Montagna M, Menin C, Chieco-Bianchi L, D'Andrea E
Institute of Oncology, Interuniversity Center for Cancer Research, Padova, Italy.
J Cancer Res Clin Oncol. 1994;120(12):732-6. doi: 10.1007/BF01194272.
The 11p15.5 chromosomal region contains one or more loci involved in congenital developmental abnormalities and in the genesis of embryonal tumors, such as Wilms' tumor, embryonal rhabdomyosarcoma, and hepatoblastoma. In these tumors, a loss of constitutive heterozygosity, selectively involving a specific parental allele, suggests both the presence of onco-suppressor genes and a phenomenon of genomic imprinting. We present evidence that both genetic events could be occasionally involved in hepatoblastoma. In fact, loss of heterozygosity at 11p15.5 could be documented in 3 of 13 patients with hepatoblastoma, and in 2 cases the paternal origin of the residual allele in the tumor was assessed. Moreover, imprinting of the paternal IGFII allele and the maternal H19 allele was confirmed in normal tissues of 5 informative patients. Finally, imprinting relaxation of IGFII was detected in the tumor tissue of 1 patient.
11p15.5染色体区域包含一个或多个与先天性发育异常以及胚胎性肿瘤发生相关的基因座,如肾母细胞瘤、胚胎性横纹肌肉瘤和肝母细胞瘤。在这些肿瘤中,组成性杂合性的丧失,选择性地涉及特定的亲本等位基因,提示了抑癌基因的存在以及基因组印记现象。我们提供的证据表明,这两种遗传事件偶尔可能与肝母细胞瘤有关。事实上,在13例肝母细胞瘤患者中有3例可检测到11p15.5处的杂合性丧失,并且在2例病例中评估了肿瘤中残留等位基因的父系起源。此外,在5例信息充分的患者的正常组织中证实了父系IGFII等位基因和母系H19等位基因的印记。最后,在1例患者的肿瘤组织中检测到IGFII印记松弛。