{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T11:39:13Z","timestamp":1771069153959,"version":"3.50.1"},"reference-count":25,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2006,7,14]],"date-time":"2006-07-14T00:00:00Z","timestamp":1152835200000},"content-version":"vor","delay-in-days":6099,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp; Cancer"],"published-print":{"date-parts":[[1989,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We have prepared karyotypes from 22 primitive neuroectodermal tumors (PNETs) from pediatric patients ranging in age from 10 months to 16 years. Twenty\u2010one cases were newly diagnosed, primary, posterior fossa tumors. One case was a recurrent tumor in a patient previously treated with radiation. Cytogenetic results were obtained from direct preparations and\/or short\u2010term (1\u201310 day) culture. Three tumors had apparently normal karyotypes. Nineteen tumors demonstrated numerical and\/or structural abnormalities. The most frequent structural chromosomal changes were deletions and nonreciprocal translocations. Four tumors contained double minutes. Several chromosomes appear to be nonrandomly involved in PNETs. These include chromosomes 5, 6, 11, 16, 17, and a sex chromosome. The most consistent change, however, was an i(17q), present in one\u2010third (8\/22) of the cases. Strikingly, in three of these eight tumors, the i(17q) was the only structural abnormality observed. An i(17q) is not specific for pediatric PNETs, as it is also seen in leukemias and other solid tumors. However, in PNETs it may be primary change related to tumor development and\/or progression. Clinically, there was no correlation of the cytogenetic findings with histologic features of the tumors, size of the tumor, extent of metastasis, or surgical resection.<\/jats:p>","DOI":"10.1002\/gcc.2870010206","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T22:38:30Z","timestamp":1172097510000},"page":"139-147","source":"Crossref","is-referenced-by-count":135,"title":["Isochromosome 17q in primitive neuroectodermal tumors of the central nervous system"],"prefix":"10.1002","volume":"1","author":[{"given":"Jaclyn A.","family":"Biegel","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucy B.","family":"Rorke","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger J.","family":"Packer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leslie 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for the expression of recessive mutation of retinoblastoma susceptibility gene in the development of osteosarcoma","volume":"48","author":"Toguchida J","year":"1988","journal-title":"Cancer Res"},{"key":"e_1_2_1_24_1","first-page":"587","article-title":"Molecular detection of microscopic and submicroscopic deletions associated with Miller\u2010Dieker syndrome","volume":"43","author":"van Tuinen P","year":"1988","journal-title":"Am J Hum Genet"},{"key":"e_1_2_1_25_1","doi-asserted-by":"publisher","DOI":"10.3171\/jns.1989.70.3.0385"},{"key":"e_1_2_1_26_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.24.9252"}],"container-title":["Genes, Chromosomes and 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