Common variants in breast cancer risk loci predispose to distinct tumor subtypes

NBCS Collaborators; ABCTB Investigators; kConFab/AOCS Investigators

doi:10.1186/s13058-021-01484-x

Common variants in breast cancer risk loci predispose to distinct tumor subtypes

NBCS Collaborators, ABCTB Investigators, kConFab/AOCS Investigators

Patrick G Johnston Centre for Cancer Research

Research output: Contribution to journal › Article › peer-review

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Abstract

Genome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear. Among 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes. Eighty-five of 173 variants were associated with at least one tumor feature (false discovery rate

Original language	English
Article number	2
Number of pages	13
Journal	Breast Cancer Research
Volume	24
Issue number	1
Early online date	04 Jan 2022
DOIs	https://doi.org/10.1186/s13058-021-01484-x
Publication status	Early online date - 04 Jan 2022

Keywords

Genetic predisposition
Etiologic heterogeneity
Breast cancer
Common breast cancer susceptibility variants

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1186/s13058-021-01484-x

Common variants in breast cancer risk loci predispose to distinct tumor subtypes
© 2021 The Authors. This is an open access article published under a Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium, provided the author and source are cited.
Final published version, 1.34 MBLicence: CC BY

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title = "Common variants in breast cancer risk loci predispose to distinct tumor subtypes",

abstract = "Genome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear. Among 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes. Eighty-five of 173 variants were associated with at least one tumor feature (false discovery rate ",

keywords = "Genetic predisposition, Etiologic heterogeneity, Breast cancer, Common breast cancer susceptibility variants",

author = "{NBCS Collaborators} and {ABCTB Investigators} and {kConFab/AOCS Investigators} and Ahearn, {Thomas U} and Haoyu Zhang and Kyriaki Michailidou and Milne, {Roger L} and Bolla, {Manjeet K} and Joe Dennis and Dunning, {Alison M} and Michael Lush and Qin Wang and Andrulis, {Irene L} and Hoda Anton-Culver and Volker Arndt and Aronson, {Kristan J} and Auer, {Paul L} and Annelie Augustinsson and Adinda Baten and Heiko Becher and Sabine Behrens and Javier Benitez and Marina Bermisheva and Carl Blomqvist and Bojesen, {Stig E} and Bernardo Bonanni and Anne-Lise B{\o}rresen-Dale and Hiltrud Brauch and Hermann Brenner and Angela Brooks-Wilson and Thomas Br{\"u}ning and Barbara Burwinkel and Buys, {Saundra S} and Federico Canzian and Castelao, {Jose E} and Jenny Chang-Claude and Chanock, {Stephen J} and Georgia Chenevix-Trench and Clarke, {Christine L} and Coll{\'e}e, {J Margriet} and Angela Cox and Cross, {Simon S} and Kamila Czene and Daly, {Mary B} and Peter Devilee and Thilo D{\"o}rk and Miriam Dwek and Eccles, {Diana M} and Evans, {D Gareth} and Fasching, {Peter A} and Jonine Figueroa and Jones, {Michael E} and Nick Orr",

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doi = "10.1186/s13058-021-01484-x",

language = "English",

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AU - NBCS Collaborators

AU - ABCTB Investigators

AU - kConFab/AOCS Investigators

AU - Ahearn, Thomas U

AU - Zhang, Haoyu

AU - Michailidou, Kyriaki

AU - Milne, Roger L

AU - Bolla, Manjeet K

AU - Dennis, Joe

AU - Dunning, Alison M

AU - Lush, Michael

AU - Wang, Qin

AU - Andrulis, Irene L

AU - Anton-Culver, Hoda

AU - Arndt, Volker

AU - Aronson, Kristan J

AU - Auer, Paul L

AU - Augustinsson, Annelie

AU - Baten, Adinda

AU - Becher, Heiko

AU - Behrens, Sabine

AU - Benitez, Javier

AU - Bermisheva, Marina

AU - Blomqvist, Carl

AU - Bojesen, Stig E

AU - Bonanni, Bernardo

AU - Børresen-Dale, Anne-Lise

AU - Brauch, Hiltrud

AU - Brenner, Hermann

AU - Brooks-Wilson, Angela

AU - Brüning, Thomas

AU - Burwinkel, Barbara

AU - Buys, Saundra S

AU - Canzian, Federico

AU - Castelao, Jose E

AU - Chang-Claude, Jenny

AU - Chanock, Stephen J

AU - Chenevix-Trench, Georgia

AU - Clarke, Christine L

AU - Collée, J Margriet

AU - Cox, Angela

AU - Cross, Simon S

AU - Czene, Kamila

AU - Daly, Mary B

AU - Devilee, Peter

AU - Dörk, Thilo

AU - Dwek, Miriam

AU - Eccles, Diana M

AU - Evans, D Gareth

AU - Fasching, Peter A

AU - Figueroa, Jonine

AU - Jones, Michael E

AU - Orr, Nick

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N2 - Genome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear. Among 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes. Eighty-five of 173 variants were associated with at least one tumor feature (false discovery rate

AB - Genome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear. Among 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes. Eighty-five of 173 variants were associated with at least one tumor feature (false discovery rate

KW - Genetic predisposition

KW - Etiologic heterogeneity

KW - Breast cancer

KW - Common breast cancer susceptibility variants

U2 - 10.1186/s13058-021-01484-x

DO - 10.1186/s13058-021-01484-x

M3 - Article

C2 - 34983606

VL - 24

JO - Breast Cancer Research

JF - Breast Cancer Research

SN - 1465-5411

IS - 1

M1 - 2

ER -

Common variants in breast cancer risk loci predispose to distinct tumor subtypes

Abstract

Keywords

UN SDGs

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