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Variant interpretation report

PMS2 c.353+7C>A, p.?

NM_000535.7:c.353+7C>A NP_000526.2:p.? Unknown · intron 4 View identifiers
Classification
Likely benign

Variant description:

The PMS2 NM_000535.7:c.353+7C>A (NP_000526.2:p.?) intronic variant has previously been reported in somatic cancers (COSMIC; COSV56220636, n = 2 times). Based on available guidelines, this variant is considered to be Likely Benign.

Five-step scale from benign to pathogenic. This variant is likely benign. Select a step to read what it means.

Likely benign.A likely benign classification under the recorded framework.

In plain language

Gene-level background from the recorded interpretation.

About PMS2

PMS2 is a DNA mismatch-repair protein that works with MLH1 to correct replication errors, including mismatches and small insertion or deletion loops. It acts as a tumor suppressor, and inherited loss of PMS2 function can cause Lynch syndrome and constitutional mismatch repair deficiency, increasing the risk of colorectal, endometrial, ovarian, urothelial, and other cancers. Loss of PMS2 function in tumors can cause hypermutation and microsatellite instability, which may make some cancers responsive to certain immunotherapies.

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.
01The reasoning

How it was classified

The recorded framework is ClinGen PMS2 VCEP v2.0. 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.

Pathogenic evidence criteria: 1 Benign evidence criteria: 2
Pathogenic criteria applied · 1
PM2Supporting
PM2 · supporting

Met at Supporting: gnomAD v4.1 AF is 6.74003e-06, below the VCEP PM2 cutoff of 0.00002.

Benign criteria applied · 2
BP4Supporting
BP4 · supporting

Met, Supporting: SpliceAI maximum delta score 0.014 satisfies the VCEP intronic BP4 threshold of <=0.1.

BP7Supporting
BP7 · supporting

Met, Supporting: c.353+7 is an intronic position at the VCEP's included +7 boundary for BP7.

Recorded classification: Likely benign

Likely Benign: PM2, BP4, and BP7 at Supporting strength satisfy the PMS2 VCEP's Rule19 requiring at least two benign Supporting criteria.

02The sources

Evidence at a glance

Evidence summaries and captured source records, where available. Missing entries should not be interpreted as negative findings.

gnomAD v4.1
gnomAD v2.1
Population frequency
10 / 1,483,674 alleles

gnomAD v4.1: 10 / 1,483,674 alleles. Recorded AF 6.74003e-06. Recorded homozygote count 0.

gnomAD v2.1

This variant is present in gnomAD v2.1 (AF= 1.50446e-05; MAF= 0.00150%, 4/265876 alleles, homozygotes = 0) and has highest observed frequency in the European (non-Finnish) population (AF= 3.21926e-05; MAF= 0.00322%, 4/124252 alleles, homozygotes = 0); grpmax FAF= 5.237e-05.

gnomAD-Canada

This variant is present in gnomAD-Canada v1.0 (AF= 5.42947116950809e-05, 1/18418 alleles, homozygotes = 0).

SpliceAI score
0.014 maximum delta

Recorded SpliceAI maximum delta score: 0.014. Refer to the recorded PP3/BP4 rationale for interpretation.

ClinVar submissions
5 reported laboratory submissions

5 Likely benign. ClinVar API review status: criteria provided, multiple submitters, no conflicts.

Context only ClinVar ↗
No screenshot for this evidence
Functional evidence
Not recorded

No standalone functional evidence summary is recorded in evidence_summary.functional.

No listed criterion applied OncoKB ↗
Somatic evidence
2 recorded samples

This variant has previously been reported in somatic cancers (COSMIC; COSV56220636, n = 2 times).

Context only COSMIC ↗
For specialists

Technical detail

ACMG/AMP criteria under ClinGen PMS2 VCEP v2.0, with the data and sources behind each one.

28 criteria with recorded statuses: 3 met · 3 not met · 10 not assessed · 12 not applicable. Open any row for the full reasoning, the rule and the evidence behind it.

Met Not met Not assessed Not applicable

PS4, PP5, and BP6 are not applicable under the PMS2 VCEP specification.

PP4 and BP5 remain not assessed because required patient-level tumor phenotype and molecular findings are unavailable.

For this intronic c.353+7C>A variant, the VCEP-specific computational/splicing criteria are PP3 not met because SpliceAI 0.014 is below 0.2, BP4_Supporting met because 0.014 is <=0.1, and BP7_Supporting met because the variant is at the included +7 intronic boundary.

The HCI-PRIORS-PMS2.txt.txt file was searched for c.353+7C>A and p.?; no exact entry was found, and the table's declared scope is missense substitutions.

Met · 3

PM2 SupportingVCEPMet at Supporting: gnomAD v4.1 AF is 6.74003e-06, below the VCEP PM2 cutoff of 0.00002. Details ▾Hide ▴
Reasoning

The governing PMS2 VCEP PM2 rule requires an absent or extremely rare allele frequency below 0.00002 in gnomAD v4. The variant is present in gnomAD v4.1 at AF 6.74003e-06 (10/1,483,674 alleles), with grpmax FAF 4.7e-06 and zero homozygotes; therefore PM2 Supporting is met. The gnomAD v2.1 non-cancer exome subset also reports AF 4.48523e-06 (1/222,954 exome alleles), but the VCEP rule specifically names gnomAD v4, so the v4 result governs. No governing-table entry for NM_000535.7:c.353+7C>A or its p.? notation was found in VCEP-pilot-variants---MMR.xlsx.txt.

VCEP rule
Absent/extremely rare allele frequency <0.00002 (<1 in 50,000 alleles ) in gnomAD v4 dataset
Evidence considered
  • gnomAD v4.1: variant 7-6003683-G-T has AF 6.74003e-06 (10/1,483,674 alleles), grpmax FAF 4.7e-06, and zero homozygotes.
  • gnomAD v2.1 non-cancer exomes: AF 4.48523e-06 (1/222,954 exome alleles), zero homozygotes; this is concordant but not the VCEP-named dataset for the rule.
  • The governing VCEP pilot table was searched for c.353+7C>A and p.?; no matching row was found.
Sources
BP4 SupportingVCEPMet, Supporting: SpliceAI maximum delta score 0.014 satisfies the VCEP intronic BP4 threshold of <=0.1. Details ▾Hide ▴
Reasoning

The variant is intronic, making the VCEP's intronic/synonymous BP4 path applicable. SpliceAI reports a maximum delta score of 0.014, which is <= 0.1; therefore the VCEP no-splicing-impact threshold is satisfied and BP4_Supporting is met. The missense HCI prior path is not applicable, and the HCI-PRIORS-PMS2 table had no exact c.353+7C>A or p.? entry.

VCEP rule
For intronic and synonymous variants: SpliceAI predicts no splicing impact with delta score <= 0.1 as per Walker et al 2023.
Evidence considered
  • SpliceAI result for NM_000535.7:c.353+7C>A: maximum delta score 0.014, indicating no predicted splicing impact under the VCEP cutoff.
  • The variant is intronic at c.353+7, which is within the VCEP's intronic BP4 scope.
  • HCI-PRIORS-PMS2.txt.txt was searched for the exact notations c.353+7C>A and p.?; no matching row was found, and the indexed HCI path is missense-only.
Still missing
  • No exact entry for c.353+7C>A or p.? was found in HCI-PRIORS-PMS2.txt.txt; the VCEP intronic SpliceAI path was evaluable independently.
Sources
BP7 SupportingVCEPMet, Supporting: c.353+7 is an intronic position at the VCEP's included +7 boundary for BP7. Details ▾Hide ▴
Reasoning

The variant is intronic at c.353+7, exactly the 3-prime intronic boundary included by the VCEP phrase at or beyond -21/+7 (5-prime/3-prime exonic). It therefore meets BP7_Supporting by location. The VCEP expressly allows BP7 and BP4 to be satisfied together; this does not double-count BP7 as a second splice prediction.

VCEP rule
A synonymous (silent) or intronic variant at or beyond -21/+7 (5′/3′ exonic). Variants may satisfy both BP7 and BP4.
Evidence considered
  • Variant normalization identifies NM_000535.7:c.353+7C>A as an intronic variant in intron 4i.
  • The VCEP BP7 rule explicitly includes intronic variants at or beyond -21/+7 and states that BP7 and BP4 may both be satisfied.
Sources

Not met · 3 · evaluated, threshold not reached

PP3 VCEPNot met: SpliceAI maximum delta score 0.014 is below the VCEP PP3 splice-defect threshold of >=0.2. Details ▾Hide ▴
Reasoning

The variant is intronic at the non-canonical +7 position, so the applicable PP3 path is the VCEP's SpliceAI splice-defect path; the governing threshold is delta score >= 0.2. SpliceAI reports a maximum delta score of 0.014 (DS_DL 0.014; DS_AG 0.003; DS_AL 0.001; DS_DG 0.000), below the threshold, so PP3 is not met. The HCI-PRIORS-PMS2 table was searched for c.353+7C>A and p.? with no exact entry; its indexed scope is missense, and no missense prior is applicable to this intronic variant.

VCEP rule
Predicted splice defect for non-canonical splicing nucleotides using SpliceAI with delta score >= 0.2 as per Walker et al 2023.
Evidence considered
  • SpliceAI result for NM_000535.7:c.353+7C>A: maximum delta score 0.014, with DS_AG 0.003, DS_AL 0.001, DS_DG 0.000, and DS_DL 0.014.
  • The variant is intronic at c.353+7 and has predicted protein consequence NP_000526.2:p.?, so the missense HCI prior path does not apply.
  • HCI-PRIORS-PMS2.txt.txt was searched for the exact notations c.353+7C>A and p.?; no matching row was found.
Still missing
  • No exact entry for c.353+7C>A or p.? was found in HCI-PRIORS-PMS2.txt.txt; that table is indexed for missense substitutions, not this intronic variant.
Sources
BA1 VCEPNot met: gnomAD v4.1 grpmax FAF is 4.7e-06, far below the VCEP BA1 threshold of 0.0028. Details ▾Hide ▴
Reasoning

The governing PMS2 VCEP BA1 threshold is a gnomAD v4 Grpmax filtering allele frequency of at least 0.0028, with exclusion as a founder pathogenic variant. The variant's gnomAD v4.1 grpmax FAF is 4.7e-06 (0.00047%), based on 10/1,483,674 total alleles and zero homozygotes, which is below 0.0028. No governing-table entry for NM_000535.7:c.353+7C>A or its p.? notation was found in VCEP-pilot-variants---MMR.xlsx.txt.

VCEP rule
GnomAD v4 Grpmax filtering allele frequency ≥ 0.0028 (0.28%) and variant is excluded as founder pathogenic variant.
Evidence considered
  • gnomAD v4.1: variant 7-6003683-G-T has total AF 6.74003e-06 (10/1,483,674 alleles), zero homozygotes, and grpmax FAF 4.7e-06.
  • The governing VCEP pilot table was searched for c.353+7C>A and p.?; no matching row was found.
Sources
BS1 VCEPNot met: gnomAD v4.1 grpmax FAF is 4.7e-06, below the VCEP BS1 lower threshold of 0.00028. Details ▾Hide ▴
Reasoning

The governing PMS2 VCEP BS1 threshold is a gnomAD v4 Grpmax filtering allele frequency of at least 0.00028 and less than 0.0028, with exclusion as a founder pathogenic variant. The variant's gnomAD v4.1 grpmax FAF is 4.7e-06 (0.00047%), below 0.00028. No governing-table entry for NM_000535.7:c.353+7C>A or its p.? notation was found in VCEP-pilot-variants---MMR.xlsx.txt.

VCEP rule
GnomAD v4 Grpmax filtering allele frequency ≥ 0.00028 and < 0.0028 (0.028-0.28%) and variant is excluded as founder pathogenic variant.
Evidence considered
  • gnomAD v4.1: variant 7-6003683-G-T has grpmax FAF 4.7e-06, total AF 6.74003e-06, 10/1,483,674 alleles, and zero homozygotes.
  • The governing VCEP pilot table was searched for c.353+7C>A and p.?; no matching row was found.
Sources

Not assessed · 10 · no assessment recorded

PS1 VCEPNot assessed: SpliceAI maximum delta is 0.014, but no qualifying VCEP-established pathogenic comparator at c.353+7 with a comparable score was identified. Details ▾Hide ▴
Reasoning

The variant is intronic, NM_000535.7:c.353+7C>A, with protein consequence p.?; therefore the same-amino-acid route does not apply. The VCEP also permits PS1 for a variant affecting the same non-canonical splice nucleotide as a confirmed Pathogenic splice variant, or a Likely Pathogenic splice variant for the Moderate route, with similar or worse SpliceAI prediction. SpliceAI predicts a maximum delta score of 0.014 for this variant, but the available evidence does not identify a qualifying VCEP-established pathogenic or likely pathogenic comparator at the same splice nucleotide or provide that comparator's SpliceAI score. The criterion cannot be evaluated from the available evidence.

VCEP rule
A predicted missense substitution that encodes the same amino acid change with a different underlying nucleotide change previously established by this VCEP as Pathogenic (not a predicted or confirmed splice defect). OR Variants affecting the same non-canonical splice nucleotide as a confirmed Pathogenic splice variant with similar or worse splicing in silico prediction using SpliceAI. OR Variants affecting the same non-canonical splice nucleotide as a Likely Pathogenic splice variant with similar or worse splicing in silico prediction using SpliceAI.
Evidence considered
  • Variant normalization: NM_000535.7:c.353+7C>A; NP_000526.2:p.? (case evidence).
  • SpliceAI result: maximum delta score 0.014 (DS_DL 0.014; DS_AG 0.003; DS_AL 0.001; DS_DG 0.000).
  • The governing VCEP rule requires a different nucleotide encoding the same amino-acid change, or a comparator at the same non-canonical splice nucleotide classified by the VCEP as Pathogenic/Likely Pathogenic with similar or worse SpliceAI prediction; no qualifying comparator was available in the case evidence.
Still missing
  • No VCEP-established Pathogenic or Likely Pathogenic comparator variant at the same non-canonical splice nucleotide, with comparator SpliceAI evidence, is available for evaluation.
Sources
PS2 VCEPNot assessed: no proband-parent testing, maternity or paternity confirmation, LS-spectrum tumor result, or de novo point assignment is provided. Details ▾Hide ▴
Reasoning

The VCEP PS2 rule assigns de novo points according to confirmed maternity and paternity, LS-spectrum tumor evidence, and tumor MSI/IHC/methylation status. The available case evidence contains no proband-level de novo observation, parental testing, maternity or paternity confirmation, LS-spectrum tumor result, or de novo point assignment, so PS2 cannot be evaluated.

Evidence considered
  • The VCEP PS2 specification provides 2 points per proband for a de novo variant with both maternity and paternity confirmed and an MMR-deficient LS-spectrum tumor, 1 point per proband when tumor data are unavailable, and 0.5 points per proband when maternity and/or paternity are unconfirmed with no tumor data.
  • No proband, parental-testing, maternity, paternity, LS-spectrum tumor, MSI/IHC/methylation, or de novo-point evidence is present in the reviewed case materials.
Still missing
  • Documented proband de novo status with maternity and paternity confirmation or the applicable unconfirmed-parent scenario.
  • LS-spectrum tumor diagnosis and MSI/IHC/methylation results, if available.
  • VCEP PS2 de novo point assignment.
Sources
PS3 VCEPNot assessed: no variant-specific functional assay result, functional odds, or demonstrated MMR defect is available for PMS2 c.353+7C>A. Details ▾Hide ▴
Reasoning

The VCEP permits PS3 from calibrated functional assays or an MMR function defect established through the functional-assay flowchart. The case materials contain no variant-specific functional assay result, functional odds, patient-derived RNA result, or other demonstrated MMR defect for PMS2 c.353+7C>A (NP_000526.2:p.?). The on-record Functional-assay-SVI-documentation-MMR.xlsx was searched for c.353+7C>A and p.? with no matching variant entry; its table documents validated assay designs and calibration controls, but does not supply a result for this variant. The on-record Functional-assay-flowchart.pdf was also searched for c.353+7C>A and p.? with no matching variant entry. Therefore PS3 cannot be evaluated from the available variant-specific evidence.

VCEP rule
Calibrated functional assays with functional odds for Pathogenicity > 18.7 OR calibrated functional assays with functional odds for pathogenicity >4.3 and <= 18.7 OR MMR function defect following functional assay flowchart* OR variants with monoallelic expression: complete loss of expression (<10% of wild-type in cDNA without puromycin) of the variant allele. Full-length transcript should be analysed with and without NMD block.
Evidence considered
  • Case normalization: NM_000535.7:c.353+7C>A; NP_000526.2:p.?; intronic variant.
  • Functional-assay-SVI-documentation-MMR.xlsx, sheet 'MMR assays': validated assay classes, control requirements, calibration thresholds, and proposed PS3 strengths are listed, but no row identifies c.353+7C>A or p.?.
  • Functional-assay-flowchart.pdf: splice-site, silent, or intronic variants require a splicing-assay path; no variant-specific result is provided for c.353+7C>A or p.?.
Still missing
  • No variant-specific functional assay result or calibrated functional odds were found in the case evidence.
  • No patient-derived RNA or other assay result demonstrating an MMR function defect was found.
  • No entry for c.353+7C>A or p.? was found in Functional-assay-SVI-documentation-MMR.xlsx.
  • No entry for c.353+7C>A or p.? was found in Functional-assay-flowchart.pdf.
Sources
PM3 VCEPNot assessed: no pathogenic PMS2 partner variant, CMMRD features, or phase evidence is available to assign the VCEP's 0.5-point phase-unknown or 1.0-point trans weight. Details ▾Hide ▴
Reasoning

The VCEP PM3 rule requires co-occurrence of this PMS2 variant with a known pathogenic or likely pathogenic variant in the same gene in a patient with clinical features consistent with CMMRD, with 1.0 point for a confirmed trans configuration or 0.5 points when phase is unknown. The available case evidence contains no affected-proband observation establishing CMMRD features, no pathogenic/likely pathogenic PMS2 partner variant, and no phase result; therefore PM3 cannot be evaluated.

VCEP rule
Co-occurrence with a known pathogenic/likely pathogenic sequence variant in the same gene in a patient with clinical features consistent with CMMRD as per Aronson et al 2022 - Refer to “Table for CMMRD diagnosis.pdf”. ... Pathogenic/Likely Pathogenic _in trans_: 1.0 point; ... Pathogenic/Likely Pathogenic - phase unknown: 0.5 points. ... Sum all cases with the above evidence to determine the PM3 strength.
Evidence considered
  • No case evidence documents a pathogenic or likely pathogenic PMS2 partner variant, an affected proband meeting CMMRD-consistent clinical features, or phase between the variants.
  • The VCEP PM3 instructions assign 1.0 point for a pathogenic/likely pathogenic variant in trans and 0.5 points when phase is unknown; no qualifying case was identified for scoring.
Still missing
  • Documented co-occurrence with a known pathogenic or likely pathogenic PMS2 variant in an affected proband with CMMRD-consistent clinical features.
  • Parental or offspring testing establishing trans phase, or an explicit phase-unknown record if applicable.
Sources
PP1 VCEPNot assessed: no pedigree segregation data or combined Bayes likelihood ratio is provided for comparison with the VCEP thresholds of >2.08, >4.3, or >18.7. Details ▾Hide ▴
Reasoning

The VCEP PP1 rule requires co-segregation in pedigrees with a combined Bayes likelihood ratio, with Supporting >2.08 and <=4.3, Moderate >4.3 and <=18.7, or Strong >18.7 in at least two families. No pedigree, affected or unaffected relative genotypes, meioses, family count, or combined Bayes likelihood ratio is provided, so PP1 cannot be evaluated.

Evidence considered
  • The VCEP PP1 thresholds are Supporting for a combined Bayes likelihood ratio >2.08 and <=4.3, Moderate for >4.3 and <=18.7, and Strong for >18.7 in at least two families.
  • No family pedigree, segregation observations, informative meioses, family count, or combined Bayes likelihood ratio is present in the reviewed case materials.
Still missing
  • Pedigree identifying affected and unaffected relatives and their variant genotypes.
  • Number of informative meioses and families.
  • Combined Bayes likelihood ratio, preferably calculated using the VCEP-recommended COOL approach.
Sources
PP4 VCEPNot assessed: no patient-level CRC/endometrial MSI-H, tumor-genome, or PMS2-loss evidence is available to meet the PP4 tumor threshold. Details ▾Hide ▴
Reasoning

PP4 is applicable, but the available case evidence does not provide the required patient-level tumor MSI/IHC findings or the number of independent qualifying tumors and families. The governing VCEP requires one or more CRC/endometrial MSI-H tumors or tumor-genome evidence and/or loss of MMR protein expression consistent with the variant location; no such patient phenotype evidence is available here. The required Table-for-CMMRD-diagnosis.pdf was searched for c.353+7C>A and p.? with no variant entry, and VCEP-pilot-variants---MMR.xlsx was searched for the same notations with no entry for this variant.

Evidence considered
  • The PP4 VCEP rule requires qualifying CRC/endometrial MSI-H tumor evidence or tumor-genome evidence and/or MMR protein loss consistent with the variant location; no such case-level result is present.
  • Table-for-CMMRD-diagnosis.pdf.txt was searched for c.353+7C>A and p.?; no variant-specific entry was found.
  • VCEP-pilot-variants---MMR.xlsx.txt was searched for c.353+7C>A and p.?; no variant-specific entry was found.
Still missing
  • Patient-level tumor MSI/IHC or tumor-genome results are unavailable for NM_000535.7:c.353+7C>A.
  • No entry for c.353+7C>A or p.? was found in Table-for-CMMRD-diagnosis.pdf.txt.
  • No entry for c.353+7C>A or p.? was found in VCEP-pilot-variants---MMR.xlsx.txt.
Sources
BS2 VCEPNot assessed: no qualifying in-trans co-occurrence, cancer-age, CMMRD, or phase-confirmation evidence is available. Details ▾Hide ▴
Reasoning

The VCEP requires co-occurrence in trans with a known pathogenic sequence variant in PMS2 in a patient with colorectal cancer after age 45 or another Lynch syndrome cancer above its median age of onset, absence of CMMRD manifestations, and phase confirmation through parents or offspring. The available case evidence contains no qualifying patient, cancer-age, CMMRD, co-occurrence, or phase-confirmation data, so BS2 cannot be evaluated.

VCEP rule
Co-occurrence in trans with a known pathogenic sequence variant in the same gene in a patient with colorectal cancer after age 45 (or other LS cancer above the median age of onset for that cancer in LS), and who has no previous or current evidence of clinical manifestations of CMMRD as per Aronson et al 2022 (Refer to 'Table for CMMRD diagnosis.pdf'). Confirmation of phase requires testing of parents or offspring.
Evidence considered
  • The case evidence bundle provides population observations but no qualifying clinical co-occurrence or phase-confirmation record for BS2.
Still missing
  • Qualifying in-trans co-occurrence with a known pathogenic PMS2 variant, affected patient's cancer age and type, CMMRD assessment, and parental or offspring phase confirmation are unavailable.
Sources
BS3 VCEPNot assessed: no NMD-inhibited RNA result, proficient protein/mRNA assay, or benign-range calibrated functional odds are available for PMS2 c.353+7C>A. Details ▾Hide ▴
Reasoning

The VCEP permits BS3 when calibrated functional odds are benign-range or when an intronic variant has no associated mRNA aberration, with laboratory assays conducted using nonsense-mediated decay inhibition; supporting BS3 can also be based on variant-specific proficient protein and mRNA function under the MMR functional-assay flowchart. The case materials contain no variant-specific RNA, splicing, allelic-imbalance, protein-function, or calibrated functional-odds result for PMS2 c.353+7C>A (NP_000526.2:p.?). The on-record Functional-assay-SVI-documentation-MMR.xlsx was searched for c.353+7C>A and p.? with no matching variant entry, and Functional-assay-flowchart.pdf was searched for the same notations with no matching entry. Therefore BS3 cannot be evaluated.

VCEP rule
Calibrated functional assays with functional odds for Pathogenicity <= 0.05 OR synonymous substitutions and intronic variants with no associated mRNA aberration (either splicing or allelic imbalance) as determined by laboratory assays conducted with nonsense-mediated decay inhibition. Whenever abnormal transcripts are identified at similar levels in controls they will be considered naturally occurring isoforms and not mRNA aberrations. OR calibrated functional assays with functional odds for Pathogenicity >0.05 & <=0.48 OR variant-specific proficient function in protein and mRNA-based lab assays as per MMR functional assay flowchart.
Evidence considered
  • Case normalization: NM_000535.7:c.353+7C>A; NP_000526.2:p.?; intronic variant.
  • Functional-assay-SVI-documentation-MMR.xlsx, sheet 'MMR assays': validated assay classes and normal/abnormal readout thresholds are documented, but no row identifies c.353+7C>A or p.? and no variant result is supplied.
  • Functional-assay-flowchart.pdf: no-impact intronic assessment requires an appropriate splicing assay with NMD inhibitors for proficient function; no such variant-specific result is available.
Still missing
  • No NMD-inhibited laboratory assay result addressing splicing or allelic imbalance was found.
  • No variant-specific proficient protein and mRNA assay result was found.
  • No calibrated functional odds for pathogenicity were found.
  • No entry for c.353+7C>A or p.? was found in Functional-assay-SVI-documentation-MMR.xlsx.
  • No entry for c.353+7C>A or p.? was found in Functional-assay-flowchart.pdf.
Sources
BS4 VCEPNot assessed: no non-segregation pedigree data or combined Bayes likelihood ratio is provided for comparison with the VCEP thresholds of <0.05 or >0.05 to 0.48. Details ▾Hide ▴
Reasoning

The VCEP BS4 rule requires lack of co-segregation with a combined Bayes likelihood ratio <0.05 for Strong or >0.05 and <=0.48 for Supporting. No pedigree, non-segregating affected relatives, informative meioses, or combined Bayes likelihood ratio is provided, so BS4 cannot be evaluated.

Evidence considered
  • The VCEP BS4 thresholds are Strong for lack of co-segregation with a combined Bayes likelihood ratio <0.05 and Supporting for >0.05 and <=0.48.
  • No non-segregation pedigree, relative genotype, informative meiosis, family count, or combined Bayes likelihood ratio is present in the reviewed case materials.
Still missing
  • Pedigree identifying affected relatives who do not carry the variant and the relevant unaffected relatives.
  • Number of informative non-segregating meioses and families.
  • Combined Bayes likelihood ratio, preferably calculated using the VCEP-recommended COOL approach.
Sources
BP5 VCEPNot assessed: COSMIC reports 2 somatic observations, but no qualifying tumor MSS/IHC or BRAF/MLH1-methylation evidence is available for BP5. Details ▾Hide ▴
Reasoning

BP5 is applicable under the PMS2 VCEP, but the case contains no qualifying tumor series. The VCEP requires 2 or 3 tumors for Supporting or at least 4 tumors for Strong when tumors show MSS and/or no MMR-protein loss, or inconsistent LS-spectrum protein loss, with an alternative BRAF V600E or MLH1-methylation pathway requiring its own qualifying tumor evidence. COSMIC reports two somatic observations, but it does not establish the required patient-level CRC/endometrial tumor MSI/IHC pattern or the specified alternative molecular basis, so BP5 cannot be assigned.

Evidence considered
  • The VCEP BP5 Supporting rule requires '2 or 3 tumors' with the specified MSS/MMR-protein inconsistency pattern or '1 BRAF V600E (Colon only)/MLH1 methylation' pathway; the Strong rule requires at least 4 tumors or at least 2 alternative-pathway tumors.
  • COSMIC record COSV56220636 reports the variant in somatic cancers 2 times, but provides no qualifying patient-level MSI/IHC or BRAF/MLH1-methylation evidence for BP5.
Still missing
  • Qualifying patient-level tumor MSI status, MMR protein expression, and any BRAF V600E or MLH1 methylation results are unavailable.
Sources
Not applicable · 12· recorded as not applicable Show reasons ▾Hide reasons ▴
PVS1 N/ANot applicable: c.353+7C>A is outside the VCEP's GT-AG 1,2 PVS1 splice-site scope, and SpliceAI's maximum delta score is 0.01. Details ▾Hide ▴
Reasoning

PVS1 is not applicable under the PMS2 VCEP rule. NM_000535.7:c.353+7C>A is a non-canonical intronic variant in exon/intron context 4i, with protein consequence NP_000526.2:p.? and no confirmed patient-mRNA splicing assay in the available evidence. The VCEP PVS1 splice-site pathway is limited to GT-AG 1,2 splice sites, whereas this variant is at +7; therefore that pathway does not apply. SpliceAI reports a maximum delta score of 0.01, but this non-canonical prediction does not establish PVS1 under the VCEP rule. The PVS1 decision-tree file and the VCEP pilot-variant table were searched for c.353+7C>A and p.?; neither contains an exact entry for this variant.

VCEP rule
GT-AG 1,2 splice sites [footnote a] | Exon skipping or use of a cryptic splice site disrupts reading frame and is predicted to undergo NMD | PVS1
Evidence considered
  • Case variant facts: NM_000535.7:c.353+7C>A, NP_000526.2:p.?, exon/intron context 4i, and canonical_splice_consensus=false.
  • SpliceAI result for NM_000535.7:c.353+7C>A: no significant splice impact, maximum delta score 0.01.
  • PVS1_DecisionTree_MMR.pdf.txt, GT-AG 1,2 splice-site row: PVS1 requires exon skipping or cryptic-site use that disrupts the reading frame and is predicted to undergo NMD.
  • PVS1_DecisionTree_MMR.pdf.txt and VCEP-pilot-variants---MMR.xlsx.txt were searched for c.353+7C>A and p.?; no exact matching variant row was found.
Still missing
  • No exact c.353+7C>A or p.? entry was found in PVS1_DecisionTree_MMR.pdf.txt.
  • No exact c.353+7C>A or p.? entry was found in VCEP-pilot-variants---MMR.xlsx.txt.
  • No confirmed patient-derived RNA or independent minigene assay demonstrating a splice aberration and loss of full-length transcript was identified in the available case evidence.
Sources
PS4 VCEPNot applicable: the PMS2 VCEP excludes PS4 proband-counting classification because tumor IHC evidence is evaluated through PP4. Details ▾Hide ▴
Reasoning

The PMS2 VCEP marks PS4 not applicable because tumor IHC data are used for variant classification through PP4 rather than proband counting. The governing source also states that PS4 has not been utilized for MMR variant classification using proband counting. No case-control calculation is therefore applicable under this VCEP rule. The literature_pass packet has an empty ai_classified_papers list, and its PS4 candidate papers were not variant-specific; paper_extracts likewise found no exact-variant case-control evidence.

VCEP rule
Due to the availability of tumor IHC data for variant classification (see PP4), PS4 has not been utilized for MMR variant classification using proband counting.
Evidence considered
  • The CSPEC entry for PS4 states: 'Due to the availability of tumor IHC data for variant classification (see PP4), PS4 has not been utilized for MMR variant classification using proband counting.'
  • literature_pass.json reports ai_classified_papers: []; the listed PS4 candidate papers were not exact-variant case-control studies.
  • paper_extracts for PMID:25741868, PMID:34012068, and PMID:34043773 do not mention PMS2 c.353+7C>A or provide variant-specific case-control counts.
Still missing
  • No variant-specific case-control study was identified in the reviewed literature packet, but this does not change the VCEP-defined PS4 inapplicability.
Sources
PM1 VCEPNot applicable: the PMS2 VCEP specification explicitly marks PM1 as Not Applicable for this framework. Details ▾Hide ▴
Reasoning

The PMS2 VCEP specification marks PM1 as Not Applicable. The governing MMR functional-domains file was searched for c.353+7C>A and p.?; it contains only the PMS2 domain schematic and no exact variant entry. PM1 is therefore not used under this VCEP specification.

VCEP rule
Not Applicable
Evidence considered
  • The PMS2 VCEP CSPEC entry for PM1 states applicability: Not Applicable.
  • MMR-Functional-domains.pdf.txt was searched for c.353+7C>A, p.?, and 353+7; no exact variant entry was found. The file lists PMS2 domains as ATPase residues 1-365, NLS residues 625-632, and MLH1 interaction residues 675-855.
Still missing
  • No exact c.353+7C>A or p.? entry was found in MMR-Functional-domains.pdf.txt.
Sources
PM4 VCEPNot applicable: the PMS2 VCEP explicitly marks PM4 Not Applicable, and this intronic variant has no evaluable protein-length change. Details ▾Hide ▴
Reasoning

PM4 is explicitly marked Not Applicable in the ClinGen InSiGHT PMS2 Version 2.0 specification. This intronic variant has no protein-length change to evaluate, and the VCEP does not provide a PM4 rule for this case.

VCEP rule
Not Applicable
Evidence considered
  • ClinGen InSiGHT PMS2 Version 2.0 CSPEC entry for PM4: applicability is Not Applicable.
Sources
PM5 N/ANot applicable: c.353+7C>A has an unknown protein consequence and is not a missense change at an amino-acid residue. Details ▾Hide ▴
Reasoning

The variant has protein consequence p.? and is an intronic splice-region variant, not a missense change at an amino-acid residue. The PMS2 VCEP PM5 rules are limited to a missense change at an amino-acid residue with a different missense comparator, so PM5 is outside the rule's named variant type and location.

VCEP rule
Missense change at an amino acid residue where a different missense change was classified by this VCEP as Pathogenic on the protein level and not due to aberrant splicing. Only use PM5 if PP3 is supporting for the missense change. Use PM5\_Supporting if other variant is Likely Pathogenic due to a missense alteration.
Evidence considered
  • Normalization identifies NM_000535.7:c.353+7C>A with NP_000526.2:p.?.
  • The PM5 candidate collection found no candidates and states that classic same-residue missense PM5 is not eligible because the consequence class is not missense.
  • The VCEP PM5 rule requires a missense change at an amino-acid residue and a different missense change classified by the VCEP as Pathogenic or Likely Pathogenic on the protein level, not due to aberrant splicing.
Sources
cspec ↗pm5_candidates
PM6 VCEPNot applicable: the PMS2 VCEP explicitly marks PM6 as not applicable in its Version 2.0 specification. Details ▾Hide ▴
Reasoning

The PMS2 VCEP explicitly marks PM6 as not applicable. Therefore, assumed de novo evidence with unconfirmed maternity and/or paternity is not evaluated under PM6 in this specification.

VCEP rule
Not applicable
Evidence considered
  • The VCEP criteria entry for PM6 has applicability set to Not applicable and provides no applicable PM6 strength rule for PMS2.
Sources
PP2 VCEPNot applicable: PP2 is explicitly excluded by the PMS2 VCEP specification, and this variant has an unknown protein consequence. Details ▾Hide ▴
Reasoning

The PMS2 VCEP specification explicitly marks PP2 as Not Applicable. In addition, this variant is intronic with protein consequence p.?, not a missense variant.

VCEP rule
Not Applicable
Evidence considered
  • The PMS2 VCEP CSPEC entry for PP2 states applicability: Not Applicable.
  • Variant normalization: NM_000535.7:c.353+7C>A; NP_000526.2:p.?
Sources
PP5 VCEPNot applicable: the PMS2 VCEP prohibits PP5, regardless of the exact variant's likely-benign ClinVar reports. Details ▾Hide ▴
Reasoning

The PMS2 VCEP explicitly marks PP5 not applicable and states that this criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee. Although ClinVar reports this exact variant as likely benign, that report cannot activate PP5 under the governing VCEP specification.

VCEP rule
This criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee.
Evidence considered
  • The VCEP CSPEC entry marks PP5 'Not Applicable for this VCEP' and gives the instruction: 'This criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee.'
  • ClinVar variation 379156 matches NM_000535.7(PMS2):c.353+7C>A and reports likely benign from five laboratories, but PP5 remains prohibited by the VCEP rule.
Sources
BP1 VCEPNot applicable: BP1 is explicitly excluded by the PMS2 VCEP specification, and this variant has an unknown protein consequence. Details ▾Hide ▴
Reasoning

The PMS2 VCEP specification explicitly marks BP1 as Not Applicable. In addition, this variant is intronic with protein consequence p.?, not a missense variant.

VCEP rule
Not Applicable
Evidence considered
  • The PMS2 VCEP CSPEC entry for BP1 states applicability: Not Applicable.
  • Variant normalization: NM_000535.7:c.353+7C>A; NP_000526.2:p.?
Sources
BP2 VCEPNot applicable: the PMS2 VCEP marks BP2 not applicable and directs use of BS2 instead. Details ▾Hide ▴
Reasoning

The PMS2 VCEP marks BP2 as not applicable and explicitly directs that BS2 is used instead. BP2 is therefore not evaluated, regardless of whether cis or trans observations are available.

VCEP rule
BS2 is used instead.
Evidence considered
  • The VCEP specification lists BP2 as not applicable and states: “BS2 is used instead.”
Sources
BP3 VCEPNot applicable: the PMS2 VCEP explicitly marks BP3 Not Applicable, and this is an intronic SNV rather than an in-frame repeat-region indel. Details ▾Hide ▴
Reasoning

BP3 is explicitly marked Not Applicable in the ClinGen InSiGHT PMS2 Version 2.0 specification. The variant is intronic rather than an in-frame deletion or insertion in a repetitive region, and the VCEP supplies no BP3 rule for it.

VCEP rule
Not Applicable
Evidence considered
  • ClinGen InSiGHT PMS2 Version 2.0 CSPEC entry for BP3: applicability is Not Applicable.
Sources
BP6 VCEPNot applicable: the PMS2 VCEP prohibits BP6, regardless of the exact variant's likely-benign ClinVar reports. Details ▾Hide ▴
Reasoning

The PMS2 VCEP explicitly marks BP6 not applicable and states that this criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee. The exact ClinVar likely-benign report therefore cannot be used as BP6 under this governing framework.

VCEP rule
This criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee.
Evidence considered
  • The VCEP CSPEC entry marks BP6 'Not Applicable for this VCEP' and gives the instruction: 'This criterion is not for use as recommended by the ClinGen Sequence Variant Interpretation VCEP Review Committee.'
  • ClinVar variation 379156 matches NM_000535.7(PMS2):c.353+7C>A and reports likely benign from five laboratories, but BP6 remains prohibited by the VCEP rule.
Sources

Identifiers

Gene
PMS2
Transcript
NM_000535.7
Coding (HGVS c.)
NM_000535.7:c.353+7C>A
Protein (HGVS p.)
NP_000526.2:p.?
GRCh38
chr7:6003683 G>T
GRCh37
chr7:6043314 G>T
Location and type
Intron 4 · unknown
ClinVar
379156
COSMIC
COSV56220636

Gene diagram

Every interpreted variant in PMS2, mapped onto the exon structure of NM_000535.7. Select a row to find it on the plot.

PMS2NM_000535.7
Fetching transcript structure from UCSC…
gnomAD v4.1 10 / 1,483,674 alleles AF 6.74e-06 · 0 homozygotes · FAF 4.7e-06
gnomAD v2.1 4 / 265,876 alleles AF 1.5e-05 · 0 homozygotes · FAF 5.24e-05
gnomAD-Canada v1.0 Allele count data not recorded

By genetic ancestry

gnomAD v4.1

AF 6.7e-06 · 10 / 1,483,674 alleles · 0 hom · FAF 4.7e-06
European (non-Finnish)10 / 1,076,372 9.3e-06
0 alternate alleles recorded in 9 other groups: Remaining individuals, Admixed American, European (Finnish), Amish, East Asian, Middle Eastern, South Asian, Ashkenazi Jewish, African/African American.

gnomAD v2.1

AF 1.5e-05 · 4 / 265,876 alleles · 0 hom · FAF 5.2e-05
European (non-Finnish)4 / 124,252 3.2e-05
0 alternate alleles recorded in 7 other groups: African/African American, Admixed American, Ashkenazi Jewish, East Asian, European (Finnish), Remaining individuals, South Asian.

gnomAD-Canada

AF not recorded · ? / ? alleles

Statements

gnomAD v4.1

This variant is present in gnomAD v4.1 (AF= 6.74003e-06; MAF= 0.00067%, 10/1483674 alleles, homozygotes = 0) and has highest observed frequency in the European (non-Finnish) population (AF= 9.29047e-06; MAF= 0.00093%, 10/1076372 alleles, homozygotes = 0); grpmax FAF= 4.7e-06.

gnomAD v2.1

This variant is present in gnomAD v2.1 (AF= 1.50446e-05; MAF= 0.00150%, 4/265876 alleles, homozygotes = 0) and has highest observed frequency in the European (non-Finnish) population (AF= 3.21926e-05; MAF= 0.00322%, 4/124252 alleles, homozygotes = 0); grpmax FAF= 5.237e-05.

gnomAD-Canada

This variant is present in gnomAD-Canada v1.0 (AF= 5.42947116950809e-05, 1/18418 alleles, homozygotes = 0).

Open the gnomAD-Canada detail page →

SpliceAI and Pangolin

SpliceAI acceptor lossat -393 bp
0.001
SpliceAI acceptor gainat +109 bp
0.003
SpliceAI donor lossat +7 bp
0.014
SpliceAI donor gainat +4 bp
0.000
Pangolin splice lossmagnitude shown
-0.022
Pangolin splice gain
0.076

Other predictors

REVEL
Not available
BayesDel
Not available

How the predictions were used

BP4 SupportingVCEPMet, Supporting: SpliceAI maximum delta score 0.014 satisfies the VCEP intronic BP4 threshold of <=0.1. Details ▾Hide ▴
Reasoning

The variant is intronic, making the VCEP's intronic/synonymous BP4 path applicable. SpliceAI reports a maximum delta score of 0.014, which is <= 0.1; therefore the VCEP no-splicing-impact threshold is satisfied and BP4_Supporting is met. The missense HCI prior path is not applicable, and the HCI-PRIORS-PMS2 table had no exact c.353+7C>A or p.? entry.

VCEP rule
For intronic and synonymous variants: SpliceAI predicts no splicing impact with delta score <= 0.1 as per Walker et al 2023.
Evidence considered
  • SpliceAI result for NM_000535.7:c.353+7C>A: maximum delta score 0.014, indicating no predicted splicing impact under the VCEP cutoff.
  • The variant is intronic at c.353+7, which is within the VCEP's intronic BP4 scope.
  • HCI-PRIORS-PMS2.txt.txt was searched for the exact notations c.353+7C>A and p.?; no matching row was found, and the indexed HCI path is missense-only.
Still missing
  • No exact entry for c.353+7C>A or p.? was found in HCI-PRIORS-PMS2.txt.txt; the VCEP intronic SpliceAI path was evaluable independently.
Sources
BP7 SupportingVCEPMet, Supporting: c.353+7 is an intronic position at the VCEP's included +7 boundary for BP7. Details ▾Hide ▴
Reasoning

The variant is intronic at c.353+7, exactly the 3-prime intronic boundary included by the VCEP phrase at or beyond -21/+7 (5-prime/3-prime exonic). It therefore meets BP7_Supporting by location. The VCEP expressly allows BP7 and BP4 to be satisfied together; this does not double-count BP7 as a second splice prediction.

VCEP rule
A synonymous (silent) or intronic variant at or beyond -21/+7 (5′/3′ exonic). Variants may satisfy both BP7 and BP4.
Evidence considered
  • Variant normalization identifies NM_000535.7:c.353+7C>A as an intronic variant in intron 4i.
  • The VCEP BP7 rule explicitly includes intronic variants at or beyond -21/+7 and states that BP7 and BP4 may both be satisfied.
Sources
PP3 VCEPNot met: SpliceAI maximum delta score 0.014 is below the VCEP PP3 splice-defect threshold of >=0.2. Details ▾Hide ▴
Reasoning

The variant is intronic at the non-canonical +7 position, so the applicable PP3 path is the VCEP's SpliceAI splice-defect path; the governing threshold is delta score >= 0.2. SpliceAI reports a maximum delta score of 0.014 (DS_DL 0.014; DS_AG 0.003; DS_AL 0.001; DS_DG 0.000), below the threshold, so PP3 is not met. The HCI-PRIORS-PMS2 table was searched for c.353+7C>A and p.? with no exact entry; its indexed scope is missense, and no missense prior is applicable to this intronic variant.

VCEP rule
Predicted splice defect for non-canonical splicing nucleotides using SpliceAI with delta score >= 0.2 as per Walker et al 2023.
Evidence considered
  • SpliceAI result for NM_000535.7:c.353+7C>A: maximum delta score 0.014, with DS_AG 0.003, DS_AL 0.001, DS_DG 0.000, and DS_DL 0.014.
  • The variant is intronic at c.353+7 and has predicted protein consequence NP_000526.2:p.?, so the missense HCI prior path does not apply.
  • HCI-PRIORS-PMS2.txt.txt was searched for the exact notations c.353+7C>A and p.?; no matching row was found.
Still missing
  • No exact entry for c.353+7C>A or p.? was found in HCI-PRIORS-PMS2.txt.txt; that table is indexed for missense substitutions, not this intronic variant.
Sources

Statement

In silico

SpliceAI predicts no significant splice impact for this variant (max delta score = 0.01).

7 paper records listed. No publication is explicitly linked to an applied criterion in the recorded metadata. None of the listed paper records explicitly indicates that the variant is named.

Recorded publications

  • 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.
    Richards S et al. · 2015
    The paper does not mention PMS2 or the exact intronic variant c.353+7C>A and provides general ACMG/AMP guidance rather than variant-specific case-control or phenotype evidence.
    Does not name this variant
    PMID 25741868 ↗
    Quoted passage
    For splice site variants, the variant may lead to exon skipping, shortening or inclusion of intronic material, due to alternative donor/acceptor site usage or creation of new sites. Although splice site variants are predicted to lead to a null effect, confirmation of impact requires functional analysis by either RNA or protein analysis.

    Proposed Criteria for Interpretation of Sequence Variants, PVS1 Null variants

  • Lynch Syndrome.
    Adam MP et al. · 1993
    No paper-specific finding is recorded.
    PMID 20301390 ↗
  • A practice guideline from the American College of Medical Genetics and Genomics and the National Society of Genetic Counselors: referral indications for cancer predisposition assessment.
    Hampel H et al. · 2015
    No paper-specific finding is recorded.
    PMID 25394175 ↗
  • ACMG SF v3.0 list for reporting of secondary findings in clinical exome and genome sequencing: a policy statement of the American College of Medical Genetics and Genomics (ACMG).
    Miller DT et al. · 2021
    This paper does not mention PMS2 or c.353+7C>A and provides no variant-specific clinical, phenotype, case-control, or population evidence.
    Does not name this variant
    PMID 34012068 ↗
  • European guidelines from the EHTG and ESCP for Lynch syndrome: an updated third edition of the Mallorca guidelines based on gene and gender.
    Seppälä TT et al. · 2021
    This paper does not explicitly mention PMS2 c.353+7C>A or a protein consequence and provides general PMS2 Lynch-syndrome guidance, not variant-specific phenotype or case-control evidence.
    Does not name this variant
    PMID 34043773 ↗
    Quoted passage
    LS is caused by inherited malfunction in one of the four MMR genes named MLH1, MSH2, MSH6 and PMS2.

    General information

  • ACMG SF v3.1 list for reporting of secondary findings in clinical exome and genome sequencing: A policy statement of the American College of Medical Genetics and Genomics (ACMG).
    Miller DT et al. · 2022
    No paper-specific finding is recorded.
    PMID 35802134 ↗
  • Sherloc: a comprehensive refinement of the ACMG-AMP variant classification criteria.
    Nykamp K et al. · 2017
    No paper-specific finding is recorded.
    PMID 28492532 ↗

Screenshots represent source records captured during evidence collection. Select one to view the recorded source content.

All source links

Statements for reports

The evidence statements recorded by the interpretation pipeline. They have not been reinterpreted by the page.

gnomAD v4.1

This variant is present in gnomAD v4.1 (AF= 6.74003e-06; MAF= 0.00067%, 10/1483674 alleles, homozygotes = 0) and has highest observed frequency in the European (non-Finnish) population (AF= 9.29047e-06; MAF= 0.00093%, 10/1076372 alleles, homozygotes = 0); grpmax FAF= 4.7e-06.

gnomAD v2.1

This variant is present in gnomAD v2.1 (AF= 1.50446e-05; MAF= 0.00150%, 4/265876 alleles, homozygotes = 0) and has highest observed frequency in the European (non-Finnish) population (AF= 3.21926e-05; MAF= 0.00322%, 4/124252 alleles, homozygotes = 0); grpmax FAF= 5.237e-05.

gnomAD-Canada

This variant is present in gnomAD-Canada v1.0 (AF= 5.42947116950809e-05, 1/18418 alleles, homozygotes = 0).

ClinVar

This variant has been reported in ClinVar as Likely benign (5 clinical laboratories). (ClinVarID = 379156)

In silico

SpliceAI predicts no significant splice impact for this variant (max delta score = 0.01).

Somatic

This variant has previously been reported in somatic cancers (COSMIC; COSV56220636, n = 2 times).