Sensitive

Prostate cancer

MAD1L1 · rs4513875

Where this position leads

Strength of the evidence

1 / 4

Its strongest genetic-study result is p = 10⁻⁸, with 1 associations in the GWAS Catalog.

How this is scored

4: ClinVar disease-causing, reviewed by an expert panel or a guideline (3–4 stars). 3: ClinVar, several labs agreeing (2 stars), or a genetic study at p ≤ 10⁻⁵⁰. 2: ClinVar from one lab (1 star), or p ≤ 10⁻²⁰. 1: ClinVar submitted without criteria (0 stars), or genome-wide significance (p ≤ 5×10⁻⁸). The higher of the two counts. It says how solid the evidence is, not whether it matters for a particular person.

What the study found

Who was studied 85,554 European ancestry cases, 10,368 African ancestry cases, 8,611 East Asian ancestry cases, 2,714 Hispanic cases, 91,972 European ancestry controls, 10,986 African ancestry controls, 18,809 East Asian ancestry controls, 5,239 Hispanic controls.

The effect Each copy of the T allele carried 1.04 times the odds of Prostate cancer (95% confidence interval 1.03-1.06); p = 1 × 10⁻⁸.

Where it sits Chromosome 7, band 7p22.3 — in an intron of MAD1L1.

What each result means

C/C No copy of the version the research linked to Prostate cancer. This is the starting point the study compared everyone against.

C/T One copy of the version the research linked to Prostate cancer. That is a smaller link than two copies.

T/T Two copies of the version the research linked to Prostate cancer. That is the strongest link of the three results. A link in a study is not a diagnosis.

Source

Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction

Conti DV, Darst BF, Moss LC, Saunders EJ, Sheng X, Chou A, Schumacher FR, Olama AAA, Benlloch S, Dadaev T, Brook MN, Sahimi A

and 220 more — show all

Hoffmann TJ, Takahashi A, Matsuda K, Momozawa Y, Fujita M, Muir K, Lophatananon A, Wan P, Le Marchand L, Wilkens LR, Stevens VL, Gapstur SM, Carter BD, Schleutker J, Tammela TLJ, Sipeky C, Auvinen A, Giles GG, Southey MC, MacInnis RJ, Cybulski C, Wokołorczyk D, Lubiński J, Neal DE, Donovan JL, Hamdy FC, Martin RM, Nordestgaard BG, Nielsen SF, Weischer M, Bojesen SE, Røder MA, Iversen P, Batra J, Chambers S, Moya L, Horvath L, Clements JA, Tilley W, Risbridger GP, Gronberg H, Aly M, Szulkin R, Eklund M, Nordström T, Pashayan N, Dunning AM, Ghoussaini M, Travis RC, Key TJ, Riboli E, Park JY, Sellers TA, Lin HY, Albanes D, Weinstein SJ, Mucci LA, Giovannucci E, Lindstrom S, Kraft P, Hunter DJ, Penney KL, Turman C, Tangen CM, Goodman PJ, Thompson IM Jr, Hamilton RJ, Fleshner NE, Finelli A, Parent MÉ, Stanford JL, Ostrander EA, Geybels MS, Koutros S, Freeman LEB, Stampfer M, Wolk A, Håkansson N, Andriole GL, Hoover RN, Machiela MJ, Sørensen KD, Borre M, Blot WJ, Zheng W, Zheng W, Yeboah ED, Mensah JE, Lu YJ, Zhang HW, Feng N, Mao X, Wu Y, Zhao SC, Sun Z, Thibodeau SN, McDonnell SK, Schaid DJ, West CML, Burnet N, Barnett G, Maier C, Schnoeller T, Luedeke M, Kibel AS, Drake BF, Cussenot O, Cancel-Tassin G, Menegaux F, Truong T, Koudou YA, John EM, Grindedal EM, Maehle L, Khaw KT, Ingles SA, Stern MC, Vega A, Gómez-Caamaño A, Fachal L, Rosenstein BS, Kerns SL, Ostrer H, Teixeira MR, Paulo P, Brandão A, Watya S, Lubwama A, Bensen JT, Fontham ETH, Mohler J, Taylor JA, Kogevinas M, Llorca J, Castaño-Vinyals G, Cannon-Albright L, Teerlink CC, Huff CD, Strom SS, Multigner L, Blanchet P, Brureau L, Kaneva R, Slavov C, Mitev V, Leach RJ, Weaver B, Brenner H, Cuk K, Holleczek B, Saum KU, Klein EA, Hsing AW, Kittles RA, Murphy AB, Logothetis CJ, Kim J, Neuhausen SL, Steele L, Ding YC, Isaacs WB, Nemesure B, Hennis AJM, Carpten J, Pandha H, Michael A, De Ruyck K, De Meerleer G, Ost P, Xu J, Razack A, Lim J, Teo SH, Newcomb LF, Lin DW, Fowke JH, Neslund-Dudas C, Rybicki BA, Gamulin M, Lessel D, Kulis T, Usmani N, Singhal S, Parliament M, Claessens F, Joniau S, Van den Broeck T, Gago-Dominguez M, Castelao JE, Martinez ME, Larkin S, Townsend PA, Aukim-Hastie C, Bush WS, Aldrich MC, Crawford DC, Srivastava S, Cullen JC, Petrovics G, Casey G, Roobol MJ, Jenster G, van Schaik RHN, Hu JJ, Sanderson M, Varma R, McKean-Cowdin R, Torres M, Mancuso N, Berndt SI, Van Den Eeden SK, Easton DF, Chanock SJ, Cook MB, Wiklund F, Nakagawa H, Witte JS, Eeles RA, Kote-Jarai Z, Haiman CA

Nature genetics · 2021 · PMID 33398198 · open access

Questions about rs4513875

What is rs4513875?

rs4513875 is a single position in the genome, in or near the MAD1L1 gene. Published research associates it with prostate cancer. A single variant does not decide an outcome — it shifts a probability, and for most common variants the shift is small.

What conditions is rs4513875 linked to?

On MyGeneLog this position is linked to Prostate Cancer. The research behind each link, and its sources, are set out on that condition page.

Does having rs4513875 mean I will get this?

No. Common variants like this one move a probability slightly and, on their own, rarely decide anything about one person. Nothing on this page is a diagnosis, and health decisions should be made with a clinician who can see your whole picture.

Where does the information about rs4513875 come from?

GWAS Catalog, Nature genetics 2021, PMID:33398198. Every variant on MyGeneLog comes from public primary sources and is published with its citation and the date it was checked.

Quoting this page

Licensed CC BY-NC 4.0: free to read, share and adapt for non-commercial use, naming MyGeneLog™ and linking the exact page. Commercial use, including training or serving a commercial AI system, needs a licence — https://www.mygenelog.com/license

Prostate cancer (rs4513875). MyGeneLog™. https://www.mygenelog.com/variants/rs4513875

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