Evaluating the role of NTHL1 p.Q90* allele in inherited breast cancer predisposition.


Journal

Molecular genetics & genomic medicine
ISSN: 2324-9269
Titre abrégé: Mol Genet Genomic Med
Pays: United States
ID NLM: 101603758

Informations de publication

Date de publication:
11 2020
Historique:
received: 15 06 2020
revised: 13 08 2020
accepted: 18 08 2020
pubmed: 20 9 2020
medline: 8 6 2021
entrez: 19 9 2020
Statut: ppublish

Résumé

Rare protein truncating variants of NTHL1 gene are causative for the recently described, recessively inherited NTHL1 tumor syndrome that is characterized by an increased lifetime risk for colorectal cancer, colorectal polyposis, and breast cancer. Although there is strong evidence for breast cancer being a part of the cancer spectrum in these families, the role of pathogenic NTHL1 variants in breast cancer susceptibility in general population remains unclear. We tested the prevalence of NTHL1 nonsense variant c.268C>T, p.Q90*, which is the major allele in NTHL1 families and also shows enrichment in the Finnish population, in a total of 1333 breast cancer patients. Genotyping was performed for DNA samples extracted from peripheral blood by using high-resolution melt analysis. Sixteen NTHL1 p.Q90* heterozygous carriers were identified (1.2%, p = 0.61): 5 in hereditary cohort (n = 234, 2.1%, p = 0.39) and 11 in unselected cohort (n = 1099, 1.0%, p = 0.36). This frequency is equal to that in the general population (19/1324, 1.4%). No NTHL1 p.Q90* homozygotes were identified. Our results indicate that NTHL1 p.Q90* heterozygous carriers do not have an increased risk for breast cancer and that the variant is unlikely to be a significant contributor to breast cancer risk at the population level.

Sections du résumé

BACKGROUND
Rare protein truncating variants of NTHL1 gene are causative for the recently described, recessively inherited NTHL1 tumor syndrome that is characterized by an increased lifetime risk for colorectal cancer, colorectal polyposis, and breast cancer. Although there is strong evidence for breast cancer being a part of the cancer spectrum in these families, the role of pathogenic NTHL1 variants in breast cancer susceptibility in general population remains unclear.
METHODS
We tested the prevalence of NTHL1 nonsense variant c.268C>T, p.Q90*, which is the major allele in NTHL1 families and also shows enrichment in the Finnish population, in a total of 1333 breast cancer patients. Genotyping was performed for DNA samples extracted from peripheral blood by using high-resolution melt analysis.
RESULTS
Sixteen NTHL1 p.Q90* heterozygous carriers were identified (1.2%, p = 0.61): 5 in hereditary cohort (n = 234, 2.1%, p = 0.39) and 11 in unselected cohort (n = 1099, 1.0%, p = 0.36). This frequency is equal to that in the general population (19/1324, 1.4%). No NTHL1 p.Q90* homozygotes were identified.
CONCLUSION
Our results indicate that NTHL1 p.Q90* heterozygous carriers do not have an increased risk for breast cancer and that the variant is unlikely to be a significant contributor to breast cancer risk at the population level.

Identifiants

pubmed: 32949222
doi: 10.1002/mgg3.1493
pmc: PMC7667375
doi:

Substances chimiques

BRCA1 Protein 0
BRCA1 protein, human 0
BRCA2 Protein 0
BRCA2 protein, human 0
Codon, Nonsense 0
Fanconi Anemia Complementation Group N Protein 0
PALB2 protein, human 0
ErbB Receptors EC 2.7.10.1
Deoxyribonuclease (Pyrimidine Dimer) EC 3.1.25.1
NTHL1 protein, human EC 3.1.25.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1493

Informations de copyright

© 2020 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals LLC.

Références

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pubmed: 26559593
Nat Genet. 2015 Jun;47(6):668-71
pubmed: 25938944
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Sci Rep. 2019 Jun 21;9(1):9020
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Breast Cancer Res Treat. 2010 Sep;123 Suppl 1:7-9
pubmed: 20711663
Mol Genet Genomic Med. 2020 Nov;8(11):e1493
pubmed: 32949222
Cancer Cell. 2019 Feb 11;35(2):256-266.e5
pubmed: 30753826
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Cold Spring Harb Perspect Biol. 2013 Apr 01;5(4):a012583
pubmed: 23545420

Auteurs

Timo Kumpula (T)

Laboratory of Cancer Genetics and Tumor Biology, University of Oulu, Oulu, Finland.

Anna Tervasmäki (A)

Laboratory of Cancer Genetics and Tumor Biology, University of Oulu, Oulu, Finland.

Tuomo Mantere (T)

Laboratory of Cancer Genetics and Tumor Biology, University of Oulu, Oulu, Finland.
Department of Human Genetics, Radboud University Medical Center, Nijmegen, Netherlands.

Susanna Koivuluoma (S)

Laboratory of Cancer Genetics and Tumor Biology, University of Oulu, Oulu, Finland.

Laura Huilaja (L)

Department of Dermatology and Medical Research Center Oulu, PEDEGO Research Unit, University of Oulu, Oulu University Hospital, Oulu, Finland.

Kaisa Tasanen (K)

Department of Dermatology and Medical Research Center Oulu, PEDEGO Research Unit, University of Oulu, Oulu University Hospital, Oulu, Finland.

Robert Winqvist (R)

Laboratory of Cancer Genetics and Tumor Biology, University of Oulu, Oulu, Finland.

Richarda M de Voer (RM)

Department of Human Genetics, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, Netherlands.

Katri Pylkäs (K)

Laboratory of Cancer Genetics and Tumor Biology, University of Oulu, Oulu, Finland.

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Classifications MeSH