TP53 encodes the p53 tumor suppressor protein, a transcription factor that responds to cellular stress such as DNA damage by switching on genes that trigger cell cycle arrest, DNA repair, senescence, or programmed cell death. In healthy cells, p53 is kept at low levels by constant degradation, but stress signals stabilize and activate it to protect against damaged cells surviving and dividing. Inherited mutations in TP53 cause Li-Fraumeni syndrome, a condition marked by a high risk of developing multiple cancers at a young age. TP53 is the most commonly mutated gene across human cancers, and loss of its normal function promotes tumor growth, spread, drug resistance, and genomic instability.
This variant
This truncating TP53 variant is consistent with loss of the p53 tumor-suppressor function that underlies the inherited cancer susceptibility of Li-Fraumeni syndrome.
Transcript
NM_000546.6
HGVS · transcript:coding
NM_000546.6:c.997_1006del
GRCh38
chr17:7670702 TCACGCCCACG>T
GRCh37
chr17:7574020 TCACGCCCACG>T
Likely Pathogenic: PVS1 very strong (+8) plus PM2 supporting (+1) total 9 points under the ClinGen TP53 Expert Panel Version 2.4 framework.
Classification rationale
PVS1PM2Likely Pathogenic
TP53 c.997_1006delframeshift · exon 10
PVS1 very strong: the exon 10 frameshift creates a premature termination codon at p.341, upstream of p.Lys351 and outside the exon 10 NMD-escape region. PM2 supporting: the variant is absent from gnomAD v4.1 and v2.1, with an observed allele frequency of 0.
PVS1 + PM2→Likely Pathogenic
LYFE Sciences is an AI system, and it can make mistakes. Criteria
may be applied incorrectly, sources may be misread, and a confident-looking
classification can still be wrong. Double-check every criterion and
its underlying evidence before relying on any call.
Gene diagram
· NM_000546.6 · variants mapped to exon structure
TP53NM_000546.6
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 TP53—click a row to locate it on the plot · use the link column to open its page
Protein
Location
Classification
Link
Applied criteria · 2 applied · 8 assessed
MetEvidence satisfies this criterion.
Not metEvaluated against available evidence; threshold not reached.
Not assessedApplies in principle, but no evidence was found to evaluate it.
N/ADoesn't apply to this variant type.
Applied · 2
Strength Supporting Moderate Strong Very strong
✓
PVS1very strongPathogenic
Met, very strong: the exon 10 frameshift creates a PTC at p.341, upstream of p.Lys351 and outside the exon 10 NMD-escape region.
The normalized consequence is NM_000546.6:c.997_1006del, a frameshift producing NP_000537.3:p.(Arg333SerfsTer9), with predicted protein position_last_predicted 341 and original terminal residue 394.Variant Validator places the deletion entirely in exon 10 of the biologically relevant NM_000546.6 transcript.The TP53 VCEP PVS1 flowchart assigns PVS1 to a frameshift-induced PTC upstream of p.Lys351 when the PTC is not in exon 11 or the 3'-most 50 nucleotides of exon 10; this variant meets that branch.
Met at supporting strength: the variant is absent from gnomAD v4.1 and v2.1, with observed frequency 0, below the TP53 PM2 threshold of <0.00003.
The TP53 VCEP Version 2.4 PM2 rule is supporting only and requires allele frequency <0.00003 in gnomAD; if multiple alleles are present in an ancestry group, that group must have frequency <0.00004.The queried frameshift variant NM_000546.6:c.997_1006del is reported absent from gnomAD v4.1 and gnomAD v2.1, corresponding to observed allele count 0 and allele frequency 0 in the reported datasets.
Assessed · not applied
· 2 not met · 6 not assessed
Pathogenic
PS2Not assessed: no proband cancer, parental testing, or confirmed parentage data are available to calculate the TP53 VCEP PS2 point total.
PS4Not assessed: no proband phenotype or PS4 point total is available to compare with the VCEP thresholds of 1-1.5, 2-3.5, 4-7.5, or >=8 points.
PP1Not assessed: no affected variant-positive relatives, obligate carriers, family structure, or documented meioses are available for PP1 assignment.
PP4Not assessed: VAF and multigene-panel context are unavailable for comparison with the VCEP PP4 ranges of 5-25% or 5-35%.
Benign
BA1Not met: the variant is absent from gnomAD v4.1 and v2.1, rather than reaching the TP53 BA1 threshold of FAF >=0.001.
BS1Not met: the variant is absent from gnomAD v4.1 and v2.1, rather than having TP53 BS1 FAF >=0.0003 and <0.001.
BS2Not assessed: no qualifying healthy female carrier count, age, cancer status, single-source provenance, or VAF data is available for the TP53 BS2 thresholds.
BS4Not assessed: no affected relatives with relevant LFS-associated cancers and documented absence of the variant are available to establish non-segregation.
SpliceAI returned NO scores for this variant, so no SpliceAI-based splice prediction is available. This is missing data, NOT evidence of absent splice impact: it must not be used to support BP4 or to argue against PP3/PVS1. Pangolin scores may be present but are not calibrated for PP3/BP4 here.