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Clinical symptoms observed in these patients were very variable as previously reported in other families and included large areas of alopecia on the vertex of the skull and serious limb reduction defects with agenesis of all toes of one foot. To identify the disease\u2010causing gene, we sequenced the <jats:italic>MSX1<\/jats:italic>, <jats:italic>CART1<\/jats:italic>, <jats:italic>P63<\/jats:italic> (<jats:italic>P73L<\/jats:italic>), <jats:italic>RUNX2<\/jats:italic>, and <jats:italic>HOXD13<\/jats:italic> genes in this family and nine previously reported families, but no disease\u2010causing mutations were found. Further investigation is ongoing in these families in order to identify the genetic cause of AOS.<\/jats:p>","DOI":"10.1111\/j.1399-0004.2006.00552.x","type":"journal-article","created":{"date-parts":[[2005,12,13]],"date-time":"2005-12-13T14:11:26Z","timestamp":1134483086000},"page":"86-92","source":"Crossref","is-referenced-by-count":18,"title":["Adams\u2013Oliver syndrome: clinical description of a four\u2010generation family and exclusion of five candidate genes"],"prefix":"10.1111","volume":"69","author":[{"given":"P","family":"Verdyck","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B","family":"Blaumeiser","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Holder\u2010Espinasse","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W","family":"Van 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