The T-ALL specific t(11;14)(p13;q11) translocation breakpoint cluster region is located near to the Wilms' tumour predisposition locus

T. Boehm, I. Lavenir, A. Forster, R. B. Wadey, John Kenneth Cowell, J. Harbott, F. Lampert, J. Waters, P. Sherrington, P. Couillin, M. Azoulay, C. Junien, V. Van Heyningen, D. J. Porteous, N. D. Hastie, T. H. Rabbitts

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Abstract

A breakpoint cluster region (T-ALL(bcr)) 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-ALL(bcr) between the genes for catalase (CAT) and the beta-subunit of follicle stimulating hormone (FSHB). This suggested a link between the T-ALL(bcr) 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-ALL(bcr) 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-ALL(bcr)-WT-aniridia-FSHB-telomere. Therefore, the T-ALL(bcr) must lie very close to but may be distinct from the Wilms' predisposition locus at 11p13.

Original languageEnglish (US)
Pages (from-to)691-695
Number of pages5
JournalOncogene
Volume3
Issue number6
StatePublished - Dec 1 1988
Externally publishedYes

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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Wilms Tumor
Aniridia
Catalase
Hybrid Cells
Beta Subunit Follicle Stimulating Hormone
Gene Order
Centromere
Telomere
Genes
Chromosomes

ASJC Scopus subject areas

  • Cancer Research
  • Genetics
  • Molecular Biology

Cite this

Boehm, T., Lavenir, I., Forster, A., Wadey, R. B., Cowell, J. K., Harbott, J., ... Rabbitts, T. H. (1988). The T-ALL specific t(11;14)(p13;q11) translocation breakpoint cluster region is located near to the Wilms' tumour predisposition locus. Oncogene, 3(6), 691-695.

The T-ALL specific t(11;14)(p13;q11) translocation breakpoint cluster region is located near to the Wilms' tumour predisposition locus. / Boehm, T.; Lavenir, I.; Forster, A.; Wadey, R. B.; Cowell, John Kenneth; Harbott, J.; Lampert, F.; Waters, J.; Sherrington, P.; Couillin, P.; Azoulay, M.; Junien, C.; Van Heyningen, V.; Porteous, D. J.; Hastie, N. D.; Rabbitts, T. H.

In: Oncogene, Vol. 3, No. 6, 01.12.1988, p. 691-695.

Research output: Contribution to journalArticle

Boehm, T, Lavenir, I, Forster, A, Wadey, RB, Cowell, JK, Harbott, J, Lampert, F, Waters, J, Sherrington, P, Couillin, P, Azoulay, M, Junien, C, Van Heyningen, V, Porteous, DJ, Hastie, ND & Rabbitts, TH 1988, 'The T-ALL specific t(11;14)(p13;q11) translocation breakpoint cluster region is located near to the Wilms' tumour predisposition locus', Oncogene, vol. 3, no. 6, pp. 691-695.
Boehm, T. ; Lavenir, I. ; Forster, A. ; Wadey, R. B. ; Cowell, John Kenneth ; Harbott, J. ; Lampert, F. ; Waters, J. ; Sherrington, P. ; Couillin, P. ; Azoulay, M. ; Junien, C. ; Van Heyningen, V. ; Porteous, D. J. ; Hastie, N. D. ; Rabbitts, T. H. / The T-ALL specific t(11;14)(p13;q11) translocation breakpoint cluster region is located near to the Wilms' tumour predisposition locus. In: Oncogene. 1988 ; Vol. 3, No. 6. pp. 691-695.
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abstract = "A breakpoint cluster region (T-ALL(bcr)) 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-ALL(bcr) between the genes for catalase (CAT) and the beta-subunit of follicle stimulating hormone (FSHB). This suggested a link between the T-ALL(bcr) 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-ALL(bcr) 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-ALL(bcr)-WT-aniridia-FSHB-telomere. Therefore, the T-ALL(bcr) must lie very close to but may be distinct from the Wilms' predisposition locus at 11p13.",
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AU - Boehm, T.

AU - Lavenir, I.

AU - Forster, A.

AU - Wadey, R. B.

AU - Cowell, John Kenneth

AU - Harbott, J.

AU - Lampert, F.

AU - Waters, J.

AU - Sherrington, P.

AU - Couillin, P.

AU - Azoulay, M.

AU - Junien, C.

AU - Van Heyningen, V.

AU - Porteous, D. J.

AU - Hastie, N. D.

AU - Rabbitts, T. H.

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N2 - A breakpoint cluster region (T-ALL(bcr)) 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-ALL(bcr) between the genes for catalase (CAT) and the beta-subunit of follicle stimulating hormone (FSHB). This suggested a link between the T-ALL(bcr) 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-ALL(bcr) 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-ALL(bcr)-WT-aniridia-FSHB-telomere. Therefore, the T-ALL(bcr) must lie very close to but may be distinct from the Wilms' predisposition locus at 11p13.

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