Topological Organization of the MYC/IGK Locus in Burkitt's Lymphoma Cells Assessed by Nuclear Halo Preparations

Rätsch, Andreas; Joos, Stefan; Kioschis, Petra; Lichter, Peter

doi:10.1006/excr.2001.5429

Cited by 23 publications

(21 citation statements)

References 41 publications

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“…38 As was demonstrated in MYC-IGK translocations, the formation of a loop of the translocation region, bringing together MYC and translocated enhancers elements, with intermediate sequences looped out could be suggested. 39 In the work abovementioned, 6 BTG1, the MYC candidate partner gene of the translocation was also overexpressed, thus suggesting a crossedregulation performed by each translocated sequences. The presence of two enhancer elements 3 0 to MYC 32 support this hypothesis.…”

Section: Discussionmentioning

confidence: 91%

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: 91%

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

et al. 2007

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“…Analysis of spatial positions of BCRs present in AML-1 and ETO genes by in situ hybridization of BCR probes with nuclear halos Visualization of specific DNA sequences on nuclear halos by hybridization opens the possibility of studying their partitioning between matrix-bound and looped-out DNA fractions (Balajee et al, 1996;Gerdes et al, 1994;Ratsch et al, 2002). In our recent experiments, this method was successfully used to study the partitioning of the human dystrophin gene into loop domains (Iarovaia et al, 2004).…”

Section: Resultsmentioning

confidence: 99%

Breakpoint cluster regions of the AML-1 and ETO genes contain MAR elements and are preferentially associated with the nuclear matrix in proliferating HEL cells

Iarovaia

Shkumatov

Razin

2004

Journal of Cell Science

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The spatial organization in interphase nuclei of the breakpoint cluster regions (BCRs) of the AML-1 and ETO genes frequently participating in reciprocal t(8;21) translocations was studied using cytological and biochemical approaches. Both BCRs were found to be localized preferentially, but not exclusively, to the nuclear matrix, as shown by hybridization of specific probes with nuclear halos. This association was not related to transcription, because the transcribed regions of both genes located far from BCRs were located preferentially in loop DNA, as shown by in situ hybridization. The sites of association with the nuclear matrix of the intensely transcribed AML-1 gene were mapped also using the biochemical PCR-based approach. Only the BCR was found to be associated with the nuclear matrix, whereas the other transcribed regions of this gene turned out to be positioned randomly in respect to the nuclear matrix. The data are discussed in the framework of the hypothesis postulating that the nuclear matrix plays an important role in determining the positions of recombination-prone areas.Key words: Nuclear matrix, Topoisomerase II, Chromosomal rearrangements, Translocations t(8;21), Nuclear halos, FISH SummaryBreakpoint cluster regions of the AML-1 and ETO genes contain MAR elements and are preferentially associated with the nuclear matrix in proliferating HEL cells

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“…Concerning neural cells, a recent study has demonstrated that N-Myc is required for brain development and that targeted loss of N-Myc function specifically disrupts the ability of neuronal progenitor cells to expand, differentiate, and populate the brain (Knoepfler et al, 2002). Regulation of Myc gene expression has been shown to occur at multiple levels, including gene transcription (Park and Wei, 2003), premature termination of translation (Krumm et al, 1992;Perez-Juste et al, 2000) and translocation (Kanda et al, 2000;Ratsch et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide negatively regulates proliferation and promotes neuronal differentiation through N-Myc downregulation

Ciani

Severi

Contestabile

et al. 2004

Journal of Cell Science

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Nitric oxide (NO) has been found to act as an important negative regulator of cell proliferation in several systems. We report here that NO negatively regulates proliferation of neuronal cell precursors and promotes their differentiation by downregulating the oncogene N-Myc. We have studied this regulatory function of NO in neuroblastoma cell lines (SK-N-BE) and in primary cerebellar granule cell cultures. In a neuronal NO synthase (nNOS) overexpressing neuroblastoma cell line exposed to the differentiative action of retinoic acid, NO slowed down proliferation and accelerated differentiation towards a neuronal phenotype. This effect was accompanied by a parallel decrease of N-Myc expression. Similar results could be obtained in parental SK-N-BE cells by providing an exogenous source of NO. Pharmacological controls demonstrated that NO's regulatory actions on cell proliferation and N-Myc expression were mediated by cGMP as an intermediate messenger. Furthermore, NO was found to modulate the transcriptional activity of N-Myc gene promoter by acting on the E2F regulatory region, possibly through the control of Rb phosphorylation state, that we found to be negatively regulated by NO. In cerebellar granule cell cultures, NOS inhibition increased the division rate of neuronal precursors, in parallel with augmented N-Myc expression. Because a high N-Myc expression level is essential for neuroblastoma progression as well as for proliferation of neuronal precursors, its negative regulation by NO highlights a novel physiopathological function of this important messenger molecule.

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Topological Organization of the MYC/IGK Locus in Burkitt's Lymphoma Cells Assessed by Nuclear Halo Preparations

Cited by 23 publications

References 41 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

Breakpoint cluster regions of the AML-1 and ETO genes contain MAR elements and are preferentially associated with the nuclear matrix in proliferating HEL cells

Nitric oxide negatively regulates proliferation and promotes neuronal differentiation through N-Myc downregulation

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