Analysis of Xq27-28 linkage in the international consortium for prostate cancer genetics (ICPCG) families View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-12

AUTHORS

Joan E Bailey-Wilson, Erica J Childs, Cheryl D Cropp, Daniel J Schaid, Jianfeng Xu, Nicola J Camp, Lisa A Cannon-Albright, James M Farnham, Asha George, Isaac Powell, John D Carpten, Graham G Giles, John L Hopper, Gianluca Severi, Dallas R English, William D Foulkes, Lovise Mæhle, Pål Møller, Rosalind Eeles, Douglas Easton, Michelle Guy, Steve Edwards, Michael D Badzioch, Alice S Whittemore, Ingrid Oakley-Girvan, Chih-Lin Hsieh, Latchezar Dimitrov, Janet L Stanford, Danielle M Karyadi, Kerry Deutsch, Laura McIntosh, Elaine A Ostrander, Kathleen E Wiley, Sarah D Isaacs, Patrick C Walsh, Stephen N Thibodeau, Shannon K McDonnell, Scott Hebbring, Ethan M Lange, Kathleen A Cooney, Teuvo LJ Tammela, Johanna Schleutker, Christiane Maier, Sylvia Bochum, Josef Hoegel, Henrik Grönberg, Fredrik Wiklund, Monica Emanuelsson, Geraldine Cancel-Tassin, Antoine Valeri, Olivier Cussenot, William B Isaacs, and the International Consortium for Prostate Cancer Genetics

ABSTRACT

BACKGROUND: Genetic variants are likely to contribute to a portion of prostate cancer risk. Full elucidation of the genetic etiology of prostate cancer is difficult because of incomplete penetrance and genetic and phenotypic heterogeneity. Current evidence suggests that genetic linkage to prostate cancer has been found on several chromosomes including the X; however, identification of causative genes has been elusive. METHODS: Parametric and non-parametric linkage analyses were performed using 26 microsatellite markers in each of 11 groups of multiple-case prostate cancer families from the International Consortium for Prostate Cancer Genetics (ICPCG). Meta-analyses of the resultant family-specific linkage statistics across the entire 1,323 families and in several predefined subsets were then performed. RESULTS: Meta-analyses of linkage statistics resulted in a maximum parametric heterogeneity lod score (HLOD) of 1.28, and an allele-sharing lod score (LOD) of 2.0 in favor of linkage to Xq27-q28 at 138 cM. In subset analyses, families with average age at onset less than 65 years exhibited a maximum HLOD of 1.8 (at 138 cM) versus a maximum regional HLOD of only 0.32 in families with average age at onset of 65 years or older. Surprisingly, the subset of families with only 2-3 affected men and some evidence of male-to-male transmission of prostate cancer gave the strongest evidence of linkage to the region (HLOD = 3.24, 134 cM). For this subset, the HLOD was slightly increased (HLOD = 3.47 at 134 cM) when families used in the original published report of linkage to Xq27-28 were excluded. CONCLUSIONS: Although there was not strong support for linkage to the Xq27-28 region in the complete set of families, the subset of families with earlier age at onset exhibited more evidence of linkage than families with later onset of disease. A subset of families with 2-3 affected individuals and with some evidence of male to male disease transmission showed stronger linkage signals. Our results suggest that the genetic basis for prostate cancer in our families is much more complex than a single susceptibility locus on the X chromosome, and that future explorations of the Xq27-28 region should focus on the subset of families identified here with the strongest evidence of linkage to this region. More... »

PAGES

46

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-2350-13-46

DOI

http://dx.doi.org/10.1186/1471-2350-13-46

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027714877

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22712434


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