A chromosome 12 coding region is juxtaposed to the <i>MYC</i> protooncogene locus in a t(8; 12)(q24;q22) translocation in a case of B‐cell chronic lymphocytic leukemia

Rimokh, Ruth; Rouault, Jean‐Pierre; Wahbi, Kamal; Gadoux, Mylène; Lafage, Marina; Archimbaud, E; Charrin, C; Gentilhomme, O; Germain, D; Samarut, Jacques; Magaud, Jean‐Pierre

doi:10.1002/gcc.2870030106

Cited by 90 publications

(61 citation statements)

References 45 publications

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“…Chromosome 8 breakpoints were found to be located 2 and 7 kb downstream from MYC, in a 10 kb region where eight other breakpoints have been sequenced previously. 6,[24][25][26][27][28][29][30] This clustering could be related to the high density of Alu sequences found in the region, whose involvement in recombination has been suggested, 31 but also to the presence of DNaseI hypersensitivity sites, mapped from 1.9 to 32 kb downstream from MYC. 32 Several breakpoints have been reported on chromosome 9 in the vicinity of those that were identified in our patients.…”

Section: Discussionmentioning

confidence: 99%

“…The hypothesis of enhancers provided by non-IG translocated sequences was suggested in one case of a t(8;12)(q24;q22). 6 However, MYC deregulation by translocated enhancers may be questionable in cases 6 and 7, with breakpoints localized several hundred kilobases from MYC. This point was discussed in a recent work.…”

Section: Discussionmentioning

confidence: 99%

“…2 Rearrangements of the 8q24 region with IG loci were also reported in other subtypes of nonHodgkin's lymphomas (NHL) and are postulated to be secondary events which could be associated with disease progression. [3][4][5] In a few number of cases, 8q24 rearrangements involving non-IG partner regions have been reported: a t(8;12)(q24;q22) in a transformed B-cell chronic lymphocytic leukaemia, 6 a t(8;9)(q24;p13) in two cases of diffuse large cell lymphomas 7 and a t(1;8)(p21;q24) in a cell line derived from a follicular lymphoma. 8 In this study, MYC rearrangements with non-IG partners were analysed by fluorescence in situ hybridization (FISH) in seventeen cases of lymphoma.…”

Section: Introductionmentioning

confidence: 99%

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Mapping of MYC breakpoints in 8q24 rearrangements involving non-immunoglobulin partners in B-cell lymphomas

et al. 2007

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Chromosomal translocations joining the immunoglobulin (IG) and MYC genes have been extensively reported in Burkitt's and non-Burkitt's lymphomas but data concerning MYC rearrangements with non-IG partners are scarce. In this study, 8q24 breakpoints from 17 B-cell lymphomas involving non-IG loci were mapped by fluorescence in situ hybridization (FISH). In seven cases the breakpoint was inside a small region encompassing MYC: in one t(7;8)(p12;q24) and two t(3;8)(q27;q24), it was telomeric to MYC whereas in four cases, one t(2;8)(p15;q24) and three t(8;9)(q24;p13) it was located in a 85 kb region encompassing MYC. In these seven cases, partner regions identified by FISH contained genes known to be involved in lymphomagenesis, namely BCL6, BCL11A, PAX5 and IKAROS. Breakpoints were cloned in two t(8;9)(q24;p13), 2.5 and 7 kb downstream from MYC and several hundred kb 5 0 to PAX5 on chromosome 9, joining MYC to ZCCHC7 and to ZBTB5 exon 2, two genes encoding zinc-finger proteins. In these seven cases, MYC expression measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR) was significantly higher when compared to that of patients without 8q24 rearrangement (P ¼ 0.006). These results suggest that these rearrangements are the consequence of a non-random process targeting MYC together with non-IG genes involved in lymphocyte differentiation and lymphoma progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mapping of MYC breakpoints in 8q24 rearrangements involving non-immunoglobulin partners in B-cell lymphomas

et al. 2007

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“…9 In addition, ported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan, a Grant-inanother case of ALL transformation in CLL carrying t(8;12) which involved c-myc and BTG1 genes was presented. 10 Aid for Cancer Research from the Ministry of Health and Welfare of Japan and a grant to NA from the Okukubo Memorial Moreover, blasts from at least two cases of ALL supervening on CLL resembled those of Burkitt's type ALL. M Osato Internal Medicine, K Horikawa Kumamoto University School The transformations detected in CLL are generally accompanied by drug resistance and poor prognosis.…”

Section: Pbl (%)mentioning

confidence: 96%

CD3−CD4+ cells with a Th2-like pattern of cytokine production in the peripheral blood of a patient with cutaneous T cell lymphoma

et al. 1997

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A case of cutaneous T cell lymphoma associated with mild autoimmune disorders were also ruled out. A diagnosis of eosinophilia and rise of IgE levels is reported. A population of CTCL was made and treatment with IFN-␣ was started (9 MU CD3 ؊ CD4 ؉ cells was observed in the peripheral blood. After × 3/week), but was stopped 2 months later due to lack of comactivation, these purified CD3 ؊ CD4 ؉ cells showed a Th2 pattern pliance without clinical benefit. Psoralene plus UV-A (P-UVA) of cytokine production, secreting higher levels of IL-5 and ILtherapy induced complete regression of the mycosis fungoides years.Keywords: Th2 cytokines, cutaneous T cell lymphoma;In September 1995, in spite of a normal blood lymphocytecount (1620/ l), two-colour immunophenotypical studies revealed a small CD3 − CD4 + T cell population (Table 1). Rare lymphocytes with convoluted nuclei were observed in the Introduction peripheral blood smears. Eosinophil count was 842/ l and total IgE level 2888 KU/l. A new cutaneous biopsy demonOver the last few years, it has become clear that human T cells strated a dense dermal infiltration by CD4 + CD7 − cells in part can be divided into distinct subsets according to the pattern of lacking TCR␤ expression, whereas a bone marrow biopsy cytokine production: Th1 cells secrete mainly IL-2 and intershowed only moderate eosinophilia. feron-␥, whereas Th2-cells produce IL-4 and IL-5. 1 The enriched CD3 − CD4 + population, obtained by depletion Recently, it has been suggested that cutaneous T cell lymof CD3 + cells from PBMC using magnetic beads, as described phoma (CTCL) represents clonal proliferation of Th2-cells. 2 elsewhere, 4 showed defective response to mitogens activating Moreover, two cases of clonal expansion of CD3 − CD4 + T the cells through crosslinking of membrane receptors (PHA cells, without clinical evidence of lymphoma, secreting Th2-and CD3), but proliferative response, and expression of actitype cytokines have been recently described. 3,4 We report vation markers such as CD69 and CD25, was partially here a new case of CTCL associated with a population of circulating CD3 − CD4 + cells with a Th2-pattern of cytokine production.

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“…The btg1 (B-cell Translocation Gene 1) gene coding sequence was isolated from a translocation break point t(8; 12) (q24; q22) in a case of B-cell Chronic Lymphocytic Leukaemia (CLL-B) (Rimokh et al, 1991;Rouault et al, 1992) and shared high homology with the previously identi®ed tis21 (Fletcher et al, 1991) and pc3 (Bradbury et al, 1991) genes. To date, seven genes have been classi®ed in the same family on the basis of their sequence homology (GueÂ henneux et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Identification of functional domains involved in BTG1 cell localization

et al. 2001

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We have previously shown that BTG1 stimulates myoblast di erentiation. In addition, this protein displays a major nuclear localization in con¯uent myoblasts, decreasing during the early steps of di erentiation, and is essentially detected in the cytoplasm of mature myotubes. To identify the domains involved in the cellular tra cking of BTG1, we observed the localization of several BTG1 sequences fused to bGalactosidase. The highly conserved B box among all members of the BTG family induces a signi®cant nuclear localization of the bGal moiety, enhanced by presence of the BTG1 carboxy-terminal sequence. In addition, a functional Nuclear Export Signal (NES) overlaps the B box. Moreover, presence of the ®rst 43 NH 2 -terminal amino acids reduced the nuclear localization of each chimeric protein tested. Last, the BTG1 amino-terminal domain bears an LxxLL motif favouring nuclear accumulation, and another region encompassing the A box inhibiting nuclear localization. In contrast to a BTG1 mutant exclusively localized in the cytoplasm, transient expression of a mutant displaying a nuclear localization enhanced myoblasts withdrawal from the cell cycle and terminal di erentiation, thus mimicking the myogenic in¯uence of BTG1. In conclusion, several regions of BTG1 are implicated in its cellular localization, and BTG1 myogenic activity is induced at the nuclear level.

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A chromosome 12 coding region is juxtaposed to the MYC protooncogene locus in a t(8; 12)(q24;q22) translocation in a case of B‐cell chronic lymphocytic leukemia

Cited by 90 publications

References 45 publications

Mapping of MYC breakpoints in 8q24 rearrangements involving non-immunoglobulin partners in B-cell lymphomas

Mapping of MYC breakpoints in 8q24 rearrangements involving non-immunoglobulin partners in B-cell lymphomas

CD3−CD4+ cells with a Th2-like pattern of cytokine production in the peripheral blood of a patient with cutaneous T cell lymphoma

Identification of functional domains involved in BTG1 cell localization

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