A new gene, BCM, on chromosome 16 is fused to the interleukin 2 gene by a t(4;16)(q26;p13) translocation in a malignant T cell lymphoma.

Laâbi, Yacine; Gras, Marjorie; Carbonnel, Franck; Jc, Brouet; Berger, Roland; Larsen, Christian‐Jacques; Tsapis, Andréas

doi:10.1002/j.1460-2075.1992.tb05482.x

Cited by 144 publications

(97 citation statements)

References 58 publications

(54 reference statements)

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“…The CREBBP (CREB binding protein) gene is located in 16p13 and is involved in recurrent translocations in acute myeloid leukemia and therapy-related acute myeloid leukemia (Borrow et al, 1996;Sobulo et al, 1997). Other genes within this region that are associated with lymphoma include CIITA, involved in translocations with BCL6 in B-cell lymphoma, and TNFRSF17 (BCM) which has been reported in translocations in T-cell lymphoma of the small intestine (Laabi et al, 1992;Yoshida et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Cytogenetic abnormalities and clinical correlations in peripheral T‐cell lymphoma

et al. 2008

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SummaryCytogenetic correlations among most types of peripheral T-cell lymphoma (PTCL) have not been very informative to date. This study aimed to identify recurrent chromosomal abnormalities in angioimmunoblastic T-cell lymphoma (AITL), ALK-negative anaplastic large cell lymphoma (ALK-ALCL) and peripheral T-cell lymphoma, unspecified (PTCL-US), and to evaluate their prognostic value. We reviewed the cytogenetic findings of 90 previously-diagnosed cases of PTCL and correlated the cytogenetic findings with the specific histological subtype. The most common abnormalities for AITL were 5q (55%), 21 (41%) and 3q (36%) gains, concurrent trisomies of 5 and 21 (41%), and loss of 6q (23%). In ALK(-) ALCL, gains of 1q (50%) and 3p (30%), and losses of 16pter (50%), 6q13q21 (30%), 15 (30%), 16qter (30%) and 17p13 (30%) were frequent findings. In PTCL-US, frequent gains involved 7q22q31 (33%), 1q (24%), 3p (20%), 5p (20%), and 8q24qter (22%), and losses of 6q22q24 (26%) and 10p13pter (26%). We did not observe any association between specific chromosomal abnormalities and overall survival (OS). However, cases with complex karyotypes, most frequently observed in ALK(-) ALCL and PTCL-US, had a significantly shorter OS. Although, genetic differences were noted in these subtypes, further studies are needed to determine the key pathogenetic events in PTCL.

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Section: Discussionmentioning

confidence: 99%

Cytogenetic abnormalities and clinical correlations in peripheral T‐cell lymphoma

et al. 2008

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“…12), and B-cell maturation antibody (BCMA; ref. 13). These receptors are expressed in variable patterns in B-cell chronic lymphocytic leukemia specimens and may describe a subset of patients with inherent resistance to therapeutic agents (14).…”

Section: Introductionmentioning

confidence: 99%

The rGel/BLyS fusion toxin specifically targets malignant B cells expressing the BLyS receptors BAFF-R, TACI, and BCMA

Lyu

Cheung

Hittelman

et al. 2007

Molecular Cancer Therapeutics

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B lymphocyte stimulator (BLyS) is crucial for B-cell survival, and the biological effects of BLyS are mediated by three cell surface receptors designated B cellactivating factor receptor (BAFF-R), transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), and B-cell maturation antibody (BCMA). Increased expression of BLyS and its receptors has been identified in numerous B-cell malignancies. We generated a fusion toxin designated rGel/BLyS for receptor-mediated delivery of the recombinant gelonin (rGel) toxin to neoplastic B cells, and we characterized its activity against various B-cell tumor lines. Three mantle cell lymphoma (MCL) cell lines (JeKo-1, Mino, and SP53) and two diffuse large B-cell lymphoma (DLBCL) cell lines (SUDHL-6 and OCI-Ly3) expressing all three distinct BLyS receptors were found to be the most sensitive to the fusion toxin (IC 50 = 2 -5 pmol/L and 0.001 -5 nmol/L for MCL and DLBCL, respectively). The rGel/BLyS fusion toxin showed specific binding to cells expressing BLyS receptors and rapid internalization of the rGel component into target cells. The cytotoxic effects of rGel/BLyS were inhibited by pretreatment with free BLyS or with soluble BAFF-R, TACI, and BCMA decoy receptors. This suggests that the cytotoxic effects of the fusion toxin are mediated through BLyS receptors. The rGel/BLyS fusion toxin inhibited MCL cell growth through induction of apoptosis associated with caspase-3 activation and poly (ADP-ribose) polymerase cleavage. Our results suggest that BLyS has the potential to serve as an excellent targeting ligand for the specific delivery of cytotoxic molecules to neoplastic B cells expressing the BLyS receptors, and that the rGel/ BLyS fusion toxin may be an excellent candidate for the treatment of B-cell malignancies especially MCL and DLBCL. [Mol Cancer Ther 2007;6(2):460 -70]

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“…TACI is not critically involved in B cell survival, but is required for Tindependent type-2 humoral responses against repetitive antigens and also functions as a tumor suppressor in controlling the size of the B cell compartment [8,9]. In contrast, no function has been assigned yet to BCMA, although its expression pattern suggests a possible role in plasma cells [3,10].…”

Section: Introductionmentioning

confidence: 99%

The anti‐apoptotic factor Bcl‐2 can functionally substitute for the B cell survival but not for the marginal zone B cell differentiation activity of BAFF

et al. 2004

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The TNF family ligand B cell-activating factor (BAFF, BLyS, TALL-1) is an essential factor for B cell development. BAFF binds to three receptors, BAFF-R, transmembrane activator and CAML interactor (TACI), and B cell maturation antigen (BCMA), but only BAFF-R is required for successful survival and maturation of splenic B cells. To test whether the effect of BAFF is due to the up-regulation of anti-apoptotic factors, TACI-Ig-transgenic mice, in which BAFF function is inhibited, were crossed with transgenic mice expressing FLICE-inhibitory protein (FLIP) or Bcl-2 in the B cell compartment. FLIP expression did not rescue B cells, while enforced Bcl-2 expression restored peripheral B cells and the ability to mount T-dependent antibody responses. However, many B cells retained immaturity markers and failed to express normal amounts of CD21. Marginal zone B cells were not restored and the Tindependent IgG3, but not IgM, response was impaired in the TACI-Ig×Bcl-2 mice. These results suggest that BAFF is required not only to inhibit apoptosis of maturating B cells, but also to promote differentiation events, in particular those leading to the generation of marginal zone B cells.

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A new gene, BCM, on chromosome 16 is fused to the interleukin 2 gene by a t(4;16)(q26;p13) translocation in a malignant T cell lymphoma.

Cited by 144 publications

References 58 publications

Cytogenetic abnormalities and clinical correlations in peripheral T‐cell lymphoma

Cytogenetic abnormalities and clinical correlations in peripheral T‐cell lymphoma

The rGel/BLyS fusion toxin specifically targets malignant B cells expressing the BLyS receptors BAFF-R, TACI, and BCMA

The anti‐apoptotic factor Bcl‐2 can functionally substitute for the B cell survival but not for the marginal zone B cell differentiation activity of BAFF

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