Boehm T, Lavenir I, Forster A, Wadey R B, Cowell J K, Harbott J, Lampert F, Waters J, Sherrington P, Couillin P
Medical Research Council Laboratory of Molecular Biology, Cambridge, UK.
Oncogene. 1988 Dec;3(6):691-5.
A breakpoint cluster region (T-ALLbcr) has been previously described on 11p13 for T-ALL carrying t(11;14)(p13;q11). One further T-ALL breakpoint is described bringing to 5 out of 6 such translocations which are found to break within a maximum of 6.7 kb on chromosome 11p13. Studies of somatic cell hybrids derived from t(11;14)(p13;q11) T-ALL placed the T-ALLbcr between the genes for catalase (CAT) and the beta-subunit of follicle stimulating hormone (FSHB). This suggested a link between the T-ALLbcr and the Wilms' tumour predisposition locus (WT) since constitutional 11p13 deletions predispose to Wilms' tumour. Utilising somatic cell hybrids from patients with Wilms' tumours and aniridia, we show that while the T-ALLbcr maps distal to the catalase gene at 11p13, it maps outside the shortest region of overlap of a series of 11p13 deletions associated with Wilms'-Aniridia. The data suggest the order of genes at 11p13 to be: centromere-CAT-T-ALLbcr-WT-aniridia-FSHB-telomere. Therefore, the T-ALLbcr must lie very close to but may be distinct from the Wilms' predisposition locus at 11p13.
先前已在11p13上描述了携带t(11;14)(p13;q11)的T细胞急性淋巴细胞白血病(T-ALL)的断裂点簇区域(T-ALLbcr)。又描述了一个T-ALL断裂点,使得6个此类易位中的5个被发现发生在11号染色体p13上最大6.7 kb范围内的断裂。对源自t(11;14)(p13;q11) T-ALL的体细胞杂种的研究将T-ALLbcr定位在过氧化氢酶(CAT)基因和促卵泡激素β亚基(FSHB)基因之间。这表明T-ALLbcr与威尔姆斯瘤易感基因座(WT)之间存在联系,因为11p13的先天性缺失易患威尔姆斯瘤。利用来自威尔姆斯瘤和无虹膜患者的体细胞杂种,我们发现,虽然T-ALLbcr定位于11p13上过氧化氢酶基因的远端,但它定位于与威尔姆斯瘤-无虹膜相关的一系列11p13缺失的最短重叠区域之外。数据表明11p13上基因的顺序为:着丝粒-CAT-T-ALLbcr-WT-无虹膜-FSHB-端粒。因此,T-ALLbcr必定非常接近但可能与11p13上的威尔姆斯瘤易感基因座不同。