PDGFRA

Chr 4Isolated casesSomatic

platelet derived growth factor receptor alpha

Also known as: CD140A, PDGFR-2, PDGFR2

The protein functions as a cell surface tyrosine kinase receptor for platelet-derived growth factors and is essential for embryonic development, gastrointestinal tract development, and mesenchymal cell differentiation. Mutations cause gastrointestinal stromal tumors (GIST), GIST-plus syndrome, and idiopathic hypereosinophilic syndrome through constitutive activation of downstream signaling pathways including PI3K/AKT, MAPK, and STAT cascades. These conditions typically occur as isolated cases or result from somatic mutations.

OMIMResearchSummary from RefSeq, OMIM, UniProt
GOFmechanismIsolated cases/SomaticLOEUF 0.172 OMIM phenotypes
Clinical SummaryPDGFRA
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Gene-Disease Validity (ClinGen)
gastrointestinal stromal tumor · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

2 total gene-disease associations curated

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
200 total variants — no pathogenic classifications of 200 total submissions
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Clinical Trials
3 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.17LOEUF
pLI 1.000
Z-score 6.31
OE 0.07 (0.040.17)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
1.94Z-score
OE missense 0.78 (0.720.84)
458 obs / 590.7 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.07 (0.040.17)
00.351.4
Missense OE0.78 (0.720.84)
00.61.4
Synonymous OE1.01
01.21.6
LoF obs/exp: 4 / 54.1Missense obs/exp: 458 / 590.7Syn Z: -0.10
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitivePDGFRA-related gastrointestinal stromal tumor/GIST-plus syndrome, somatic or familialGOFAD
DN
0.5279th %ile
GOF
0.6931th %ile
LOF
0.52top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and gain-of-function). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFLOEUF 0.17
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

200 submitted variants in ClinVar

Classification Summary

Likely Benign149
Benign47
Conflicting4
149
Likely Benign
47
Benign
4
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
0
0
0
Likely Pathogenic
0
0
0
0
0
VUS
0
0
0
0
0
Likely Benign
0
0
90
59
149
Benign
0
0
47
0
47
Conflicting
4
Total0013759200

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

PDGFRA · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗