Endometrial Cancer Risk in Women With Germline BRCA1 or BRCA2 Mutations: Multicenter Cohort Study.


Journal

Journal of the National Cancer Institute
ISSN: 1460-2105
Titre abrégé: J Natl Cancer Inst
Pays: United States
ID NLM: 7503089

Informations de publication

Date de publication:
04 09 2021
Historique:
received: 20 11 2020
revised: 17 01 2021
accepted: 03 02 2021
pubmed: 13 3 2021
medline: 25 2 2022
entrez: 12 3 2021
Statut: ppublish

Résumé

Endometrial cancer (EC) risk in BReast CAncer gene 1/2 (BRCA1/2) mutation carriers is uncertain; therefore, we assessed this in a large Dutch nationwide cohort study. We selected 5980 BRCA1/2 (3788 BRCA1, 2151 gBRCA2, 41 both BRCA1/BRCA2) and 8451 non-BRCA1/2 mutation carriers from the Hereditary Breast and Ovarian cancer study, the Netherlands cohort. Follow-up started at the date of the nationwide Dutch Pathology Registry coverage (January 1, 1989) or at the age of 25 years (whichever came last) and ended at date of EC diagnosis, last follow-up, or death (whichever came first). EC risk in BRCA1/2 mutation carriers was compared with 1) the general population, estimating standardized incidence ratios (SIRs) based on Dutch population-based incidence rates; and 2) non-BRCA1/2 mutation carriers, using Cox-regression analyses, expressed as hazard ratio (HR). Statistical tests were 2-sided. Fifty-eight BRCA1/2 and 33 non-BRCA1/2 mutation carriers developed EC over 119 296 and 160 841 person-years, respectively (SIR = 2.83, 95% confidence interval [CI] = 2.18 to 3.65; and HR = 2.37, 95% CI = 1.53 to 3.69, respectively). gBRCA1 mutation carriers showed increased risks for EC overall (SIR = 3.51, 95% CI = 2.61 to 4.72; HR = 2.91, 95% CI = 1.83 to 4.66), serous-like EC (SIR = 12.64, 95% CI = 7.62 to 20.96; HR = 10.48, 95% CI = 2.95 to 37.20), endometrioid EC (SIR = 2.63, 95% CI = 1.80 to 3.83; HR = 2.01, 95% CI = 1.18 to 3.45), and TP53-mutated EC (HR = 15.71, 95% CI = 4.62 to 53.40). For BRCA2 mutation carriers, overall (SIR = 1.70, 95% CI = 1.01 to 2.87) and serous-like EC risks (SIR = 5.11, 95% CI = 1.92 to 13.63) were increased compared with the general population. Absolute risks by 75 years remained low (overall EC = 3.0%; serous-like EC = 1.1%). BRCA1/2 mutation carriers have a two- to threefold increased risk for EC, with highest risk observed for the rare subgroups of serous-like and p53-abnormal EC in BRCA1 mutation carriers.

Sections du résumé

BACKGROUND
Endometrial cancer (EC) risk in BReast CAncer gene 1/2 (BRCA1/2) mutation carriers is uncertain; therefore, we assessed this in a large Dutch nationwide cohort study.
METHODS
We selected 5980 BRCA1/2 (3788 BRCA1, 2151 gBRCA2, 41 both BRCA1/BRCA2) and 8451 non-BRCA1/2 mutation carriers from the Hereditary Breast and Ovarian cancer study, the Netherlands cohort. Follow-up started at the date of the nationwide Dutch Pathology Registry coverage (January 1, 1989) or at the age of 25 years (whichever came last) and ended at date of EC diagnosis, last follow-up, or death (whichever came first). EC risk in BRCA1/2 mutation carriers was compared with 1) the general population, estimating standardized incidence ratios (SIRs) based on Dutch population-based incidence rates; and 2) non-BRCA1/2 mutation carriers, using Cox-regression analyses, expressed as hazard ratio (HR). Statistical tests were 2-sided.
RESULTS
Fifty-eight BRCA1/2 and 33 non-BRCA1/2 mutation carriers developed EC over 119 296 and 160 841 person-years, respectively (SIR = 2.83, 95% confidence interval [CI] = 2.18 to 3.65; and HR = 2.37, 95% CI = 1.53 to 3.69, respectively). gBRCA1 mutation carriers showed increased risks for EC overall (SIR = 3.51, 95% CI = 2.61 to 4.72; HR = 2.91, 95% CI = 1.83 to 4.66), serous-like EC (SIR = 12.64, 95% CI = 7.62 to 20.96; HR = 10.48, 95% CI = 2.95 to 37.20), endometrioid EC (SIR = 2.63, 95% CI = 1.80 to 3.83; HR = 2.01, 95% CI = 1.18 to 3.45), and TP53-mutated EC (HR = 15.71, 95% CI = 4.62 to 53.40). For BRCA2 mutation carriers, overall (SIR = 1.70, 95% CI = 1.01 to 2.87) and serous-like EC risks (SIR = 5.11, 95% CI = 1.92 to 13.63) were increased compared with the general population. Absolute risks by 75 years remained low (overall EC = 3.0%; serous-like EC = 1.1%).
CONCLUSIONS
BRCA1/2 mutation carriers have a two- to threefold increased risk for EC, with highest risk observed for the rare subgroups of serous-like and p53-abnormal EC in BRCA1 mutation carriers.

Identifiants

pubmed: 33710348
pii: 6169002
doi: 10.1093/jnci/djab036
pmc: PMC8418438
doi:

Substances chimiques

BRCA1 Protein 0
BRCA1 protein, human 0
BRCA2 Protein 0
BRCA2 protein, human 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1203-1211

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press.

Auteurs

Marthe M de Jonge (MM)

Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands.

Cornelis D de Kroon (CD)

Department of Gynaecology, Leiden University Medical Center, Leiden, the Netherlands.

Denise J Jenner (DJ)

Department of Epidemiology, the Netherlands Cancer Institute, Amsterdam, the Netherlands.

Jan Oosting (J)

Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands.

Joanne A de Hullu (JA)

Department of Gynaecology, RadboudUMC, Nijmegen, the Netherlands.

Marian J E Mourits (MJE)

Department of Gynaecology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.

Encarna B Gómez Garcia (EB)

Department of Clinical Genetics, Maastricht University Medical Center, Maastricht, the Netherlands.

Margreet G E M Ausems (MGEM)

Department of Genetics, Division Laboratories, Pharmacy and Biomedical Genetics, University Medical Center Utrecht, Utrecht, the Netherlands.

J Margriet Collée (J)

Department of Clinical Genetics, Erasmus MC, University Medical Center, Rotterdam, the Netherlands.

Klaartje van Engelen (K)

Department of Clinical Genetics, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.

Irma van de Beek (I)

Department of Clinical Genetics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.

Vincent T H B M Smit (VTHBM)

Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands.

Matti A Rookus (MA)

Department of Epidemiology, the Netherlands Cancer Institute, Amsterdam, the Netherlands.

Geertruida H de Bock (GH)

Department of Epidemiology, University Medical Center Groningen, Groningen, the Netherlands.

Flora E van Leeuwen (FE)

Department of Epidemiology, the Netherlands Cancer Institute, Amsterdam, the Netherlands.

Tjalling Bosse (T)

Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands.

Olaf M Dekkers (OM)

Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, the Netherlands.

Christi J van Asperen (CJ)

Department of Clinical Genetics, Leiden University Medical Center, Leiden, the Netherlands.

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