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The incidence is estimated to be about 1 in 25,000, and PWS is the most common syndromal cause of human obesity. DNA abnormalities, usually deletions or duplications of chromosome 15, have been identified in individuals with PWS with or without recognizable chromosome 15 deletions. Paternal origin of the chromosome 15 deletion by cytogenetic and DNA studies has been found in nearly all PWS individuals studied. No cytogenetic evidence for chromosome breakage has been identified, although an environmental cause (e.g., paternal hydrocarbon\u2010exposed occupations) of the chromosome 15 abnormality has been proposed. PWS patients with the chromosome 15 deletion are more prone to hypopigmentation compared with PWS individuals with normal chromosomes, but no other clinical differences are consistently identified between those with and without the chromosome deletion. Anthropometric, dermatoglyphic, and other clinical findings indicate homogeneity of PWS patients with the chromosome deletion and heterogeneity of the nondeletion patients. A review of our current understanding of the major clinical, cytogenetic, and DNA findings is presented, and clinical manifestations and cytogenetic abnormalities are summarized from the literature.<\/jats:p>","DOI":"10.1002\/ajmg.1320350306","type":"journal-article","created":{"date-parts":[[2005,6,12]],"date-time":"2005-06-12T03:45:23Z","timestamp":1118547923000},"page":"319-332","source":"Crossref","is-referenced-by-count":461,"title":["Prader\u2010Willi syndrome: Current understanding of cause and diagnosis"],"prefix":"10.1002","volume":"35","author":[{"given":"Merlin G.","family":"Butler","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,6,5]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0022-510X(69)90058-6"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00278725"},{"key":"e_1_2_1_4_1","doi-asserted-by":"publisher","DOI":"10.1136\/adc.56.11.882"},{"key":"e_1_2_1_5_1","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.26.9.874"},{"issue":"5","key":"e_1_2_1_6_1","first-page":"237","article-title":"Prader\u2010Willi syndrome associated with an interstitial deletion of chromosome 15","volume":"151","author":"Bonuccelli CM","year":"1982","journal-title":"Johns Hopkins Med J"},{"key":"e_1_2_1_7_1","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-198303000-00001"},{"key":"e_1_2_1_8_1","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.147.4.673"},{"key":"e_1_2_1_9_1","first-page":"140","article-title":"Hypopigmentation: A common feature of Prader\u2010 Labhart\u2010Willi syndrome","volume":"45","author":"Butler MG","year":"1989","journal-title":"Am J Hum Genet"},{"key":"e_1_2_1_10_1","first-page":"417","article-title":"The use of skinfold measurements to judge obesity during the early phase of Prader\u2010Labhart\u2010Willi syndrome","volume":"12","author":"Butler MG","year":"1988","journal-title":"Int J Obes"},{"key":"e_1_2_1_11_1","unstructured":"ButlerMG HaynesJL MeaneyFJ(1989a):Intra\u2010familial and midparental\u2010PWS child correlations and heritability estimates of anthropometric measurements in Prader\u2010Willi syndrome families. 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