Pooled analysis indicates that the GSTT1 deletion, GSTM1 deletion, and GSTP1 Ile105Val polymorphisms do not modify breast cancer risk in BRCA1 and BRCA2 mutation carriers
Pooled analysis indicates that the GSTT1 deletion, GSTM1 deletion, and GSTP1 Ile105Val polymorphisms do not modify breast cancer risk in BRCA1 and BRCA2 mutation carriers
The GSTP1, GSTM1, and GSTT1 detoxification genes all have functional polymorphisms that are common in the general population. A single study of 320 BRCA1/2 carriers previously assessed their effect in BRCA1 or BRCA2 mutation carriers. This study showed no evidence for altered risk of breast cancer for individuals with the GSTT1 and GSTM1 deletion variants, but did report that the GSTP1 Ile105Val (rs1695) variant was associated with increased breast cancer risk in carriers. We investigated the association between these three GST polymorphisms and breast cancer risk using existing data from 718 women BRCA1 and BRCA2 mutation carriers from Australia, the UK, Canada, and the USA. Data were analyzed within a proportional hazards framework using Cox regression. There was no evidence to show that any of the polymorphisms modified disease risk for BRCA1 or BRCA2 carriers, and there was no evidence for heterogeneity between sites. These results support the need for replication studies to confirm or refute hypothesis-generating studies.
281-285
Spurdle, A. B.
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Fahey, P.
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Chen, Xiaoqing
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McGuffog, L.
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Easton, D.
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Peock, S.
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Cook, M.
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Simard, J.
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Rebbeck, T. R.
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Antoniou, A. C.
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Chenevix-Trench, G
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Lucassen, Anneke
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18 November 2009
Spurdle, A. B.
79a08784-9f45-4c4f-9bd2-cf1db78f2cda
Fahey, P.
a3c95eaf-5ece-4085-8561-fb36f7f9717a
Chen, Xiaoqing
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McGuffog, L.
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Easton, D.
1bccdadd-da65-418d-90ea-483a8fe7dafb
Peock, S.
078d7af2-b419-40af-a52d-df59456d03b3
Cook, M.
b693d851-afb5-4cf6-ad02-4bb9169b5fe3
Simard, J.
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Rebbeck, T. R.
b9b2a9f6-d199-4f8f-9968-64ce622cae9f
Antoniou, A. C.
e5c475a7-25bb-4973-b7aa-689c00c7edab
Chenevix-Trench, G
e90da721-7c34-4695-902f-34496a53526f
Lucassen, Anneke
2eb85efc-c6e8-4c3f-b963-0290f6c038a5
Spurdle, A. B., Fahey, P., Chen, Xiaoqing, McGuffog, L., Easton, D., Peock, S., Cook, M., Simard, J., Rebbeck, T. R., Antoniou, A. C. and Chenevix-Trench, G
,
kConFab, EMBRACE and INHERIT
(2009)
Pooled analysis indicates that the GSTT1 deletion, GSTM1 deletion, and GSTP1 Ile105Val polymorphisms do not modify breast cancer risk in BRCA1 and BRCA2 mutation carriers.
Breast Cancer Research and Treatment, 122, .
(doi:10.1007/s10549-009-0601-0).
Abstract
The GSTP1, GSTM1, and GSTT1 detoxification genes all have functional polymorphisms that are common in the general population. A single study of 320 BRCA1/2 carriers previously assessed their effect in BRCA1 or BRCA2 mutation carriers. This study showed no evidence for altered risk of breast cancer for individuals with the GSTT1 and GSTM1 deletion variants, but did report that the GSTP1 Ile105Val (rs1695) variant was associated with increased breast cancer risk in carriers. We investigated the association between these three GST polymorphisms and breast cancer risk using existing data from 718 women BRCA1 and BRCA2 mutation carriers from Australia, the UK, Canada, and the USA. Data were analyzed within a proportional hazards framework using Cox regression. There was no evidence to show that any of the polymorphisms modified disease risk for BRCA1 or BRCA2 carriers, and there was no evidence for heterogeneity between sites. These results support the need for replication studies to confirm or refute hypothesis-generating studies.
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Published date: 18 November 2009
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Local EPrints ID: 472041
URI: http://eprints.soton.ac.uk/id/eprint/472041
ISSN: 0167-6806
PURE UUID: 0a1513df-f086-4a25-9d3d-6a4c3247547d
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Date deposited: 24 Nov 2022 17:36
Last modified: 17 Mar 2024 02:54
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Contributors
Author:
A. B. Spurdle
Author:
P. Fahey
Author:
Xiaoqing Chen
Author:
L. McGuffog
Author:
D. Easton
Author:
S. Peock
Author:
M. Cook
Author:
J. Simard
Author:
T. R. Rebbeck
Author:
A. C. Antoniou
Author:
G Chenevix-Trench
Corporate Author: kConFab
Corporate Author: EMBRACE
Corporate Author: INHERIT
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