Reddy K S, Sulcova V, Schwartz S, Noble J E, Phillips J, Brasel J A, Huff K, Lin H J
Cytogenetics Laboratory, Quest Diagnostics Inc., San Juan Capistrano, California, USA.
Am J Med Genet. 2000 May 1;92(1):69-76.
We observed an analphoid marker chromosome stable through cell division in a 16-year-old girl with developmental delay, short stature, limb contractures, and ovaries containing multiple cysts. She also developed myasthenia gravis at 15 years. The marker chromosome, present in 75% of metaphases (and in 90% of transformed lymphoblastoid cells), was C-band negative, and had no pan alpha-satellite sequences detectable by fluorescence in situ hybridization (FISH). The 8q origin of the marker was determined by use of subtelomeric probes and was confirmed by chromosome 8 painting probes. The marker was shown to be an inversion duplication of 8q when subtelomeric, telomeric, and c-myc FISH probes hybridized to both ends of the marker. The karyotype was 47,XX,+inv dup(8)(qter--> q23.3::q23.3-->[neocen]-->qter), resulting in tetrasomy for 8q23.3qter. The parents had normal karyotypes. Centromeric proteins CENP-C and CENP-E were present, but alpha associated centromere protein CENP-B was absent at a position defining a neocentromere.
我们在一名16岁发育迟缓、身材矮小、肢体挛缩且卵巢有多个囊肿的女孩中观察到一条在细胞分裂过程中稳定存在的无着丝粒标记染色体。她在15岁时还患上了重症肌无力。这条标记染色体存在于75%的中期细胞(以及90%的转化淋巴母细胞)中,C带阴性,荧光原位杂交(FISH)检测不到泛α卫星序列。通过使用亚端粒探针确定了该标记的8q起源,并经8号染色体涂染探针证实。当亚端粒、端粒和c-myc FISH探针与该标记的两端杂交时,显示该标记为8q的倒位重复。核型为47,XX,+inv dup(8)(qter--> q23.3::q23.3-->[新着丝粒]-->qter),导致8q23.3qter四体。其父母核型正常。着丝粒蛋白CENP-C和CENP-E存在,但在定义新着丝粒的位置缺乏与α相关的着丝粒蛋白CENP-B。