Traits - Frontal fibrosing alopecia susceptibility

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Frontal fibrosing alopecia susceptibility

Hair & Skin

Frontal fibrosing alopecia is a form of scarring hair loss that mostly affects post-menopausal women, with a frontal hairline pattern.

GWAS work has identified variants near HLA and immune genes (such as CYP1B1) linked to frontal fibrosing alopecia.

This result reflects research-level variation in this specific form of hair loss and is not a clinical diagnosis.

Hormones, environmental triggers, skin care, and other immune conditions also influence whether the condition develops.

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Report markers
37 SNP entries
Genes
0
Research
1 study
Your report

Genetic tendency

Higher frontal fibrosing alopecia susceptibility tendency

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Behind this report

Review the genes, tested markers and supporting research.

SNPs tested

These are the unique genetic markers analyzed for this trait. Genotypes showing "--" were not identified in your DNA file. Report marker totals can include repeated study entries; this table shows each SNP once.

Genotypes and reported variant frequencies
SNPChromosomeGenotypeVariant alleleFrequency
rs1461070GAA1.70%
rs277580AGG83.70%
rs10045403--G26.60%
rs10507508--G4.40%
rs111463574--T91.50%
rs112198986--T3.70%
rs112659862--C0.50%
rs114108912--C1.00%
rs116806118--T0.50%
rs117687547--T3.10%
rs12951836--G50.70%
rs13032164--83.60%
rs13078360--G20.00%
rs142366299--T1.20%
rs148661203--T0.70%
rs1800440--81.00%
rs2523616--19.00%
rs34097647--T19.70%
rs34560261--T22.00%
rs6540122--T16.00%
rs6731286--T65.80%
rs73062921--A11.30%
rs760327--C39.00%
rs78504246--A0.50%
rs79459566--T4.00%
rs8065764--C87.70%
rs7749944--0.60%
rs7806494--72.30%
rs2773871--80.20%
HLA-A*11:01--5.90%
HLA-A*33:01--0.60%
HLA-B*07:02--14.10%
rs112115472--96.30%
rs147324178--14.40%
rs2021162--27.60%
rs62388754--5.80%
rs6975452--50.40%

DNA Genics reports genotypes based on the 'positive' strand of the human genome reference sequence (build 37/HG19). Other companies may use the opposite strand, so genotypes may need conversion for comparison.

Research studies

The following peer-reviewed scientific studies support the genetic associations analyzed in this report.

03/08/2019 Nat Commun

Authors: Tziotzios C, Petridis C, Dand N, Ainali C, Saklatvala JR, Pullabhatla V, Onoufriadis A, Pramanik R, Baudry D, Lee SH, Wood K, Liu L, Seegobin S, Michelotti GA, Lwin SM, Christou EAA, Curtis CJ, de Rinaldis E, Saxena A, Holmes S, Harries M, Palamaras I, Cunningham F, Parkins G, Kaur M, Farrant P, McDonagh A, Messenger A, Jones J, Jolliffe V, Ali I, Ardern-Jones M, Mitchell C, Burrows N, Atkar R, Banfield C, Alexandroff A, Champagne C, Cooper HL, Vañó-Galván S, Molina-Ruiz AM, Perez NO, Patel GK, Macbeth A, Page M, Bryden A, Mowbray M, Wahie S, Armstrong K, Cooke N, Goodfield M, Man I, de Berker D, Dunnill G, Takwale A, Rao A, Siah TW, Sinclair R, Wade MS, Dlova NC, Setterfield J, Lewis F, Bhargava K, Kirkpatrick N, Estivill X, Stefanato CM, Flohr C, Spector T, Watt FM, Smith CH, Barker JN, Fenton DA, Simpson MA, McGrath JA

Study sample: 5,161 individuals (european ancestry)

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Coverage: 2/37 SNP entries detected (5%).

Reference: Human Genome Build 37 (HG19). Other testing companies may report using the opposite strand, requiring conversion for comparison.

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