Jumping Translocation of Homogeneously Staining Region and Tetraploidy with Double Minutes in Acute Myelomonocytic Leukemia

Yoshida, Takemi; Kimura, N.; Akiyoshi, T; Ohshima, Koichi; Nagano, Mitsuyuki; Morioka, Eiji; Hisano, Shusuke; Ohyashiki, Kazuma; Kamada, Nanao; Tamura, Kazuo

doi:10.1016/s0165-4608(98)00144-7

Cited by 20 publications

(19 citation statements)

References 24 publications

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“…Jumping translocations may occur in multiple myeloma, 6 non-Hodgkin's lymphoma, 7 and acute de novo or secondary leukemia. 7,8 To our knowledge, only 13 cases of AML associated with JT have been described: one case of AML0, 7 one case of AML2, 8 two cases of APL, 9,10 seven cases of AML4/5, 8,[11][12][13][14][15][16] and one case of AML7. 17 One other unclassified AML case following juvenile chronic myelomonocytic leukemia has been reported.…”

Section: Discussionmentioning

confidence: 99%

Jumping translocation in acute leukemia of myelomonocytic lineage: a case report and review of the literature

et al. 2000

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Jumping translocation (JT) is a very rare cytogenetic event, occurring especially in cancer. We describe a case of secondary acute monocytic leukemia (AML5b) with a JT involving the 3q13-3qter segment and leading to a partial trisomy 3. Each clone with JT was associated with trisomy 8 or tetrasomy 8. The literature of JT in AML cases is reviewed: only 13 cases of AML associated with JT have been previously described, seven of which are AML4/5 FAB subtype. Jumping translocation involvement in leukemogenesis is discussed. Leukemia (2000) 14, 119-122.

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Section: Discussionmentioning

confidence: 99%

Jumping translocation in acute leukemia of myelomonocytic lineage: a case report and review of the literature

et al. 2000

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“…hsr-only cells (see Balaban-Malenbaum and Gilbert 1977;Yoshida et al 1999). The complete loss of dmin can follow.…”

Section: Double Minutes and Hsr In Solid Tumorsmentioning

confidence: 99%

“…The complete loss of dmin can follow. The patient reported by Yoshida et al (1999) initially showed a hsr/dmin mosaic, then, after therapy, only hsr cells were found. Similar results have been observed also in cultured tumor cells (Quinn et al 1979;George and Francke 1980;George and Powers 1982).…”

Section: Double Minutes and Hsr In Solid Tumorsmentioning

confidence: 99%

Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure

Storlazzi¹,

Lonoce²,

et al. 2010

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Double minutes (dmin) and homogeneously staining regions (hsr) are the cytogenetic hallmarks of genomic amplification in cancer. Different mechanisms have been proposed to explain their genesis. Recently, our group showed that the MYC-containing dmin in leukemia cases arise by excision and amplification (episome model). In the present paper we investigated 10 cell lines from solid tumors showing MYCN amplification as dmin or hsr. Particularly revealing results were provided by the two subclones of the neuroblastoma cell line STA-NB-10, one showing dmin-only and the second hsr-only amplification. Both subclones showed a deletion, at 2p24.3, whose extension matched the amplicon extension. Additionally, the amplicon structure of the dmin and hsr forms was identical. This strongly argues that the episome model, already demonstrated in leukemias, applies to solid tumors as well, and that dmin and hsr are two faces of the same coin. The organization of the duplicated segments varied from very simple (no apparent changes from the normal sequence) to very complex. MYCN was always overexpressed (significantly overexpressed in three cases). The fusion junctions, always mediated by nonhomologous end joining, occasionally juxtaposed truncated genes in the same transcriptional orientation. Fusion transcripts involving NBAS (also known as NAG), FAM49A, BC035112 (also known as NCRNA00276), and SMC6 genes were indeed detected, although their role in the context of the tumor is not clear.

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“…Deleterious mutations of PRDM1 associated with loss of BLIMP1 protein have also been reported in primary central nervous system lymphoma 63 . Finally, ETS-1, the transcription factor, which is amplified in certain leukemias, interacts with BLIMP1 leading to a block in BLIMP1 DNA binding activity and a reduction in the ability of BLIMP1 to repress target genes [64][65][66][67][68] . In contrast, the over-expression of the BLIMP1β isoform has been reported in multiple myeloma, DLBCL and in some T cell lymphomas 6,[69][70][71] .…”

Section: Blimp1 Is a Tumour Suppressor Genementioning

confidence: 99%

BLIMP1α, the master regulator of plasma cell differentiation is a tumor supressor gene in B cell lymphomas

Vrzalikova¹,

Woodman²,

Murray³

2012

BIOMED PAP

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Aims. The aim of this review was to summarize recent knowledge of the structure and function of a transcriptional repressor, B lymphocyte induced maturation protein 1 (BLIMP1) and its participation in the pathogenesis of B lymphomas. Methods and results. This review summarizes the structure and function of BLIMP1, its major target genes and its role as a tumour suppressor in B cell lymphomas. We review our recent data implicating the loss of BLIMP1α as an important step in the pathogenesis of the Epstein-Barr virus (EBV) associated B cell lymphomas. Conclusions. BLIMP1 is a transcriptional repressor essential for the differentiation of germinal centre (GC) B cells to plasma cells. The loss of BLIMP1 in GC B cells could contribute to the pathogenesis of EBV-associated lymphomas by preventing plasma cell differentiation and viral replication.

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Jumping Translocation of Homogeneously Staining Region and Tetraploidy with Double Minutes in Acute Myelomonocytic Leukemia

Cited by 20 publications

References 24 publications

Jumping translocation in acute leukemia of myelomonocytic lineage: a case report and review of the literature

Jumping translocation in acute leukemia of myelomonocytic lineage: a case report and review of the literature

Gene amplification as double minutes or homogeneously staining regions in solid tumors: Origin and structure

BLIMP1α, the master regulator of plasma cell differentiation is a tumor supressor gene in B cell lymphomas

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