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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.

Type

Journal article

Journal

Oncogene

Publication Date

12/1988

Volume

3

Pages

691 - 695

Keywords

Aniridia, Chromosome Banding, Chromosome Mapping, Chromosomes, Human, Pair 11, Chromosomes, Human, Pair 14, Gene Deletion, Genetic Predisposition to Disease, Humans, Hybrid Cells, Kidney Neoplasms, Leukemia-Lymphoma, Adult T-Cell, Multigene Family, Oncogenes, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcr, Proto-Oncogenes, Translocation, Genetic, Wilms Tumor