Cloning of the chromosome translocation breakpoint junction of the t(14;19) in chronic lymphocytic leukemia.

McKeithan, Timothy W.; Rowley, Janet D.; Shows, Thomas B.; Dı́az, Manuel O.

doi:10.1073/pnas.84.24.9257

Cited by 102 publications

(57 citation statements)

References 21 publications

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“…The constitutive NF-kB activity seen in most haematological disorders occurs through several mechanisms, including the chromosomal translocation and subsequent overexpression of BCL-3 in a subset of human B-cell chronic lymphotic leukaemias (McKeithan et al, 1987) and mutations of the IkBa gene that impair its inhibitory function in some cases of Hodgkin's lymphomas (Cabannes et al, 1999;Emmerich et al, 1999;Jungnickel et al, 2000). Gene amplification of NIK or loss of function mutations for inhibitory signalling molecules such as TRAF3 and CYLD have been reported in multiple myelomas (Annunziata et al, 2007;Keats et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

et al. 2009

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Constitutive nuclear factor (NF)-jB activation in haematological malignancies is caused in several cases by loss of function mutations within the coding sequence of NF-jB inhibitory molecules such as IjBa or p100. Hut-78, a truncated form of p100, constitutively generates p52 and contributes to the development of T-cell lymphomas but the molecular mechanism underlying this oncogenic potential remains unclear. We show here that MMP9 gene expression is induced through the alternative NF-jB-activating pathway in fibroblasts and also on Hut-78 or p52 overexpression in fibroblasts as well as in lymphoma cells. p52 is critical for Hut-78-mediated MMP9 gene induction as a Hut-78 mutant as well as other truncated NF-jB2 proteins that are not processed into p52 failed to induce the expression of this metalloproteinase. Conversely, MMP9 gene expression is impaired in p52-depleted HUT-78 cells. Interestingly, MLL1 and MLL2 H3K4 methyltransferase complexes are tethered by p52 on the MMP9 but not on the IjBa promoter, and the H3K4 trimethyltransferase activity recruited on the MMP9 promoter is impaired in p52-depleted HUT-78 cells. Moreover, MLL1 and MLL2 are associated with Hut-78 in a native chromatin-enriched extract. Thus, we identified a molecular mechanism by which the recruitment of a H3K4 histone methyltransferase complex on the promoter of a NF-jB-dependent gene induces its expression and potentially the invasive potential of lymphoma cells harbouring constitutive activity of the alternative NF-jB-activating pathway.

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Section: Introductionmentioning

confidence: 99%

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

et al. 2009

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“…Four months after starting treatment with dasatinib, the patient was also evaluated for CML: bone marrow analysis showed complete cytogenetic response and undetectable bcr-abl transcript by real-time PCR. 1 This case report leaves us with some open questions: firstly, what mechanisms of dasatinib are involved in gynecomastia? Secondly, why did our patient develop gynecomastia during dasatinib treatment and not when taking imatinib?…”

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confidence: 99%

“…The chromosomal rearrangement of the immunoglobulin heavy chain (IGH) gene locus resulted in upregulated expression of a new gene, named BCL3, encoding a protein member of the IkB family. 1 It was then reported that t(14;19) was not entirely specific to CLL, because it was also found in other types of chronic B-cell malignancies (for review, see Soma et al 2 ). The Groupe Francophone de Cytogénétique Hématologique (GFCH) collected 43 chronic lymphoproliferative disorders with t(14; 19) or variant BCL3-translocations between 1988 and 2007, to analyze to what extent this uncommon abnormality could define a subgroup among B-cell malignancies, and to document the consequences of the rearrangement.…”

mentioning

confidence: 99%

“…Treatment with oncogenic tyrosine kinase inhibitors has led to a dramatic change in the overall survival rates of patients with chronic myeloid leukemia (CML). 1 Dasatinib is an oral tyrosine kinase inhibitor of bcr-abl, Src, c-kit and the platelet-derived growth factor receptor-alpha and -beta (PDGFR-a, PDGFR-b). Like imatinib, it has been shown to be safe and effective in patients with CML.…”

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confidence: 99%

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The most frequent t(14;19)(q32;q13)-positive B-cell malignancy corresponds to an aggressive subgroup of atypical chronic lymphocytic leukemia

et al. 2008

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“…B-cell leukemia/lymphoma 3 (Bcl-3) is a protooncogene and was initially identified from the patients with chronic lymphocytic leukemia (B-CLL) (McKeithan et al, 1987;Ohno et al, 1990). Elevated Bcl-3 was found in a number of solid tumors, as well as in leukemia and lymphoma.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of Bcl-3 Inhibits Cell Growth and Induces DNA Damage in HTLV-1-infected Cells)

Gao

Wang²,

Chen³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Oncoprotein Bcl-3 is perceived as an unusual member of IκB family since it can both stimulate and suppress NF-κB activation. Aberrant Bcl-3 results in increased cell proliferation and survival, suggesting a contribution to malignant potential and elevated levels of Bcl-3 have been observed in many HTLV-1-infected T cell lines and ATL cells. To investigate the specific roles of Bcl-3 in HTLV-1-infected cells, we knocked down Bcl-3 expression using shRNA and then examined the consequences with regard to DNA damage and cell proliferation, as well as NF-κB activation. The HTLV-1 encoded protein Tax promotes Bcl-3 expression and nuclear translocation. In HTLV-1-infected cells, Bcl-3 knockdown obviously induced DNA damage. Cell growth and NF-κB activation were reduced in HTLV-1-infected or Tax positive cells when Bcl-3 expression was decreased. Together, our results revealed positive roles of Bcl-3 in DNA stabilization, growth and NF-κB activation in HTLV-1-infected cells.

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Cloning of the chromosome translocation breakpoint junction of the t(14;19) in chronic lymphocytic leukemia.

Abstract: Our laboratory has reported that t(14;19)(q32; q13

Cited by 102 publications

References 21 publications

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

The most frequent t(14;19)(q32;q13)-positive B-cell malignancy corresponds to an aggressive subgroup of atypical chronic lymphocytic leukemia

Knockdown of Bcl-3 Inhibits Cell Growth and Induces DNA Damage in HTLV-1-infected Cells)

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