Evidence for an association between markers on chromosome 19q and non-syndromic cleft lip with or without cleft palate in two groups of multiplex families |
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| Authors: | D. F. Wyszynski Nancy Maestri Iain McIntosh E. Anne Smith Amy F. Lewanda Constanza Garcia-Delgado Enrique Vinageras-Guarneros Eric Wulfsberg Terri H. Beaty |
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| Affiliation: | (1) Department of Epidemiology, School of Hygiene and Public Health, The Johns Hopkins University, 615 N. Wolfe Street, Baltimore, MD 21205, USA Tel.: +1 410 955-7961; Fax: +1 410 955-0863 e-mail: dfw@welchlink.welch.jhu.edu, TP;(2) Department of Pediatrics, School of Medicine, The Johns Hopkins University, Baltimore, USA, TP;(3) Department of Medicine, School of Medicine, The Johns Hopkins Universitiy, Baltimore, USA, TP;(4) Medical Genetics Branch, National Center for Human Genome Research, National Institues of Health, Bethesda, USA, US;(5) Department of Medical Genetics, Children’s National Medical Center, Washington, DC, USA, US;(6) Department of Medical Genetics, Hospital Infantil de Mexico “Federico Gomez”, Mexico, DF, MX;(7) Department of Plastic and Reconstructive Surgery, Hospital Infantil de Mexico “Federico Gomez”, Mexico, DF, MX;(8) Division of Human Genetics, University of Maryland at Baltimore, Baltimore, Maryland, USA, TP |
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| Abstract: | It has been reported that BCL3 on chromosome 19q, or a nearby gene, may play a role in the etiology of non-syndromic cleft lip with or without cleft palate (NSCL/P) in some families. We tested 30 USA and 11 Mexican multiplex NSCL/P families for four markers on chromosome 19q: D19S178, APOC2/AC1, APOC2/007, and BCL3. While likelihood-based linkage analysis failed to show significant evidence of linkage, the transmission disequilibrium test indicated highly significant deviation from independent assortment of allele 3 at the BCL3 marker in both data sets (USA:P = 0.001; Mexican: P = 0.018; both combined: P < 0.001) and for allele 13 of the D19S178 marker in the Mexican data set (P = 0.004). These results support an association, possibly due to linkage disequilibrium, between chromosome 19 markers and a putative NSCL/P locus. Received: 10 May 1996 / Revised: 31 July 1996 |
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