{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T16:18:27Z","timestamp":1779293907388,"version":"3.51.4"},"reference-count":25,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2002,9,26]],"date-time":"2002-09-26T00:00:00Z","timestamp":1032998400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genesis"],"published-print":{"date-parts":[[2002,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cloned animals suffer a wide range of severe fetal and placental malformations. Whether these malformations arise from insufficient epigenetic modifications or mutations has not yet been determined. To address this question, we examined siblings from both cloned XO and XY parents. These parents, which exhibited hypertrophic placentas, increased body weights, and open eyelids at birth, were created from the same ES cell sublines. The siblings from all three cloned pairs showed normal body and placenta weights and no open eyelids at birth. The results clearly showed that the phenotypic abnormalities seen in cloned mice were not transmitted to the progeny, a finding that suggests that abnormalities in cloned mice are responsible for insufficient epigenetic modifications\/reprogramming. genesis 2:203\u2013207, 2002. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gene.10143","type":"journal-article","created":{"date-parts":[[2002,10,23]],"date-time":"2002-10-23T12:54:30Z","timestamp":1035377670000},"page":"203-207","source":"Crossref","is-referenced-by-count":73,"title":["Abnormalities in cloned mice are not transmitted to the 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