Genetic Information

Gene & Transcript Details

Gene
TP53
Transcript
NM_000546.5 MANE Select
Total Exons
Reference Sequence
NC_000017.10
Alternative Transcripts
IDStatusDetails
NM_000546.3 Alternative 2640 nt | 252–1433
NM_000546.5 RefSeq Select 2591 nt | 203–1384
NM_000546.6 MANE Select 2512 nt | 143–1324
NM_000546.4 Alternative 2586 nt | 198–1379
NM_000546.2 Alternative 2629 nt | 252–1433

Variant Details

HGVS Notation
NM_000546.5:c.490A>G
Protein Change
K164E
Location
Exon 5 (Exon 5 of )
5
5'Exon Structure3'
Functional Consequence
Loss of Function
Alternate Identifiers

Clinical & Population Data

Population Frequency

gnomAD
Global Frequency
0.0 in 100,000
Extremely Rare
ACMG Criteria Applied PM2
This variant is absent or extremely rare in population databases (PM2 criteria applies).

ClinVar

Open
Classification
Likely Pathogenic
3 publications
Publications List
PMID: 32817165

This sequence change replaces lysine, which is basic and polar, with glutamic acid, which is acidic and polar, at codon 164 of the TP53 protein (p.Lys164Glu). This variant is not present in population databases (gnomAD no frequency). This missense change has been observed in individuals with clinical features of Li-Fraumeni syndrome (PMID: 32817165, 33138793, 38050059). ClinVar contains an entry for this variant (Variation ID: 246416). Invitae Evidence Modeling incorporating data from in vitro experimental studies (PMID: 12826609, 29979965, 30224644) indicates that this missense variant is expected to disrupt TP53 function with a positive predictive value of 97.5%. Experimental studies have shown that this missense change affects TP53 function (PMID: 12826609, 29979965, 30224644). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic.

PMID: 29979965

This variant is considered pathogenic. Functional studies indicate this variant impacts protein function [PMID: 29979965]. This variant is expected to disrupt protein structure [Myriad internal data]. This variant has been reported in multiple individuals with clinical features of gene-specific disease [PMID: 38050059, 33138793].

Clinical Statement

"This variant has been reported in ClinVar as Uncertain significance (3 clinical laboratories) and as Likely pathogenic (1 clinical laboratories) and as Pathogenic (1 clinical laboratories) and as Pathogenic by ClinGen TP53 Variant Curation Expert Panel, ClinGen expert panel."

COSMIC Somatic Evidence

Open
COSMIC ID
COSM3820721
Recurrence
31 occurrences
PM1 Criteria
Applied
COSMIC Database Preview
COSMIC Preview
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Functional Impact & Domains

Functional Domain

Hotspot Status
Not a hotspot
Domain Summary
This variant is not located in a mutational hotspot or critical domain.
Related Variants in This Domain
No evidence of other pathogenic variants at this position in gene TP53.

Functional Studies & Therapeutic Relevance

Functional Summary

Error in OpenAI Consolidation. OncoKB: TP53K164ETP53K164ESomaticNCBI Gene:7157|Show additional gene information Variant OverviewTP53, a tumor suppressor in the DNA damage pathway, is the most frequently mutated gene in cancer.The TP53 K164E mutation is likely oncogenic.Hide mutation effect description The TP53 K164E mutation is located in the DNA-binding domain of the protein. This mutation has been identified in ovarian cancer and is a statistically significant hotspot (PMID: 9699640). In vivo studies with yeast expressing TP53 K164E demonstrated that the mutation is inactivating as measured by the loss of transactivational activity as compared to wildtype (PMID: 27328919, 12826609). In vitro studies with various human cancer cell lines expressing TP53 K164E also demonstrated the mutation is inactivating as measured by reduced growth suppression activity as compared to wildtype (PMID: 29979965, 30224644). JAX-CKB: TP53 K164E lies within the DNA-binding domain of the Tp53 protein (PMID: 22713868). K164E confers a loss of function to the Tp53 protein as demonstrated by decreased transactivation of Tp53 target genes, decreased growth suppression, and loss of DNA binding in culture (PMID: 38050059).

Database Previews
OncoKB
OncoKB Preview
JAX-CKB
JAX-CKB Preview

Click on previews to view full database entries. External databases may require institutional access.

Computational Analysis

Pathogenicity Predictions

SpliceAI
Predictor Consensus
Mixed/VUS
PP3 Applied
No
REVEL Score
0.0
Threshold: ≥0.75 = PP3 applied

SpliceAI Scores

Window: ±500bp
Effect Type Score Position
- Acceptor Loss (AL) 0.0 -151 bp
- Donor Loss (DL) 0.0 -268 bp
+ Acceptor Gain (AG) 0.0 -168 bp
+ Donor Gain (DG) 0.0 -23 bp
High impact (≥0.5) Medium impact (0.2-0.49) Low impact (<0.2)

VCEP Guidelines

Applied ACMG/AMP Criteria (VCEP Specific)

Filter Criteria:
PS3

PS3 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)

PM2

PM2 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)

PP5

PP5 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)

BP4

BP4 (Unknown (Pre-LLM))

From pre-LLM assessment (LLM Failed)