作者: Anthony E. Reeve , Michael R. Eccles , Richard J. Wilkins , Graeme I. Bell , Lynn J. Millow
DOI: 10.1038/317258A0
关键词: Gene mapping 、 Wilms' tumor 、 Genetics 、 Cancer research 、 Gene 、 Regulator gene 、 Chromosome 、 Oncogene 、 Gene expression 、 Germline 、 Biology
摘要: Wilms' tumour probably arises from embryonal kidney cells and occurs in both hereditary sporadic forms1. Knudson Strong have suggested that forms of the disease are initiated by two mutational events2. In case inherited form, cytogenetic evidence indicates a germline deletion chromosome band 11p13 may correspond to one mutations3–5. DNA mapping is consistent with notion susceptibility gene (Wg) on 11 actually recessive6–9. Comings has proposed dominantly tumours arise inactivation or loss diploid pair regulatory genes which normally suppress expression structural transforming (Tg)10. It recently been N-myc oncogene serve as retinoblas-toma11, although no such yet identified tumour. We now report four cases tumour, insulin-like growth factor-II (IGF-II) transcripts highly elevated compared adjacent normal kidney. addition, we mapped for IGF-II 11p14.1, immediate vicinity Wg. These findings suggest be involved aetiology