Myeloid- and lymphoid-specific breakpoint cluster regions in chromosome band 13q14 in acute leukemia

Coignet, Lionel; Lima, Carmen S. P.; Min, Toon; Streubel, Berthold; Swansbury, John; Telford, Nick; Swanton, S; Bowen, A; Nagai, Masami; Catovsky, Daniel; Fonatsch, Christa; Dyer, Martin J. S.

doi:10.1002/(sici)1098-2264(199907)25:3<222::aid-gcc4>3.0.co;2-c

Cited by 27 publications

(17 citation statements)

References 36 publications

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“…Interestingly, the ETV6 gene has been shown to be fused to the homeobox gene CDX2 in a patient with acute myeloid leukemia and a t(12;13)(p13;q12), 28 and a preliminary study by Coignet et al 29 suggests that myeloid-and lymphoid-specific breakpoint cluster regions are present within chromosome 13q14 in patients with acute leukemia and with a t(12;13)(p12;q12-14).…”

Section: Discussionmentioning

confidence: 99%

Cytogenetic abnormalities associated with the t(12;21): a collaborative study of 169 children with t(12;21)-positive acute lymphoblastic leukemia

Raynaud¹,

Dastugue²,

Zoccola³

et al. 1999

Leukemia

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The t(12;21)(p13;q22) is a cryptic abnormality observed in 25% of children with B-lineage acute lymphoblastic leukemia (ALL), associated with a favorable prognosis. To determine whether specific cytogenetic abnormalities accompany the t(12;21), we analyzed the cytogenetic profiles of blast cells from 169 ALL cases positive for the t(12;21), previously identified by molecular methods. Only 13.6% of samples had normal karyotypes. Structural changes were detected in 89.7% of abnormal karyotypes, and numerical abnormalities in 47%. Rearrangements of 12p were the most frequent structural aberration (57 out of 146 patients with chromosomal abnormalities). Nonspecific deletions of chromosomes 6 and 9 were also found. The most frequent numerical abnormalities was trisomy for chromosomes 21. Blast cells were pseudodiploid (45.6%), hyperdiploid with 47 to 51 chromosomes (24.3%), hypodiploid with 44 to 45 chromosomes (10%), near-triploid (0.6%), or near-tetraploid (5.9%). Our results show that the t(12;21) is not associated with hyperdiploidy of 52 to 68 chromosomes or with the prognostic t(1;19), t(4;11) or t(9;22). Only children with B-lineage ALL who lack these abnormalities detected by conventional cytogenetics will probably benefit from additional testing by molecular methods to detect the t(12;21).

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Section: Discussionmentioning

confidence: 99%

Cytogenetic abnormalities associated with the t(12;21): a collaborative study of 169 children with t(12;21)-positive acute lymphoblastic leukemia

Raynaud¹,

Dastugue²,

Zoccola³

et al. 1999

Leukemia

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“…The clones were obtained from the HGMP Resource Centre, DNA was extracted with the QiaFilter Maxi DNA extraction kit (Qiagen, Valencia, CA, USA) and their gene specificity was confirmed by Southern blot. FISH was performed according to standard protocols as described previously (Coignet et al, 1999). Briefly, the probes were labeled by nick translation with digoxigenin-11-deoxyuridine triphosphate (Roche, Indianapolis, IN, USA).…”

Section: Chromosomal Localizationmentioning

confidence: 99%

NOL7 is a nucleolar candidate tumor suppressor gene in cervical cancer that modulates the angiogenic phenotype

et al. 2005

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Cervical cancer is associated with human papilloma virus infection. However, this infection is insufficient to induce transformation and progression. Loss of heterozygosity analyses suggest the presence of a tumor suppressor gene (TSG) on chromosome 6p21.3-p25. Here we report the cloning NOL7, its mapping to chromosome band 6p23, and localization of the protein to the nucleolus. Fluorescence in situ hybridization analysis demonstrated an allelic loss of an NOL7 in cultured tumor cells and human tumor samples. Transfection of NOL7 into cervical carcinoma cells inhibited their growth in mouse xenografts, confirming its in vivo tumor suppressor activity. The induction of tumor dormancy correlated with an angiogenic switch caused by a decreased production of vascular endothelial growth factor and an increase in the production of the angiogenesis inhibitor thrombospondin-1. These data suggest that NOL7 may function as a TSG in part by modulating the expression of the angiogenic phenotype.

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“…10 in Ref. 13). Chromosome band 12p13 had been known to be involved in many different balanced leukemic translocations (reviewed in Ref.…”

Section: Figurementioning

confidence: 91%

Establishment of the B cell precursor acute lymphoblastic leukemia cell line MUTZ-5 carrying a (12;13) translocation

et al. 2001

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Myeloid- and lymphoid-specific breakpoint cluster regions in chromosome band 13q14 in acute leukemia

Cited by 27 publications

References 36 publications

Cytogenetic abnormalities associated with the t(12;21): a collaborative study of 169 children with t(12;21)-positive acute lymphoblastic leukemia

Cytogenetic abnormalities associated with the t(12;21): a collaborative study of 169 children with t(12;21)-positive acute lymphoblastic leukemia

NOL7 is a nucleolar candidate tumor suppressor gene in cervical cancer that modulates the angiogenic phenotype

Establishment of the B cell precursor acute lymphoblastic leukemia cell line MUTZ-5 carrying a (12;13) translocation

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