Details der Publikation - Two-locus genome-wide linkage scan for prostate cancer susceptibility genes with an interaction effect

Two-locus genome-wide linkage scan for prostate cancer susceptibility genes with an interaction effect

Abstract Prostate cancer represents a significant worldwide public health burden. Epidemiological and genetic epidemiological studies have consistently provided data supporting the existence of inherited prostate cancer susceptibility genes. Segregation analyses of prostate cancer suggest that a multigene model may best explain familial clustering of this disease. Therefore, modeling gene–gene interactions in linkage analysis may improve the power to detect chromosomal regions harboring these disease susceptibility genes. In this study, we systematically screened for prostate cancer linkage by modeling two-locus gene–gene interactions for all possible pairs of loci across the genome in 426 prostate cancer families from Johns Hopkins Hospital, University of Michigan, University of Umeå, and University of Tampere. We found suggestive evidence for an epistatic interaction for six sets of loci (target chromosome-wide/reference marker-specific P≤0.0001). Evidence for these interactions was found in two independent subsets from within the 426 families. While the validity of these results requires confirmation from independent studies and the identification of the specific genes underlying this linkage evidence, our approach of systematically assessing gene–gene interactions across the entire genome represents a promising alternative approach for gene identification for prostate cancer..

Medienart:	E-Artikel

Erscheinungsjahr:	2005
Erschienen:	2005

Enthalten in:	Zur Gesamtaufnahme - volume:118
Enthalten in:	Human genetics - 118(2005), 6 vom: 23. Nov., Seite 716-724

Sprache:	Englisch

Beteiligte Personen:	Chang, Bao-Li [VerfasserIn] Lange, Ethan M. [VerfasserIn] Dimitrov, Latchezar [VerfasserIn] Valis, Christopher J. [VerfasserIn] Gillanders, Elizabeth M. [VerfasserIn] Lange, Leslie A. [VerfasserIn] Wiley, Kathleen E. [VerfasserIn] Isaacs, Sarah D. [VerfasserIn] Wiklund, Fredrik [VerfasserIn] Baffoe-Bonnie, Agnes [VerfasserIn] Langefeld, Carl D [VerfasserIn] Zheng, S. Lilly [VerfasserIn] Matikainen, Mika P. [VerfasserIn] Ikonen, Tarja [VerfasserIn] Fredriksson, Henna [VerfasserIn] Tammela, Teuvo [VerfasserIn] Walsh, Patrick C. [VerfasserIn] Bailey-Wilson, Joan E. [VerfasserIn] Schleutker, Johanna [VerfasserIn] Gronberg, Henrik [VerfasserIn] Cooney, Kathleen A. [VerfasserIn] Isaacs, William B. [VerfasserIn] Suh, Edward [VerfasserIn] Trent, Jeffrey M. [VerfasserIn] Xu, Jianfeng [VerfasserIn]

Links:	Volltext [lizenzpflichtig]

Themen:	Epistatic Interaction Johns Hopkins Hospital Linkage Analysis Prostate Cancer Reference Marker

Anmerkungen:	© Springer-Verlag 2005

doi:	10.1007/s00439-005-0099-4

funding:
Förderinstitution / Projekttitel:

PPN (Katalog-ID):	OLC210642776X

Internformat


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520			\|a Abstract Prostate cancer represents a significant worldwide public health burden. Epidemiological and genetic epidemiological studies have consistently provided data supporting the existence of inherited prostate cancer susceptibility genes. Segregation analyses of prostate cancer suggest that a multigene model may best explain familial clustering of this disease. Therefore, modeling gene–gene interactions in linkage analysis may improve the power to detect chromosomal regions harboring these disease susceptibility genes. In this study, we systematically screened for prostate cancer linkage by modeling two-locus gene–gene interactions for all possible pairs of loci across the genome in 426 prostate cancer families from Johns Hopkins Hospital, University of Michigan, University of Umeå, and University of Tampere. We found suggestive evidence for an epistatic interaction for six sets of loci (target chromosome-wide/reference marker-specific P≤0.0001). Evidence for these interactions was found in two independent subsets from within the 426 families. While the validity of these results requires confirmation from independent studies and the identification of the specific genes underlying this linkage evidence, our approach of systematically assessing gene–gene interactions across the entire genome represents a promising alternative approach for gene identification for prostate cancer.
650		4	\|a Prostate Cancer
650		4	\|a Linkage Analysis
650		4	\|a Epistatic Interaction
650		4	\|a Reference Marker
650		4	\|a Johns Hopkins Hospital
700	1		\|a Lange, Ethan M. \|4 aut
700	1		\|a Dimitrov, Latchezar \|4 aut
700	1		\|a Valis, Christopher J. \|4 aut
700	1		\|a Gillanders, Elizabeth M. \|4 aut
700	1		\|a Lange, Leslie A. \|4 aut
700	1		\|a Wiley, Kathleen E. \|4 aut
700	1		\|a Isaacs, Sarah D. \|4 aut
700	1		\|a Wiklund, Fredrik \|4 aut
700	1		\|a Baffoe-Bonnie, Agnes \|4 aut
700	1		\|a Langefeld, Carl D \|4 aut
700	1		\|a Zheng, S. Lilly \|4 aut
700	1		\|a Matikainen, Mika P. \|4 aut
700	1		\|a Ikonen, Tarja \|4 aut
700	1		\|a Fredriksson, Henna \|4 aut
700	1		\|a Tammela, Teuvo \|4 aut
700	1		\|a Walsh, Patrick C. \|4 aut
700	1		\|a Bailey-Wilson, Joan E. \|4 aut
700	1		\|a Schleutker, Johanna \|4 aut
700	1		\|a Gronberg, Henrik \|4 aut
700	1		\|a Cooney, Kathleen A. \|4 aut
700	1		\|a Isaacs, William B. \|4 aut
700	1		\|a Suh, Edward \|4 aut
700	1		\|a Trent, Jeffrey M. \|4 aut
700	1		\|a Xu, Jianfeng \|4 aut
773	0	8	\|i Enthalten in \|t Human genetics <Berlin> \|d Springer-Verlag, 1964 \|g 118(2005), 6 vom: 23. Nov., Seite 716-724 \|h Online-Ressource \|w (DE-627)253723973 \|w (DE-600)1459188-1 \|w (DE-576)072373008 \|x 1432-1203 \|7 nnns
773	1	8	\|g volume:118 \|g year:2005 \|g number:6 \|g day:23 \|g month:11 \|g pages:716-724
856	4	0	\|u https://dx.doi.org/10.1007/s00439-005-0099-4 \|z lizenzpflichtig \|3 Volltext
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912			\|a GBV_ILN_2034
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912			\|a GBV_ILN_2049
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912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2059
912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2070
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912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2093
912			\|a GBV_ILN_2106
912			\|a GBV_ILN_2107
912			\|a GBV_ILN_2108
912			\|a GBV_ILN_2110
912			\|a GBV_ILN_2111
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912			\|a GBV_ILN_4037
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912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
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912			\|a GBV_ILN_4251
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4326
912			\|a GBV_ILN_4328
912			\|a GBV_ILN_4333
912			\|a GBV_ILN_4334
912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4336
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951			\|a AR
952			\|d 118 \|j 2005 \|e 6 \|b 23 \|c 11 \|h 716-724

Two-locus genome-wide linkage scan for prostate cancer susceptibility genes with an interaction effect

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