Molecular cytogenetic characterization of the mantle cell lymphoma cell line GRANTA-519

Rudolph, Cornelia; Steinemann, Doris; Neuhoff, Nils von; Gadzicki, Dorothea; Ripperger, Tim; Drexler, Hans; Mrasek, Kristin; Liehr, Thomas; Claussen, Uwe; Emura, M.; Schröck, Evelin; Schlegelberger, Brigitte

doi:10.1016/j.cancergencyto.2004.01.006

Cited by 36 publications

(26 citation statements)

References 18 publications

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“…by guest www.bloodjournal.org From including Granta-519 cells. 19,41 However, the expression of Cyclin D1, one of the most specific markers of MCL development, was not affected by DPN treatment (data not shown). Although previous studies have demonstrated that estrogens activate the expression of Cyclin D1 via ERa but inhibit via ERb in HeLa cells in vitro, 42 the mechanisms of the inhibitory effects of ERb agonist in lymphoid cells on tumor cell proliferation do not seem to involve Cyclin D1.…”

Section: 28mentioning

confidence: 99%

“…Murine mouse T-cell lymphoma line EG7, 18 human MCL cell line Granta-519, 19 human BL line Raji, 17 and human breast cancer MDA-MB-231 20 cells were maintained in RPMI 1640 medium (EG7, Granta-519, Raji) or Dulbecco's modified Eagle's medium (MDA-MB-231) supplemented with 10% fetal bovine serum, 2 mM L-glutamine, 100 IU penicillin/mL, and 100 mg/mL streptomycin at 37°C in 5% CO 2 .…”

Section: Cell Linesmentioning

confidence: 99%

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Inhibition of lymphoma vascularization and dissemination by estrogen receptor β agonists

Yakimchuk

Hasni

Guan

et al. 2014

Blood

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Section: 28mentioning

confidence: 99%

Section: Cell Linesmentioning

confidence: 99%

Inhibition of lymphoma vascularization and dissemination by estrogen receptor β agonists

Yakimchuk

Hasni

Guan

et al. 2014

Blood

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“…Granta-519 and HBL-2 cells showed high levels of Bcl-2 protein in accordance with the described amplification of the 18q21 region involving the BCL-2 gene. 26,27 In contrast, Bcl-2 protein was not detected in UPN-1 cells that harbor a deletion at 18q12-22 (Silvia Bea, unpublished data, May 2006). Densitometric analysis of these proteins revealed an inverse correlation between the sensitivity to GX15-070 and the total amount of these antiapoptotic proteins, Bcl-2 being the protein that most contributed to the whole ( Figure 2B).…”

Section: Relationship Between Gx15-070 Cytotoxicity and Expression Ofmentioning

confidence: 99%

The BH3-mimetic GX15-070 synergizes with bortezomib in mantle cell lymphoma by enhancing Noxa-mediated activation of Bak

Pérez-Galán

Roué

Villamor

et al. 2007

Blood

177

161

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IntroductionMantle cell lymphoma (MCL) is a well-defined lymphoid neoplasm genetically characterized by the t(11;14)(q13;q32) translocation leading to a constitutive overexpression of cyclin D1. 1 In addition to classical MCL, a blastoid variant of this disease has been described, characterized by high proliferation and associated with INK4a/ARF deletions, p53 mutations, and complex karyotypes. [2][3][4] The clinical behavior is aggressive, and few patients reach long survival or can be considered cured with current therapies. Recent results from clinical trials using the proteasome inhibitor bortezomib have shown promising results in the management of patients with MCL. [5][6][7][8] Bcl-2 family proteins are key regulators of apoptosis, determining cellular fate in response to numerous stress. 9,10 In mammalian cells, the prosurvival members (Bcl-2, Bcl-X L , Mcl-1, Bcl-w, and A1) oppose 2 proapoptotic groups: the multidomain proteins (Bax, Bak, and Bok) and the BH-3-only proteins (Bim, Puma, Noxa, Bad, Bid, Bmf, Bik, and Hrk). A balance between prosurvival and prodeath Bcl-2 members dictates the outcome of many deathinitiating signaling pathways. The BH3-only members function as sensors of cellular well-being, and when activated by cytotoxic signals, selectively engage the prosurvival members by inserting its BH3 domain into a hydrophobic groove on the antiapoptotic member surfaces. 11 This event allows Bax and Bak displacement from antiapoptotic members, their oligomerization and permeabilization of the mitochondrion, provoking the release of proapoptotic factors, caspase activation and finally cell death. 12,13 There is growing evidence that the Bcl-2 pathway is deregulated in most neoplasms. Several studies have described high levels of Bcl-2 in MCL cells. 14,15 Bcl-X L overexpression has also been described in MCL cells, linked to constitutive activation of the NF-B pathway. 16 Moreover, Mcl-1 overexpression has been correlated with high-grade MCL. 17 In addition, we have recently shown that bortezomib induces both the accumulation of the antiapoptotic protein Mcl-1 and the activation of the proapoptotic BH3-only protein Noxa, which counteracts, at least partially, the effect of its antiapoptotic partner. 18 It is conceivable that Mcl-1 accumulation may delay bortezomib-induced apoptosis. In this context, the emergence of small-molecule inhibitors that modulate Bcl-2 pathway represents a rational approach for the treatment of this neoplasm and may synergize with bortezomib activity. GX15-070 (GeminX Biotechnologies, Montreal, QC, Canada) is a small-molecule pan-Bcl-2 inhibitor that belongs to the polypirrole class of molecules, which binds to Bcl-2, Bcl-w, Bcl-X L , and Mcl-1 with a K d in the range of 0.5 M. 19 This compound has been designed to mimic proapoptotic BH3-only proteins in its binding to the antiapoptotic Bcl-2 family members, and appears to fall into the class of BH3 "sensitizers." 20 GX15-070 is currently in phase 1 clinical trials for the treatment of refractory solid tumors, and in phases...

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“…13 Although tumor cell lines may display a greater extent of CpG island hypermethylation than the primary tumors, they still carry the characteristic aberrant methylation modifications 14 and could therefore be used as methylotype models of the primary tumors. 15 To search for novel candidate genes probably involved in the progression of t(11;14)-positive MCL, we treated the human MCL cell line Granta-519 16,17 with 5-aza-2'-deoxycytidine (5-aza-CdR) to identify epigenetically silenced genes. This inactivating substrate of DNA methyltransferase 18 induces an indirect genomic demethylation 19 and chromatin remodeling 20 and can, therefore, lead to the reactivation of transcriptionally silenced genes.…”

mentioning

confidence: 99%

Promoter methylation of PARG1, a novel candidate tumor suppressor gene in mantle cell lymphomas

Ripperger¹,

Neuhoff²,

Kamphues³

et al. 2007

Haematologica

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Molecular cytogenetic characterization of the mantle cell lymphoma cell line GRANTA-519

Cited by 36 publications

References 18 publications

Inhibition of lymphoma vascularization and dissemination by estrogen receptor β agonists

Inhibition of lymphoma vascularization and dissemination by estrogen receptor β agonists

The BH3-mimetic GX15-070 synergizes with bortezomib in mantle cell lymphoma by enhancing Noxa-mediated activation of Bak

Promoter methylation of PARG1, a novel candidate tumor suppressor gene in mantle cell lymphomas

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