A new characteristic karyotypic anomaly in lymphoproliferative disorders

Berghe, Herman Van den; Parloir, C.; Gourichon, David; Michaux, Jean‐Louis; Sokal, G.

doi:10.1002/1097-0142(197907)44:1<188::aid-cncr2820440131>3.0.co;2-f

Cited by 92 publications

(17 citation statements)

References 24 publications

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“…Unlike c-rel, however, chromosomal aberrations involving rela are only infrequently found in human lymphoid tumors. There have been sporadic reports of rela gene translocation in nonHodgkin's lymphomas and multiple myelomas, and ampli®cation was observed in a few cases of DLLC (Table 1; Houldsworth et al, 1996;Lai et al, 1995;Van den Berghe et al, 1979). In one multiple myeloma, rela contains a point mutation in its transactivation domain that reduces its transactivation potential (Table 1; Trecca et al, 1997).…”

Section: Rela Gene Alterations In Leukemias and Lymphomasmentioning

confidence: 99%

Aberrant rel/nfkb genes and activity in human cancer

1999

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Rel/NF-kB transcription factors are key regulators of immune, in¯ammatory and acute phase responses and are also implicated in the control of cell proliferation and apoptosis. Remarkable progress has been made in understanding the signal transduction pathways that lead to the activation of Rel/NF-kB factors and the consequent induction of gene expression. Evidence linking deregulated Rel/NF-kB activity to oncogenesis in mammalian systems has emerged in recent years, consistent with the acute oncogenicity of the viral oncoprotein v-Rel in animal models. Chromosomal ampli®cation, overexpression and rearrangement of genes coding for Rel/NF-kB factors have been noted in many human hematopoietic and solid tumors. Persistent nuclear NF-kB activity was also described in several human cancer cell types, as a result of constitutive activation of upstream signaling kinases or mutations inactivating inhibitory IkB subunits. Studies point to a correlation between the activation of cellular gene expression by Rel/NF-kB factors and their participation in the malignant process. Experiments implicating NFkB in the control of the apoptotic response also support a role in oncogenesis and in the resistance of tumor cells to chemotherapy. This review focuses on the status of the rel, nfkb and ikb genes and their activity in human tumors and their association with the onset or progression of malignancies.

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Section: Rela Gene Alterations In Leukemias and Lymphomasmentioning

confidence: 99%

Aberrant rel/nfkb genes and activity in human cancer

1999

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“…The t(11;14)(ql3;q32) translocation is an important abnormality associated with B-lymphocytic malignancy (9,32,48,50). Breakpoints at chromosome 14q32 occur in the joining region of the immunoglobulin heavy-chain (IgH) gene (25,46,47).…”

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confidence: 99%

Characterization of a candidate bcl-1 gene.

Withers¹,

Harvey²,

Faust³

et al. 1991

Mol. Cell. Biol.

318

134

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The t(11;14)(q13;q32) translocation has been associated with human B-lymphocytic malignancy. Several examples of this translocation have been cloned, documenting that this abnormality joins the immunoglobulin heavy-chain gene to the bcl-1 locus on chromosome 11. However, the identification of the bcl-1 gene, a putative dominant oncogene, has been elusive. In this work, we have isolated genomic clones covering 120 kb of the bcl-1 locus. Probes from the region of an HpaII-tiny-fragment island identified a candidate bcl-1 gene. cDNAs representing the bcl-1 mRNA were cloned from three cell lines, two with the translocation. The deduced amino acid sequence from these clones showed bcl-1 to be a member of the cyclin gene family. In addition, our analysis of expression of bcl-1 in an extensive panel of human cell lines showed it to be widely expressed except in lymphoid or myeloid lineages. This observation may provide a molecular basis for distinct modes of cell cycle control in different mammalian tissues. Activation of the bcl-1 gene may be oncogenic by directly altering progression through the cell cycle.

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“…Translocations of either the long arm of chromosome 11 (ql3-+qter) or the long arm of chromosome 18 (q21-*qter) to band q32 of chromosome 14 have been observed in diffuse large-cell lymphoma (12), diffuse small-cell lymphoma (13,14), chronic lymphocytic leukemia of the B-cell type (15), multiple myeloma (16), and follicular lymphoma (13,14). Recently, we have cloned the chromosomal breakpoint of B-cell leukemias and lymphomas with the t(11;14)(q13;q32) translocation (12) and have shown that the breakpoints in three separate tumors with this translocation occurred within a 4-kilobase (kb) stretch of DNA (unpublished observations). We have inferred that at band q13 of human chromosome 11 is located a locus, which we named bcl-J, that is activated by its proximity to the heavy chain locus and is involved in the expression of neoplasia in B cells carrying the 11;14 translocation (17,18).…”

mentioning

confidence: 99%

A 14;18 and an 8;14 chromosome translocation in a cell line derived from an acute B-cell leukemia.

Pegoraro¹,

Palumbo²,

Erikson³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

208

118

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We have established a cell line, which we named 380, from a young male with acute lymphoblastic leukemia (FAB type L2). Karyologic analysis of this cell line indicates that it carries an 8;14 and a 14;18 chromosome translocation, which are characteristic of Burkitt lymphoma and of follicular lymphoma, respectively. This cell line is Epstein-Barr virus antigen-negative, reacts with monoclonal antibodies specific for B cells, and contains rearranged immunoglobulin heavy and light chain genes, but does not express human immunoglobulins. In this cell line, both mu heavy chain constant (C mu) loci are rearranged within the joining (JH) DNA segment. One of the JH segments on one of the 14q+ chromosomes is rearranged with a segment of chromosome 8, where the c-myc oncogene resides, while the other is rearranged with a segment of chromosome 18 where a putative oncogene, which we have called bcl-2, is located. The c-myc oncogene, which is translocated to one of the 14q+ chromosomes, is in its germ-line configuration more than 14 kilobases away from both the JH segment and the heavy chain enhancer that is located between the JH and mu switch region. Based on these findings, we propose a model of some aspects of B-cell oncogenesis according to which B-cell neoplasms carrying translocations involving the heavy chain loci on both human chromosomes 14 are the result of a multiple step process.

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A new characteristic karyotypic anomaly in lymphoproliferative disorders

Cited by 92 publications

References 24 publications

Aberrant rel/nfkb genes and activity in human cancer

Aberrant rel/nfkb genes and activity in human cancer

Characterization of a candidate bcl-1 gene.

A 14;18 and an 8;14 chromosome translocation in a cell line derived from an acute B-cell leukemia.

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