1 requires the same amino acid change as a previously established pathogenic variant, regardless of nucleotide change, or a different variant at the same nucleotide position as a pathogenic splicing variant with equal or greater predicted impact.
Rodríguez-Escudero et al. report T131I and T131L in a yeast PIP3 phosphatase assay, but the extracted paper finding does not establish an alternate T131 missense variant as pathogenic.
Still missing
A previously established pathogenic variant producing the same p.Thr131Ile amino acid change through a different nucleotide change, or a qualifying pathogenic-splicing comparator at c.392, is required.
PS2VCEPNot assessed: presumed de novo status is reported, but the PS2 Strong requirement for confirmed maternity and paternity is not documented.
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Reasoning
The available evidence describes presumed de novo observations without confirmation of maternity and paternity. The PTEN VCEP PS2 rule requires both maternity and paternity to be confirmed for the Strong level, and no evidence establishes the Very Strong PS2 observation counts.
VCEP rule
Strong: De novo (both maternity and paternity confirmed) observation in a patient with the disease and no family history. Very Strong: Two proven OR four assumed OR one proven + two assumed de novo observations in a patient with the disease and no family history.
Evidence considered
The ClinGen PTEN Expert Panel submission audit records a signal for presumed de novo occurrence but does not provide confirmed maternity and paternity; it therefore does not satisfy the VCEP PS2 Strong rule.
The available literature extraction for PMID:23160955 reports a de novo PTEN mutation burden in an autism cohort but does not explicitly report PTEN c.392C>T (p.Thr131Ile).
Still missing
Confirmation of both maternity and paternity for a qualifying affected proband is not available.
The number of proven or assumed de novo observations qualifying for PS2 Very Strong is not independently documented.
PS4VCEPNot assessed: no variant-specific odds ratio, confidence interval, p-value, or phenotype-specificity score is available for the PS4 thresholds.
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Reasoning
The PTEN VCEP permits PS4 from a case-control result with odds ratio >2, p<0.05, and a 95% confidence-interval lower limit >1.5, or from independent proband phenotype-specificity scores. The available evidence provides no case-control odds ratio, p-value, confidence interval, Cleveland Clinic score, pediatric phenotype score, or aggregate specificity score for this variant. The reviewed literature describes PTEN-associated cohorts or phenotypes but does not provide the required variant-specific PS4 metric. Therefore PS4 cannot be evaluated under the VCEP rule.
VCEP rule
This criterion may not be applied if BS1 applies. Phenotype specificity scores are added across independent probands and calculated as follows: ... PS4: Probands with specificity score of 4-15.5. ... PS4_Supporting: Proband(s) with specificity score of 1-1.5.
Evidence considered
ClinGen PTEN VCEP specification v3.2: PS4 may use a sufficiently powered case-control study with odds ratio >2, p<0.05, and 95% confidence-interval lower limit >1.5, or phenotype-specificity scores summed across independent probands.
ClinVar record for NM_000314.8:c.392C>T (p.Thr131Ile) lists disease conditions including macrocephaly-autism syndrome, diffuse pediatric-type high-grade glioma, and PTEN hamartoma tumor syndrome, but supplies no PS4 specificity score or case-control statistic.
PMID:23160955 reports macrocephaly in individuals with PTEN mutations but does not explicitly report c.392C>T/p.(T131I) or a qualifying variant-specific PS4 metric.
PMID:22748663 reports pediatric glioma PTEN mutation/deletion frequencies but does not mention c.392C>T/p.(T131I) or provide the VCEP-required variant-specific case-control statistic.
PMID:23335809 reports a 146-person PTEN cohort and genotype-phenotype analyses but does not mention c.392C>T/p.(T131I) or provide a qualifying specificity score for this variant.
Still missing
Variant-specific case-control odds ratio, p-value, and 95% confidence interval, or qualifying independent-proband Cleveland Clinic/pediatric phenotype scores, are unavailable.
PM5VCEPNot assessed: no same-residue pathogenic or likely pathogenic comparator with the required BLOSUM62 comparison is available.
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Reasoning
The variant is p.Thr131Ile. The VCEP PM5 rule requires a different missense change at the same amino acid residue that has been determined pathogenic or likely pathogenic, plus a BLOSUM62 score for the queried variant equal to or lower than that known variant. The available PM5 candidate collection found no same-residue candidates and supplies no qualifying comparator or BLOSUM62 comparison; therefore PM5 is not assessed.
VCEP rule
Missense change at an amino acid residue where a different missense change determined to be pathogenic or likely pathogenic has been seen before. In addition, variant being interrogated must have BLOSUM62 score equal to or less than the known variant.
Evidence considered
The variant is NP_000305.3:p.(Thr131Ile), affecting residue 131.
The VCEP PM5 rule requires a different missense change at the same residue that is pathogenic or likely pathogenic and requires the queried variant's BLOSUM62 score to be equal to or lower than the known variant's score.
The PM5 candidate artifact reports zero same-residue candidates, zero expert-panel pathogenic/likely pathogenic candidates, and zero non-expert majority pathogenic/likely pathogenic candidates; it provides no BLOSUM62 comparator calculation.
Still missing
A different p.Thr131 missense variant determined pathogenic or likely pathogenic and its applicable BLOSUM62 score are required.
PP1VCEPNot assessed: no variant-specific affected relatives, co-segregation observations, or meiosis count are documented.
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Reasoning
No case-level segregation observations, affected relatives, or meiosis count are available for this variant. The literature extraction does not report variant-specific segregation, so none of the VCEP PP1 thresholds can be evaluated.
VCEP rule
Strong: Co-segregation with disease in multiple affected family members, with ≥7 meioses observed across at least two families. Moderate: Co-segregation with disease in multiple affected family members, with 5 or 6 meioses observed. Supporting: Co-segregation with disease in multiple affected family members, with 3 or 4 meioses observed.
Evidence considered
The available evidence contains no variant-specific co-segregation results or meiosis count for PTEN c.392C>T (p.Thr131Ile).
Still missing
Variant-level segregation data in affected family members are not available.
The number of observed meioses across families is not available.
PP2VCEPNot assessed: VCEP-specific evidence establishing both low benign missense variation and a common PTEN missense disease mechanism is unavailable.
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Reasoning
The VCEP PP2 rule requires both a low rate of benign missense variation in the gene and missense variants being a common disease mechanism. The available VCEP-governed evidence does not provide a gene-level benign-missense-rate assessment or an explicit VCEP determination that missense variation is a common PTEN disease mechanism. The criterion therefore cannot be assessed without importing a non-VCEP threshold or assumption.
VCEP rule
Missense variant in a gene that has a low rate of benign missense variation and where missense variants are a common mechanism of disease.
Evidence considered
The VCEP PP2 rule requires a low rate of benign missense variation and missense variants to be a common mechanism of disease.
The available case evidence does not contain a VCEP-specific benign-missense-rate value or an explicit VCEP statement satisfying both PP2 conditions.
Still missing
A VCEP-governed assessment of PTEN benign missense variation rate and missense disease-mechanism prevalence is required.
BS2VCEPNot assessed: no homozygous observation in a healthy or PHTS-unaffected individual is available for this absent variant.
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Reasoning
The PTEN VCEP requires observation of the variant in the homozygous state in a healthy or PHTS-unaffected individual. The available population evidence reports the variant as absent from gnomAD v2.1, v4.1, v2.1 non-cancer, and v3.1 non-cancer, and provides no homozygote observations, parental confirmation, or clinical-status information. Therefore BS2 cannot be evaluated.
VCEP rule
Observed in the homozygous state in a healthy or PHTS-unaffected individual. One observation if homozygous status confirmed, two if not confirmed. To be applied at supporting evidence level if BS1 is also applied.
Evidence considered
ClinGen PTEN VCEP specification v3.2, BS2 Strong rule: observed in the homozygous state in a healthy or PHTS-unaffected individual; one observation if homozygous status is confirmed and two if not confirmed; apply at supporting level if BS1 is also applied.
gnomAD v2.1, gnomAD v4.1, gnomAD v2.1 non-cancer, and gnomAD v3.1 non-cancer all report the variant absent and provide no homozygote observation or clinical-status record.
Still missing
A confirmed or appropriately documented homozygous observation in a healthy or PHTS-unaffected individual is required.
BS4VCEPNot assessed: no affected family members with documented lack of variant segregation are reported in one or more families.
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Reasoning
No affected family members carrying the variant are described as non-segregating, and no family-level segregation data are available. Therefore, the VCEP BS4 thresholds for one or two or more families cannot be evaluated.
VCEP rule
Strong: Lack of segregation in affected members of two or more families. Supporting: Lack of segregation in affected members of one family.
Evidence considered
The available evidence contains no affected-family non-segregation observation for PTEN c.392C>T (p.Thr131Ile).
Still missing
Family-level non-segregation data are not available.
BP2VCEPNot assessed: no documented trans, cis, or phase-unknown observation with a different pathogenic or likely pathogenic PTEN variant is available.
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Reasoning
The VCEP BP2 rule requires either observation of the queried variant in trans with a pathogenic or likely pathogenic PTEN variant, or at least three observations in cis and/or phase unknown with different pathogenic or likely pathogenic PTEN variants. The available case evidence does not document a qualifying trans observation, three qualifying cis or phase-unknown observations, or the relevant phase and partner-variant details. The criterion therefore cannot be evaluated.
VCEP rule
Observed in trans with a pathogenic or likely pathogenic PTEN variant OR at least three observations in cis and/or phase unknown with different pathogenic/likely pathogenic PTEN variants.
Evidence considered
No case-level report in the reviewed evidence documents NM_000314.8:c.392C>T in trans with a pathogenic or likely pathogenic PTEN variant.
No set of at least three observations in cis and/or phase unknown with different pathogenic or likely pathogenic PTEN variants is documented; ClinVar classification and functional observations do not establish this allelic evidence.
Still missing
A qualifying pathogenic or likely pathogenic PTEN partner variant and its phase relative to NM_000314.8:c.392C>T are not documented.
There are not three documented cis and/or phase-unknown observations involving different pathogenic or likely pathogenic PTEN variants.
BP5VCEPNot assessed: no two qualifying cases with a highly penetrant alternate disorder and non-overlapping personal or family histories are documented.
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Reasoning
The PTEN VCEP requires a variant found in a case with an alternate molecular basis, at least two such cases, a highly penetrant other gene/disorder, and personal or family history showing no overlap between that disorder and PTEN. The available case bundle contains no qualifying alternate-gene diagnoses, two-case series, or documented non-overlapping personal/family histories for NM_000314.8:c.392C>T. Therefore BP5 cannot be evaluated.
VCEP rule
At least two such cases are required for criteria to apply. In addition, the other gene/disorder must be considered highly penetrant AND the patient’s personal/family history must demonstrate no overlap between the other gene and PTEN. ... Variant found in a case with an alternate molecular basis for disease. Other gene/disorder must be considered highly penetrant AND patient’s personal/family history must demonstrate no overlap between other gene and PTEN.
Evidence considered
ClinGen PTEN VCEP specification v3.2 requires at least two cases, a highly penetrant alternate gene/disorder, and personal/family history demonstrating no overlap between the alternate disorder and PTEN.
No case-level alternate molecular basis or qualifying non-overlapping personal/family history is provided for this variant.
Still missing
At least two qualifying cases with an alternate highly penetrant molecular diagnosis and documented absence of phenotype overlap with PTEN are unavailable.
Not applicable · 8· recorded as not applicableShow reasons ▾Hide reasons ▴PVS1N/ANot applicable: c.392C>T is a missense variant (p.Thr131Ile), outside the PTEN decision tree's null-variant consequence classes.
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Reasoning
NM_000314.8:c.392C>T (NP_000305.3:p.(Thr131Ile), p.(T131I)) is a missense substitution in exon 5, not a nonsense, frameshift, canonical splice-site, exon-deletion, duplication, or initiation-codon variant covered by the PTEN PVS1 decision tree. The governing CSPEC entry directs use of the PTEN decision tree, and the consulted PVS1_DecisionTree_PTEN.pdf contains no notation of c.392C>T, p.Thr131Ile, or p.T131I. Therefore, the null-variant PVS1 pathway does not apply; NMD and the p.D375 threshold are not applicable to this missense consequence.
VCEP rule
Use PTEN PVS1 decision tree.
Evidence considered
Case normalization: NM_000314.8:c.392C>T corresponds to NP_000305.3:p.(Thr131Ile) / p.(T131I); the variant assessment classifies it as missense in exon 5.
ClinGen PTEN VCEP CSPEC PVS1 entry: the rule is to use the PTEN PVS1 decision tree.
PVS1_DecisionTree_PTEN.pdf is declared for PVS1 and was searched for c.392C>T, p.Thr131Ile, and p.T131I; no variant-specific row was found.
Still missing
No entry for c.392C>T, p.Thr131Ile, or p.T131I was found in PVS1_DecisionTree_PTEN.pdf.txt; the file was searched directly.
PM3VCEPNot applicable: the PTEN VCEP explicitly marks PM3 as not applicable, so recessive-allelic evidence is not evaluated.
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Reasoning
The ClinGen PTEN VCEP Version 3.2 CSPEC explicitly marks PM3 as not applicable. Therefore, PM3 is not evaluated for this PTEN variant, regardless of the absence or presence of available phase observations.
VCEP rule
Not Applicable
Evidence considered
ClinGen PTEN Expert Panel Specifications Version 3.2 CSPEC entry for PM3: applicability is "Not Applicable".
PM4N/ANot applicable: p.(Thr131Ile) is a missense substitution with no protein-length change, whereas PM4 requires an in-frame indel or stop-loss extension.
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Reasoning
The variant is missense, p.(Thr131Ile), and does not change protein length. The PTEN VCEP PM4 rule is limited to protein length changes from in-frame insertions/deletions in a non-repeat region or stop-loss variants, including in-frame changes affecting a catalytic motif and protein extensions. None of those consequence classes applies to c.392C>T.
VCEP rule
Protein length changes due to in-frame deletions/insertions in a non-repeat region or stop-loss variants. Applies to in-frame insertions or deletions impacting at least one residue in a catalytic motif (see PM1), and variants causing protein extension.
Evidence considered
The case variant assessment identifies NM_000314.8:c.392C>T as missense, encoding NP_000305.3:p.(Thr131Ile) / p.(T131I).
Mighell et al. 2018 supplementary Table S2, row T131I / Thr131Ile: the variant is explicitly listed as missense; no protein-length change is reported.
The PTEN VCEP PM4 rule requires protein length changes due to in-frame deletions/insertions in a non-repeat region or stop-loss variants, including catalytic-motif indels and protein extensions.
BP3VCEPNot applicable: the PTEN VCEP CSPEC explicitly marks BP3 as Not Applicable for this framework.
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Reasoning
The PTEN VCEP CSPEC entry marks BP3 as Not Applicable. Accordingly, BP3 is not evaluated for this missense variant, regardless of its exon or repeat-region context.
VCEP rule
Not Applicable
Evidence considered
ClinGen PTEN VCEP CSPEC BP3 entry: applicability is explicitly listed as Not Applicable.
BP7N/ANot applicable: p.(Thr131Ile) is a missense change, whereas PTEN VCEP BP7 covers only synonymous or qualifying intronic variants.
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Reasoning
NM_000314.8:c.392C>T produces NP_000305.3:p.(Thr131Ile), making it a missense rather than a synonymous or intronic variant. The PTEN VCEP BP7 rule is limited to synonymous or intronic variants at or beyond +7/-21, so this missense variant lies outside BP7 scope and no predictor result is needed.
VCEP rule
A synonymous (silent) or intronic variant at or beyond +7/-21 for which splicing prediction algorithms predict no impact to the splice consensus sequence nor the creation of a new splice.
Evidence considered
ClinGen PTEN VCEP v3.2 BP7 rule applies to a synonymous (silent) or intronic variant at or beyond +7/-21.
NM_000314.8:c.392C>T is a missense variant encoding NP_000305.3:p.(Thr131Ile), not a synonymous or intronic variant; BP7 is therefore outside its governing scope.
Every interpreted variant in PTEN, mapped onto the exon structure of NM_000314.8. Select a row to find it on the plot.
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—Select a row to find it on the plot; use the link to open its page.
Protein
Location
Classification
Link
gnomAD v4.1Allele count data not recorded
gnomAD v2.1Allele count data not recorded
gnomAD-Canada v1.0Allele count data not recorded
Statements
gnomAD v4.1
Absent from gnomAD v4.1.
gnomAD v2.1
Absent from gnomAD v2.1.
gnomAD-Canada
Absent from gnomAD-Canada v1.0.
SpliceAI and Pangolin
SpliceAI acceptor lossat -156 bp
0.004
SpliceAI acceptor gainat +344 bp
0.000
SpliceAI donor lossat +79 bp
0.000
SpliceAI donor gainat -22 bp
0.000
Pangolin splice lossmagnitude shown
-0.003
Pangolin splice gain
0.001
Other predictors
REVEL
0.965
BayesDel
0.585
How the predictions were used
PP3SupportingVCEPMet: REVEL score 0.965 exceeds the PTEN VCEP PP3 missense threshold of >0.7.
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Reasoning
NM_000314.8:c.392C>T, NP_000305.3:p.(Thr131Ile), is a missense variant. The PTEN VCEP PP3 rule names REVEL for missense variants and requires a REVEL score > 0.7. The exact-variant REVEL score is 0.965, which exceeds the VCEP threshold; the available SpliceAI result was not used because SpliceAI is named by this rule only for splicing variants, not for this missense situation. PP3 is met at supporting strength.
VCEP rule
Multiple lines of computational evidence support a deleterious effect on the gene or gene product.
* Splicing variants: Concordance of SpliceAl and VarSeak
* Missense variants: REVEL score > 0.7
Evidence considered
ClinGen PTEN VCEP v3.2 PP3 rule: for missense variants, the named predictor is REVEL and the cutoff is >0.7.
Local REVEL predictor lookup for NM_000314.8:c.392C>T / NP_000305.3:p.(Thr131Ile): REVEL score = 0.965; this exceeds the VCEP PP3 missense cutoff.
SpliceAI max delta score = 0.004 was not used for PP3 because the VCEP rule assigns SpliceAI to its splicing-variant path, whereas this variant is missense.
BP4VCEPNot met: REVEL score 0.965 is above, rather than below, the PTEN VCEP BP4 missense threshold of <0.5.
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Reasoning
NM_000314.8:c.392C>T, NP_000305.3:p.(Thr131Ile), is a missense variant. The PTEN VCEP BP4 rule names REVEL for missense variants and requires a REVEL score < 0.5. The exact-variant REVEL score is 0.965, so the VCEP BP4 missense condition is not met. The available SpliceAI result was not used because SpliceAI is named by this rule only for splicing variants, not for this missense situation.
VCEP rule
Multiple lines of computational evidence suggest no impact on gene or gene product.
* Splicing variants: Concordance of SpliceAl and VarSeak
* Missense variants: REVEL scores < 0.5
Evidence considered
ClinGen PTEN VCEP v3.2 BP4 rule: for missense variants, the named predictor is REVEL and the cutoff is <0.5.
Local REVEL predictor lookup for NM_000314.8:c.392C>T / NP_000305.3:p.(Thr131Ile): REVEL score = 0.965; this does not satisfy the VCEP BP4 missense cutoff.
SpliceAI max delta score = 0.004 was not used for BP4 because the VCEP rule assigns SpliceAI to its splicing-variant path, whereas this variant is missense.
BP7N/ANot applicable: p.(Thr131Ile) is a missense change, whereas PTEN VCEP BP7 covers only synonymous or qualifying intronic variants.
Details ▾Hide ▴
Reasoning
NM_000314.8:c.392C>T produces NP_000305.3:p.(Thr131Ile), making it a missense rather than a synonymous or intronic variant. The PTEN VCEP BP7 rule is limited to synonymous or intronic variants at or beyond +7/-21, so this missense variant lies outside BP7 scope and no predictor result is needed.
VCEP rule
A synonymous (silent) or intronic variant at or beyond +7/-21 for which splicing prediction algorithms predict no impact to the splice consensus sequence nor the creation of a new splice.
Evidence considered
ClinGen PTEN VCEP v3.2 BP7 rule applies to a synonymous (silent) or intronic variant at or beyond +7/-21.
NM_000314.8:c.392C>T is a missense variant encoding NP_000305.3:p.(Thr131Ile), not a synonymous or intronic variant; BP7 is therefore outside its governing scope.
SpliceAI predicts no significant splice impact for this variant (max delta score = 0.00). REVEL score = 0.965. BayesDel score = 0.585205.
6 paper records listed. 1 cited in the classification.
Cited in the classification
A comprehensive functional analysis of PTEN mutations: implications in tumor- and autism-related syndromes.
Rodríguez-Escudero I et al. · 2011 Nov 1
The paper explicitly evaluates PTEN p.(T131I) and p.(T131L) in a heterologous Saccharomyces cerevisiae assay measuring PIP3 phosphatase activity; both were reported among mutations that fully abrogated activity, but the extracted finding does not establish T131L as a pathogenic or likely pathogenic comparator for PS1 or PM5.
A group of mutations (H123Y, C124N, A126D, G127N, K128T, G129D, R130A, R130K, T131I and T131L) fully abrogated the PIP3 phosphatase activity of PTEN in yeast
Location Results, “Functional analysis of mutations at the PTEN P-loop mimicking PTEN-like proteins”; Results, “Functional analysis of tumor-related mutations targeting PTEN active site residues”
Context Heterologous S. cerevisiae reconstitution assay with PTEN, PI3K p110α-CAAX and GFP-Akt1; PIP3 phosphatase activity was assessed by GFP-Akt1 localization and rescue of PI3K-induced yeast growth inhibition.
Other recorded publications
Multi-model functionalization of disease-associated PTEN missense mutations identifies multiple molecular mechanisms underlying protein dysfunction.
The paper does not mention PTEN c.392C>T or NP_000305.3:p.(T131I). It reports PTEN deletions and mutations in pediatric high-grade glioma cohorts, including poorer prognosis when PTEN alterations are present.
The CCG trial reported that 24% of pediatric GBMs and AAs had PTEN deletions.21 Although mutations in PTEN are rare in pediatric GBM than in GBM in adults, if present, a poorer prognosis can be expected. PTEN mutation is rare (8%) in pediatric AA, but if present is associated with poor prognosis.23
The paper does not explicitly report PTEN c.392C>T (NP_000305.3:p.(T131I)). It reports that PTEN was one of six genes with evidence of de novo mutation burden in 2,446 ASD probands and that macrocephaly was observed in individuals with de novo and inherited PTEN mutations.
Macrocephaly was also observed in individuals with de novo and inherited PTEN mutations (22).
Results, paragraph discussing phenotypic data and head circumference
High cumulative risks of cancer in patients with PTEN hamartoma tumour syndrome.
Bubien V et al. · 2013
The paper does not explicitly mention PTEN c.392C>T or NP_000305.3:p.(T131I). It reports a cohort of 146 individuals with deleterious germline PTEN mutations and genotype-phenotype analyses, without a variant-specific PS4 score or alternate molecular basis for this variant.
The evidence statements recorded by the interpretation pipeline. They have not been reinterpreted by the page.
gnomAD v4.1
Absent from gnomAD v4.1.
gnomAD v2.1
Absent from gnomAD v2.1.
gnomAD-Canada
Absent from gnomAD-Canada v1.0.
ClinVar
This variant has been reported in ClinVar as Likely pathogenic (1 clinical laboratory) and as Pathogenic by Clingen PTEN Variant Curation Expert Panel, Clingen (expert panel). (ClinVarID = 39669)
In silico
SpliceAI predicts no significant splice impact for this variant (max delta score = 0.00). REVEL score = 0.965. BayesDel score = 0.585205.
Functional
OncoKB identified variant-specific curated literature and context relevant to functional review; biological-effect context: Loss-of-function; curated oncogenicity label: Oncogenic.
Somatic
This variant does not lie in a statistically significant hotspot. This variant has previously been reported in somatic cancers (COSMIC; COSV64300549, n = 2 times).
Cancer Hotspots
This variant does not lie in a statistically significant hotspot.