CHROMOSOME REARRANGEMENT, t(6 : 14) (p21.1:q32.3), IN MULTIPLE MYELOMA

Nishida, Kazuhiro; Yashige, H; Maekawa, Taira; Fujii, Hiroshi; Horiike, Shigeo; Misawa, Shinichi; Inazawa, Johji; Abe, Tatsuo

doi:10.1111/j.1365-2141.1989.tb04272.x

Cited by 17 publications

(5 citation statements)

References 6 publications

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“…This tumour met all the entry criteria for this study, thus it is apparently a MCL that possesses a 6;14 translocation. To date, t(6;14)(p21;q32) has not been described in MCL, although it has rarely been demonstrated in multiple myeloma and plasma‐cell leukaemia ( Tominaga et al , 1988 ; Nishida et al , 1989 ).…”

Section: Discussionmentioning

confidence: 99%

Diagnostic utility of fluorescence in situ hybridization in mantle‐cell lymphoma

et al. 2000

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Summary. Mantle-cell lymphoma (MCL) has a poorer prognosis than other small B-cell lymphomas, thus a definitive diagnosis is essential. The t(11;14)(q13;q32) associated with MCL juxtaposes portions of CCND1 (11q13) and IGH (14q32), resulting in over-expression of cyclin D1. In this study, a highly sensitive two-colour fluorescence in situ hybridization (FISH) method was developed to detect t(11;14)(q13;q32) in nuclei isolated from paraffin-embedded tissue. Twenty-three MCLs, 13 normal controls and nine small B-cell lymphomas other than MCL were studied by FISH. Each MCL had been previously investigated to detect genomic IGH±CCND1 fusion by polymerase chain reaction (PCR) using DNA extracted from frozen tissue. The IGH±CCND1 fusion detection rate in the MCLs was 96% by FISH compared with 35% by PCR. By FISH, one MCL and three small B-cell lymphomas other than MCL harboured abnormalities involving only IGH. Less than 1% of cells showed falsepositive IGH±CCND1 fusion in normal specimens by FISH. Thus, this highly sensitive FISH assay is very useful in confirming the diagnosis of MCL, has wide applicability as it may be performed on both paraffin-embedded and fresh tissue, and may also facilitate detection of translocations involving these loci in tumours other than MCL.

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Section: Discussionmentioning

confidence: 99%

Diagnostic utility of fluorescence in situ hybridization in mantle‐cell lymphoma

et al. 2000

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“…When c-myc is translocated and controlled by an Ig intronic or distal enhancer, its expression becomes dysregulated from the translocated allele and sustained by up-stream c-myc regulators such as NF-κB [146] and Bcl-6 [147]. In addition, somatic mutations contributing to c-myc activation are B-cell malignancies such as myeloma, plasma cell leukemia, SMZLs and DLBCLs [163][164][165][166][167][168]. Overexpressed cyclin D2 has also been observed in some B-CLLs and LPLs [169] but its role in tumorigenesis has not been defined.…”

Section: Cellular Origin Of Human B Cell Lymphomamentioning

confidence: 98%

Lymphoma and the Control of B Cell Growth and Differentiation

Goodnow²

2006

CMM

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It is now widely accepted that lymphomagenesis is a multistep transformation process. A number of genetic changes and environmental and infectious factors contributing to the development and malignant progression of B-cell lymphoproliferative disorders are well documented. Reciprocal chromosomal translocations involving the immunoglobulin loci are a hallmark of most mature B cell lymphomas and lead to dysregulated expression of proto-oncogenes (c-myc) important for cell proliferation or genes involved in cell cycle progression (cyclin D1), differentiation block (bcl-6, PAX5) and cell survival (bcl-2, NF-kappaB). In addition, genetic alterations that inactivate tumor suppressor genes (p53, p16) have been frequently detected in some lymphoma tissues. Many of these genes are normally regulated by signals from the B cell antigen receptor. The high prevalence of bacterial and viral infection in lymphoma patients supports the hypothesis that infectious agents may play a contributory role in the development and evolution of B cell lymphoproliferative disorders by either directly inducing polyclonal B cell hyperactivation (EBV, HCV), or providing a chronic antigenic stimulus (EBV, HCV, HBV, H. pylori), or mimicking B cell antigen receptor signaling (EBV, HCV, HHV8), although whether these are causative factors or they are secondary to genetic changes in lymphomagenesis remains to be defined. Stimulatory signals from reactive T cells, local cytokines and growth factors can also contribute, to some extent, to the progression of transformation. Modulation of B cell antigen receptor signaling therefore emerges as a potentially powerful strategy for controlling the growth of certain B cell lymphomas.

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“…12,13 The t(6;14)(p12ϳp21;q32) has been previously reported in a variety of B-cell malignancies, principally in myeloma and plasma cell leukemia but also in DLBCL and splenic marginal zone lymphomas (SMZLs). [14][15][16][17][18] Here we report the recurrent involvement of a third cell-cycle regulatory gene, cyclin D3/CCND3, in 6 cases of mature B-cell malignancy, including one case of CD5 ϩ DLBCL, through its direct involvement in t(6;14)(p21.1;q32.3).…”

Section: Introductionmentioning

confidence: 99%

Cyclin D3 is a target gene of t(6;14)(p21.1;q32.3) of mature B-cell malignancies

Sawada

Harder

Horsman

et al. 2001

Blood

116

103

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Chromosomal translocation t(6;14)(p21.1; q32.3) has been reported as a rare but recurrent event not only in myeloma and plasma cell leukemia but also in diffuse large B-cell non-Hodgkin lymphoma (B-NHL) (diffuse large B-cell lymphoma [DLBCL]) and splenic lymphoma with villous lymphocytes (SLVL); however, the nature of the target gene(s) has not been determined. This study identified t(6; 14)(p21.1;q32.3) in 3 cases of transformed extranodal marginal zone B-NHL, in 1 case of SLVL, and in 1 case of a low-grade B-cell lymphoproliferative disorder. In a sixth case, a CD5 ؉ DLBCL, the translocation was identified by molecular cloning in the absence of cytogenetically detectable change. Two chromosomal translocation breakpoints were cloned by using long-distance inverse polymerase chain reaction methods. IntroductionThe lymphomas and leukemias of mature B cells are a biologically and histologically heterogeneous group of malignancies. 1 Their molecular pathogenesis for the most part remains unknown, although cloning of chromosomal translocations targeted to the immunoglobulin (IG) loci continues to allow the identification of novel dominant oncogenes and to define new pathogenic mechanisms. 2 These translocations result in the deregulated expression of genes involved in several pathways, including the control of programmed cell death (apoptosis) and proliferation.IG translocations that involve genes controlling progression through the cell cycle have been described. Cyclin D1 (CCND1) on chromosome 11q13 is involved in the t(11;14)(q13;q32.3). This translocation is found in nearly all cases of mantle cell lymphoma but also in some cases of myeloma, in marginal zone malignancies, such as splenic lymphoma with villous lymphocytes (SLVL), and in B-cell prolymphocytic leukemia. [3][4][5][6] The cyclin-dependent kinase gene (CDK6) in chromosome band 7q22 is involved in t(7;14)(q22;q32) or more commonly in t(2;7)(p12;q22); these translocations appear to be specific for a subset of SLVL. 7,8 The involvement of the cell-cycle regulatory genes in marginal zone B-cell malignancies was unanticipated, because they are characteristically indolent diseases. Whether these genes might have functions in B-cell differentiation other than cell-cycle regulation in mature B cells is not yet clear; cyclin D3 expression, for example, is associated with differentiation of some cell types. 9 Cytogenetic abnormalities of chromosome band 6p21 reported in mature B-cell malignancies are various and include translocations, amplifications, and deletions. 10,11 Such translocations in diffuse large B-cell lymphoma (DLBCL) often involve the BCL6 gene on chromosome band 3q27 and may juxtapose BCL6 with either the histone H4 gene or the PIM1 oncogene. 12,13 The t(6;14)(p12ϳp21;q32) has been previously reported in a variety of B-cell malignancies, principally in myeloma and plasma cell leukemia but also in DLBCL and splenic marginal zone lymphomas (SMZLs). 14-18 Here we report the recurrent involvement of a For personal use only. on May 12, 2018. by gues...

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CHROMOSOME REARRANGEMENT, t(6 : 14) (p21.1:q32.3), IN MULTIPLE MYELOMA

Cited by 17 publications

References 6 publications

Diagnostic utility of fluorescence in situ hybridization in mantle‐cell lymphoma

Diagnostic utility of fluorescence in situ hybridization in mantle‐cell lymphoma

Lymphoma and the Control of B Cell Growth and Differentiation

Cyclin D3 is a target gene of t(6;14)(p21.1;q32.3) of mature B-cell malignancies

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