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PTCH1c.2438C>TUncertain significance
Print report
Variant interpretation report

PTCH1 c.2438C>T, p.(Pro813Leu)

NM_000264.5:c.2438C>T NP_000255.2:p.(Pro813Leu) View identifiers
Classification
Uncertain significance

Variant description:

No variant summary was recorded for this case.

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

Uncertain.The recorded classification is uncertain significance.

In plain language

Gene-level background from the recorded interpretation.

About PTCH1

No gene-level summary was recorded for this case.

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 Not recorded. 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: 1
Pathogenic criteria applied · 1
PM2Moderate
PM2 · moderate

This variant is absent from gnomAD v2.1 and is present at extremely low frequency in gnomAD v4.1 (4/1,612,430 alleles; AF=2.48e-6; 0 homozygotes; grpmax FAF=7.9e-7). The allele frequency of 0.00025% is well below the 0.1% PM2 threshold for non-VCEP frameworks. The submitting laboratory (Labcorp/Invitae) also applied PM2 for this variant.

Benign criteria applied · 1
BP4Supporting
BP4 · supporting

Multiple lines of computational evidence suggest this variant does not have a significant impact on the gene product. BayesDel score is 0.0037, which strongly predicts a benign effect. SpliceAI max delta is 0.01, indicating no predicted splicing alteration. The REVEL score of 0.656 is borderline and does not outweigh the preponderance of benign computational evidence.

Recorded classification: Uncertain significance

gene-specific framework lacked a usable explicit final combination framework, so generic ACMG/AMP 2015 final-combination rules were applied as fallback; applied criteria: PM2 moderate, BP4 supporting benign; combination = 1 moderate + 1 supporting benign, which maps to VUS.

02The sources

Evidence at a glance

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

SpliceAI score
0.010 maximum delta

Recorded SpliceAI maximum delta score: 0.010. Refer to the recorded PP3/BP4 rationale for interpretation.

Applied · BP4 → SpliceAI ↗
ClinVar submissions
1 reported laboratory submissions

1 Uncertain significance.

Context only ClinVar ↗
Functional evidence
Statement recorded

OncoKB did not identify variant-specific reviewed functional evidence for this variant; gene-level curated context is available for reviewer follow-up. PTCH1, a tumor suppressor and inhibitor of the hedgehog pathway, is recurrently mutated in basal cell carcinoma.

No listed criterion applied OncoKB ↗
COSMIC
Cancer Hotspots
Somatic evidence
2 recorded samples

This variant has previously been reported in somatic cancers (COSMIC; COSV59468245, n = 2 times).

Cancer Hotspots

This variant does not lie in a statistically significant hotspot.

Context only
COSMIC ↗Cancer Hotspots ↗
For specialists

Technical detail

ACMG/AMP criteria under Not recorded, with the data and sources behind each one.

29 criteria with recorded statuses: 2 met · 21 not met · 0 not assessed · 6 not applicable. Open any row for the full reasoning, the rule and the evidence behind it.

Pathogenic
PVS1PS1PS2PS3PS4PM1PM2PM3PM4PM5PM6PP1PP2PP3PP4PP5PS5
Benign
BA1BS1BS2BS3BS4BP1BP2BP3BP4BP5BP6BP7
Met Not met Not assessed Not applicable

NM_000264.5:c.2438C>T (p.Pro813Leu) is a missense variant in exon 15 of PTCH1, a gene in which loss-of-function variants are an established cause of Gorlin syndrome (nevoid basal cell carcinoma syndrome).

This variant is absent from gnomAD v2.1 and present at extremely low frequency in gnomAD v4.1 (4/1,612,430 alleles, AF=2.48e-6, 0 homozygotes), meeting PM2 at moderate strength.

Multiple lines of computational evidence suggest no significant impact on the gene product: BayesDel score is 0.0037 (strongly predicts benign) and SpliceAI max delta is 0.01 (no splicing impact), meeting BP4 at supporting benign level.

The variant has been reported in ClinVar as Uncertain significance by a single clinical laboratory (Labcorp/Invitae, SCV005813886). It has been observed somatically in COSMIC (COSV59468245, n=2) but this does not inform germline pathogenicity.

No variant-specific functional studies, segregation data, case-control analyses, or de novo observations were identified. Five literature-triage papers (PMIDs 15604628, 20301330, 21304560, 26389210, 26389333) were reviewed; none mention NM_000264.5:c.2438C>T.

Applying generic ACMG/AMP 2015 combination rules (PMID:25741868): one moderate pathogenic criterion (PM2) and one supporting benign criterion (BP4) are present. These do not meet the threshold for Likely Pathogenic, Likely Benign, Pathogenic, or Benign. The variant is classified as a Variant of Uncertain Significance.

Met · 2

PM2 ModerateThis variant is absent from gnomAD v2.1 and is present at extremely low frequency in gnomAD v4.1 (4/1,612,430 alleles; AF=2.48e-6; 0 homozygotes; grpmax FAF=7.9e-7). The allele frequency of 0.00025% is well below the 0.1% PM2 threshold for non-VCEP frameworks. The submitting laboratory (Labcorp/Invitae) also applied PM2 for this variant. Details ▾Hide ▴
Evidence considered
  • gnomAD v2.1: absent
  • gnomAD v4.1: 4/1
  • 612
  • 430 alleles
  • AF=2.48e-6
  • gnomAD-Canada v1.0: absent
  • ClinVar submitter also applied PM2
Sources
gnomad_v2 ↗gnomad_v4 ↗gnomad_canada ↗clinvar ↗
BP4 SupportingMultiple lines of computational evidence suggest this variant does not have a significant impact on the gene product. BayesDel score is 0.0037, which strongly predicts a benign effect. SpliceAI max delta is 0.01, indicating no predicted splicing alteration. The REVEL score of 0.656 is borderline and does not outweigh the preponderance of benign computational evidence. Details ▾Hide ▴
Evidence considered
  • BayesDel: 0.0037 (strongly predicts benign)
  • SpliceAI max delta: 0.01 (no splice impact)
  • REVEL: 0.656 (borderline
  • does not outweigh benign predictions)
Sources
revelbayesdelspliceai ↗

Not met · 21 · evaluated, threshold not reached

PS1 No known pathogenic missense variant at Pro813 arising from a different nucleotide change has been identified. The same-residue PM5 candidate search returned zero comparator variants, and no reputable source has established P813L as pathogenic via any other nucleotide substitution. Details ▾Hide ▴
Evidence considered
  • Zero same-residue comparator variants identified by PM5 candidate search
Still missing
  • No ClinVar or literature evidence of a pathogenic missense at Pro813 via a different nucleotide change
Sources
pm5_candidates
PS2 No de novo observation with confirmed maternity and paternity has been reported for this variant in any available source. Details ▾Hide ▴
Evidence considered
  • No de novo data in ClinVar
  • gnomAD
  • or reviewed publications
Still missing
  • No parental testing data available
PS3 No well-established in vitro or in vivo functional studies demonstrate a damaging effect for NM_000264.5:c.2438C>T (p.Pro813Leu). OncoKB reports no variant-specific reviewed functional evidence. COSMIC reports n=2 somatic observations (COSV59468245), but somatic occurrence alone does not constitute functional evidence of germline pathogenicity. Details ▾Hide ▴
Evidence considered
  • OncoKB: no variant-specific functional evidence
  • COSMIC: 2 somatic observations
  • not functional data
Still missing
  • No functional assay data for this variant
Sources
oncokb ↗
PS4 The prevalence of this variant in affected individuals has not been shown to be significantly increased compared to controls. A single clinical laboratory submission in ClinVar (Labcorp/Invitae) classifies it as VUS without reporting patient counts or case-control statistics. The variant is present in gnomAD v4.1 at AF=2.48e-6 (4 alleles), which does not independently establish enriched prevalence in affected populations. Details ▾Hide ▴
Evidence considered
  • ClinVar: 1 submitter
  • VUS
  • no patient counts
  • gnomAD v4.1: 4/1
  • 612
  • 430 alleles
Still missing
  • No case-control study
  • No proband phenotype data
Sources
clinvar ↗gnomad_v4 ↗
PM1 Residue Pro813 does not lie within a statistically significant mutational hotspot as determined by cancerhotspots.org. No evidence was identified that this residue resides in a well-characterized critical functional domain without benign variation. PTCH1 is a large multi-pass transmembrane protein; domain-level PM1 evidence was not established for this residue. Details ▾Hide ▴
Evidence considered
  • cancerhotspots.org: residue Pro813 not a significant hotspot
Still missing
  • No domain-specific benign variation tolerance data for Pro813
PM6 No de novo observation (without confirmed parentage) has been reported for this variant in ClinVar, the reviewed literature, or any other source. Details ▾Hide ▴
Evidence considered
  • No de novo data in any available source
Still missing
  • No de novo testing data
PP1 No co-segregation data are available for this variant. No family studies were identified in the reviewed literature. Details ▾Hide ▴
Evidence considered
  • No co-segregation data in any available source
Still missing
  • No family segregation data
PP2 While PTCH1 loss-of-function is an established disease mechanism for Gorlin syndrome, missense variants are also well-documented as causative in this disorder. Insufficient evidence that PTCH1 meets the PP2 threshold of a gene with a low rate of benign missense variation where missense is a common disease mechanism. No HCI prior or custom PP2 score was available. Details ▾Hide ▴
Evidence considered
  • PTCH1 missense variants are a recognized cause of Gorlin syndrome
  • not exclusively truncating
  • No HCI prior score for PTCH1
Still missing
  • No gene-specific benign missense rate data for PTCH1
PP3 In silico predictions are conflicting and do not provide multiple lines of computational support for a deleterious effect. REVEL score is 0.656 (borderline, below the >0.75 threshold for strong evidence). BayesDel score is 0.0037, which strongly predicts a benign effect. SpliceAI max delta is 0.01, indicating no predicted splicing impact. The preponderance of computational evidence does not support a deleterious effect. Details ▾Hide ▴
Evidence considered
  • REVEL: 0.656 (borderline)
  • BayesDel: 0.0037 (predicts benign)
  • SpliceAI max delta: 0.01 (no splice impact)
Sources
revelbayesdelspliceai ↗
PP4 No proband phenotype information is available. The variant's specificity for Gorlin syndrome / nevoid basal cell carcinoma syndrome cannot be assessed without clinical data. Details ▾Hide ▴
Evidence considered
  • No proband phenotype data available
Still missing
  • Proband clinical phenotype not provided
PP5 No reputable source has classified this variant as pathogenic. The single ClinVar submission classifies it as Uncertain significance. Although five papers (PMIDs 15604628, 20301330, 21304560, 26389210, 26389333) were flagged by literature triage as candidate PP5/PS4 sources, none mention the specific variant NM_000264.5:c.2438C>T. They are gene-level or general guideline publications. Details ▾Hide ▴
Evidence considered
  • ClinVar: Uncertain significance
  • 1 submitter
  • Five literature-triage papers reviewed
  • none mention the variant
Sources
clinvar ↗
BA1 The allele frequency in gnomAD v4.1 is 2.48e-6 (0.00025%), far below the 1% BA1 threshold for non-VCEP frameworks. The variant is absent from gnomAD v2.1 and gnomAD-Canada. Details ▾Hide ▴
Evidence considered
  • gnomAD v4.1 AF=0.00025%
  • well below BA1 threshold of 1%
Sources
gnomad_v2 ↗gnomad_v4 ↗gnomad_canada ↗
BS1 The allele frequency in gnomAD v4.1 is 0.00025%, below the 0.3% BS1 threshold for non-VCEP frameworks. Details ▾Hide ▴
Evidence considered
  • gnomAD v4.1 AF=0.00025%
  • below BS1 threshold of 0.3%
Sources
gnomad_v2 ↗gnomad_v4 ↗gnomad_canada ↗
BS2 This variant has not been observed in the homozygous state (0 homozygotes in gnomAD v4.1, 0 in v2.1) and no control population data demonstrate observation in healthy adults at a frequency that would meet BS2. Details ▾Hide ▴
Evidence considered
  • 0 homozygotes in gnomAD v2.1 and v4.1
  • No healthy adult control data
Still missing
  • No specific healthy adult control data for this variant
Sources
gnomad_v2 ↗gnomad_v4 ↗
BS3 No well-established in vitro or in vivo functional studies demonstrate no damaging effect for this variant. While BayesDel predicts a benign score (0.0037), computational prediction alone does not meet the BS3 threshold, which requires experimental functional evidence showing no deleterious effect. Details ▾Hide ▴
Evidence considered
  • BayesDel: 0.0037 (predicts benign
  • but computational only)
  • No experimental functional data available
Still missing
  • No experimental functional studies for this variant
Sources
bayesdel
BS4 No segregation data are available for this variant. Lack of segregation in affected family members cannot be assessed. Details ▾Hide ▴
Evidence considered
  • No segregation data available
Still missing
  • No family segregation data
BP1 Although PTCH1 loss-of-function is an established disease mechanism for Gorlin syndrome, missense variants in PTCH1 are also well-documented as causative. The gene is not characterized by a disease mechanism that is primarily truncating to the exclusion of missense changes. Details ▾Hide ▴
Evidence considered
  • PTCH1 missense variants are established as causative for Gorlin syndrome alongside truncating variants
Sources
pvs1_gene_context
BP2 No observation of this variant in trans with a known pathogenic PTCH1 variant has been reported. No data are available to assess BP2. Details ▾Hide ▴
Evidence considered
  • No trans configuration data available
Still missing
  • No phase data with other PTCH1 variants
BP5 No observation of this variant in a case with an alternative molecular basis for disease has been reported. Details ▾Hide ▴
Evidence considered
  • No alternate molecular cause data available
Still missing
  • No proband genetic testing data for alternative diagnoses
BP6 No reputable source has classified this variant as benign. The sole ClinVar classification is Uncertain significance. Details ▾Hide ▴
Evidence considered
  • ClinVar: Uncertain significance
  • no benign classification
Sources
clinvar ↗
PS5 No reputable source has classified this variant as pathogenic. The sole ClinVar submission (Labcorp/Invitae, SCV005813886) classifies it as Uncertain significance. Details ▾Hide ▴
Evidence considered
  • ClinVar: Uncertain significance
  • 1 submitter
  • criteria provided
  • single submitter
Still missing
  • No expert panel or multi-submitter pathogenic classification
Sources
clinvar ↗
Not applicable · 6· recorded as not applicable Show reasons ▾Hide reasons ▴
PVS1 N/AThis is a missense variant (c.2438C>T, p.Pro813Leu) in exon 15 of PTCH1. It does not fall into the generic PVS1 null-variant buckets (nonsense, frameshift, or canonical ±1,2 splice consensus). The pvs1_variant_assessment confirms bucket='other' and apply_generic_pvs1_framework=false. Details ▾Hide ▴
Evidence considered
  • Missense variant
  • not a null variant
  • ClinGen SVI PVS1 framework (PMC6185798) does not apply to missense variants
Sources
pvs1_generic_framework ↗pvs1_gene_contextpvs1_variant_assessment
PM3 N/ASkipped: PTCH1-associated Gorlin syndrome is autosomal dominant; PM3 (in trans with pathogenic variant) is designed for recessive disorders. Details ▾Hide ▴

No further detail was recorded.

PM4 N/ASkipped: this is a substitution variant, not an in-frame deletion/insertion or stop-loss. Details ▾Hide ▴

No further detail was recorded.

PM5 N/ANo same-residue pathogenic missense comparator variant at Pro813 was identified by the automated PM5 candidate search. The pm5_candidates search returned zero candidates. Without a confirmed pathogenic missense at Pro813 as comparator, PM5 cannot be applied. Details ▾Hide ▴
Evidence considered
  • PM5 candidate search: zero same-residue pathogenic comparators at Pro813
Sources
pm5_candidates
BP3 N/ASkipped: this is a substitution variant, not an in-frame indel. Details ▾Hide ▴

No further detail was recorded.

BP7 N/AThis is a missense variant (c.2438C>T, p.Pro813Leu), not a synonymous or intronic variant. BP7 is restricted to synonymous variants with no predicted splicing impact. Details ▾Hide ▴
Evidence considered
  • Missense variant
  • BP7 does not apply

Identifiers

Gene
PTCH1
Transcript
NM_000264.5
Coding (HGVS c.)
NM_000264.5:c.2438C>T
Protein (HGVS p.)
NP_000255.2:p.(Pro813Leu)
GRCh38
chr9:95467238 G>A
GRCh37
chr9:98229520 G>A
ClinVar
3705147, 524555
COSMIC
COSV59468245

Gene diagram

Every interpreted variant in PTCH1, mapped onto the exon structure of NM_000264.5. Select a row to find it on the plot.

PTCH1NM_000264.5
Fetching transcript structure from UCSC…
gnomAD v4.1 4 / 1,612,430 alleles AF 2.48e-06 · 0 homozygotes · FAF 7.9e-07
gnomAD v2.1 Allele count data not recorded
gnomAD-Canada v1.0 Allele count data not recorded

By genetic ancestry

gnomAD v4.1

AF 2.5e-06 · 4 / 1,612,430 alleles · 0 hom · FAF 7.9e-07
European (non-Finnish)4 / 1,179,474 3.4e-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.

Statements

gnomAD v4.1

This variant is present in gnomAD v4.1 (AF= 2.48073e-06; MAF= 0.00025%, 4/1612430 alleles, homozygotes = 0) and has highest observed frequency in the European (non-Finnish) population (AF= 3.39134e-06; MAF= 0.00034%, 4/1179474 alleles, homozygotes = 0); grpmax FAF= 7.9e-07.

gnomAD v2.1

Absent from gnomAD v2.1.

gnomAD-Canada

Absent from gnomAD-Canada v1.0.

SpliceAI and Pangolin

SpliceAI acceptor lossat +183 bp
0.000
SpliceAI acceptor gainat +21 bp
0.000
SpliceAI donor lossat +270 bp
0.000
SpliceAI donor gainat -122 bp
0.010
Pangolin splice lossmagnitude shown
-0.020
Pangolin splice gain
0.010

Other predictors

REVEL
0.656
BayesDel
0.004

How the predictions were used

BP4 SupportingMultiple lines of computational evidence suggest this variant does not have a significant impact on the gene product. BayesDel score is 0.0037, which strongly predicts a benign effect. SpliceAI max delta is 0.01, indicating no predicted splicing alteration. The REVEL score of 0.656 is borderline and does not outweigh the preponderance of benign computational evidence. Details ▾Hide ▴
Evidence considered
  • BayesDel: 0.0037 (strongly predicts benign)
  • SpliceAI max delta: 0.01 (no splice impact)
  • REVEL: 0.656 (borderline
  • does not outweigh benign predictions)
Sources
revelbayesdelspliceai ↗
PP3 In silico predictions are conflicting and do not provide multiple lines of computational support for a deleterious effect. REVEL score is 0.656 (borderline, below the >0.75 threshold for strong evidence). BayesDel score is 0.0037, which strongly predicts a benign effect. SpliceAI max delta is 0.01, indicating no predicted splicing impact. The preponderance of computational evidence does not support a deleterious effect. Details ▾Hide ▴
Evidence considered
  • REVEL: 0.656 (borderline)
  • BayesDel: 0.0037 (predicts benign)
  • SpliceAI max delta: 0.01 (no splice impact)
Sources
revelbayesdelspliceai ↗
BP7 N/AThis is a missense variant (c.2438C>T, p.Pro813Leu), not a synonymous or intronic variant. BP7 is restricted to synonymous variants with no predicted splicing impact. Details ▾Hide ▴
Evidence considered
  • Missense variant
  • BP7 does not apply

Statement

In silico

SpliceAI predicts no significant splice impact for this variant (max delta score = 0.01). REVEL score = 0.656. BayesDel score = 0.00372277.

5 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

  • Genetic cancer risk assessment and counseling: recommendations of the national society of genetic counselors.
    Trepanier A et al. · 2004
    Practice guidelines from the National Society of Genetic Counselors describing the cancer genetic risk assessment and counseling process. Discusses hereditary cancer syndromes at the gene level, including PTCH/Gorlin syndrome in a summary table. No specific PTCH1 variants are mentioned.
    Does not name this variant
    PMID 15604628 ↗
  • Nevoid Basal Cell Carcinoma Syndrome.
    Adam MP et al. · 1993
    GeneReviews clinical summary for Nevoid Basal Cell Carcinoma Syndrome (Gorlin syndrome). Provides gene-level overview of PTCH1-associated disease, clinical features, and genetic counseling recommendations. This is a continuously updated reference work that does not catalog individual variants.
    Does not name this variant
    PMID 20301330 ↗
  • Clinical utility gene card for: Gorlin syndrome.
    Lo Muzio L et al. · 2011
    Clinical utility gene card for Gorlin syndrome published in the European Journal of Human Genetics. Summarizes the clinical utility of PTCH1 genetic testing, including analytical sensitivity, clinical sensitivity, and recommendations for test indications. Discusses the PTCH1 gene and mutation spectrum generally but does not mention any individual missense variant.
    Does not name this variant
    PMID 21304560 ↗
    Quoted passage
    PTCH1 gene analysis includes full gene sequencing covering all coding exons, flanking intronic sequences and MLPA analysis to detect large intragenic deletions and duplications.

    Entire full text reviewed; no individual PTCH1 variants are listed

  • Genetics of Breast and Gynecologic Cancers (PDQ®): Health Professional Version.
    PDQ Cancer Genetics Editorial Board · 2002
    PDQ cancer genetics summary covering breast and gynecologic cancer predisposition. Provides gene-level reviews of BRCA1, BRCA2, and other hereditary cancer genes. PTCH1 is not the focus of this summary.
    Does not name this variant
    PMID 26389210 ↗
  • Genetics of Skin Cancer (PDQ®): Health Professional Version.
    PDQ Cancer Genetics Editorial Board · 2002
    PDQ cancer genetics summary covering skin cancer predisposition, including Gorlin syndrome and PTCH1. Reviews PTCH1 gene function, associated clinical features of nevoid basal cell carcinoma syndrome, and genetic testing recommendations. No individual variants are discussed.
    Does not name this variant
    PMID 26389333 ↗

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

gnomAD v4.1 4 / 1,612,430 recorded alleles Open source ↗
gnomAD v2.1 Captured gnomAD v2.1 source record Open source ↗
SpliceAI Lookup Recorded maximum delta 0.010 Open source ↗
ClinVar 1 Uncertain significance Open source ↗
COSMIC Captured COSMIC source record Open source ↗
Cancer hotspots Captured Cancer Hotspots source record Open source ↗
OncoKB Captured OncoKB source record Open source ↗

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= 2.48073e-06; MAF= 0.00025%, 4/1612430 alleles, homozygotes = 0) and has highest observed frequency in the European (non-Finnish) population (AF= 3.39134e-06; MAF= 0.00034%, 4/1179474 alleles, homozygotes = 0); grpmax FAF= 7.9e-07.

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 Uncertain significance (1 clinical laboratory). (ClinVarID = 3705147)

In silico

SpliceAI predicts no significant splice impact for this variant (max delta score = 0.01). REVEL score = 0.656. BayesDel score = 0.00372277.

Functional

OncoKB did not identify variant-specific reviewed functional evidence for this variant; gene-level curated context is available for reviewer follow-up. PTCH1, a tumor suppressor and inhibitor of the hedgehog pathway, is recurrently mutated in basal cell carcinoma.

Somatic

This variant does not lie in a statistically significant hotspot. This variant has previously been reported in somatic cancers (COSMIC; COSV59468245, n = 2 times).

Cancer Hotspots

This variant does not lie in a statistically significant hotspot.