{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T22:34:51Z","timestamp":1755038091688},"reference-count":22,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,7,17]],"date-time":"2006-07-17T00:00:00Z","timestamp":1153094400000},"content-version":"vor","delay-in-days":3897,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[1995,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Whdlms' tumor development, like most tumors, involves multiple genetic alterations affecting divershd genes. Only one of these has thus far been identified, the Wilms' tumor I (<jats:italic>WTI<\/jats:italic>) gene on 11p 13, which functions as a tumor suppressor gene. We assessed the involvement of the <jats:italic>WTI<\/jats:italic> gene constitutionally and somatically in 26 Wilms' tumor patients. Of these, the clinical data suggest a constitutional pre\u2010disposition in 12 bilateral cases and 7 cases with early onset. We employed Southern blot analysis and PCR\u2010based markers for analyses of somatic allelic losses in chromosome bands 11 p 13, 11 p 15 and 16q and screened for point mutations in exons 2\u201310 of the <jats:italic>WTI<\/jats:italic> gene with denaturing gradient gel electrophoresis (DGGE). Of the 12 cases with multiple tumors, I exhibited a constitutional 11 p 13 deletion and a somatic stop mutation in exon 4 of the <jats:italic>WTI<\/jats:italic> gene and 2 harbored constitutional mutations in the <jats:italic>WTI<\/jats:italic> gene: a pre\u2010mature stop codon in exon 6 in a boy with bilateral cryptorchidism and bilateral Wilms' tumors and an intragenic deletion in a girl with bilateral WT. Three additional bilateral tumors displayed <jats:italic>WTI<\/jats:italic> rearrangements or allelic losses with 11 p 13 markers. Four of 7 patients with an early onset of unilateral tumor had losses of 11p 13, though no <jats:italic>WTI<\/jats:italic> mutations were detected. Two of the remaining cases that did not show any somatic or constitutional 11 p 13 alterations had Beckwith\u2010Wiedemann syndrome, known to involve the 11 p 15 region.<\/jats:p>","DOI":"10.1002\/ijc.2910630410","type":"journal-article","created":{"date-parts":[[2007,2,20]],"date-time":"2007-02-20T01:11:41Z","timestamp":1171933901000},"page":"516-522","source":"Crossref","is-referenced-by-count":23,"title":["Constitutional and somatic mutations in the <i>WTI<\/i> gene in wilms' tumor patients"],"prefix":"10.1002","volume":"63","author":[{"given":"Agneta","family":"Nordenskj\u00f6ld","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eitan","family":"Friedman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bengt","family":"Sandstedt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan","family":"S\u00f6derh\u00e4ll","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria","family":"Anvret","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,17]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng0594-91"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/gcc.2870080203"},{"key":"e_1_2_1_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90601-A"},{"key":"e_1_2_1_5_1","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.7.10.8393819"},{"key":"e_1_2_1_6_1","first-page":"595","article-title":"Structural rearrangements of the WT1 gene in Wilms' tumor cells","volume":"6","author":"Cowell J.","year":"1991","journal-title":"Oncogene"},{"key":"e_1_2_1_7_1","doi-asserted-by":"publisher","DOI":"10.1159\/000131375"},{"key":"e_1_2_1_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/343774a0"},{"key":"e_1_2_1_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/336374a0"},{"key":"e_1_2_1_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(90)90690-G"},{"key":"e_1_2_1_11_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.21.9618"},{"key":"e_1_2_1_12_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ge.28.120194.002515"},{"key":"e_1_2_1_13_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.9.3247"},{"key":"e_1_2_1_14_1","first-page":"711","article-title":"Familial Beckwith\u2010Wiedemanns syndrome and a second Wilms' tumor locus both map to 11p15.5","volume":"44","author":"Koufos A.","year":"1989","journal-title":"Amer. J. hum. Genet."},{"key":"e_1_2_1_15_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00283727"},{"key":"e_1_2_1_16_1","first-page":"3094","article-title":"A third Wilms' tumor locus on chromosome 16 q","volume":"52","author":"Maw M. 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