TY  - JOUR
AU  - Klapproth, Kay
AU  - Sander, Sandrine
AU  - Marinković, Dragan
AU  - Baumann, Bernd
AU  - Wirth, Thomas
PY  - 2009
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/309
AB  - Deregulated c-MYC is found in a variety of cancers where it promotes proliferation as well as apoptosis. In many hematologic malignancies, enhanced NF-kappa B exerts prosurvival functions. Here we investigated the role of NF-kappa B in mouse and human c-MYC-transformed lymphomas. The NF-kappa B pathway is extinguished in murine lymphoma cells, and extrinsic stimuli typically inducing NF-kappa B activity fail to activate this pathway. Genetic activation of the NF-kappa B pathway induces apoptosis in these cells, whereas inhibition of NF-kappa B by an I kappa B alpha superrepressor provides a selective advantage in vivo. Furthermore, in human Burkitt lymphoma cells we find that NF-kappa B activation induces apoptosis. NF-kappa B up-regulates Fas and predisposes to Fas-induced cell death, which is caspase-8 mediated and can be prevented by CFLAR overexpression. We conclude that c-MYC overexpression sensitizes cells to NF-kappa B-induced apoptosis, and persistent inactivity of NF-kappa B signaling is a prerequisite for MYC-mediated tumorigenesis. We could also show that low immunogenicity and Fas insensitivity of MYC-driven lymphoma cells are reversed by activation of NF-kappa B. Our observations provide a molecular explanation for the described absence of the NF-kappa B signaling in Burkitt lymphoma and question the applicability of NF-kappa B inhibitors as candidates for treatment of this cancer. (Blood. 2009; 114: 2448-2458)
PB  - Amer Soc Hematology, Washington
T2  - Blood
T1  - The IKK2/NF-kappa B pathway suppresses MYC-induced lymphomagenesis
EP  - 2458
IS  - 12
SP  - 2448
VL  - 114
DO  - 10.1182/blood-2008-09-181008
ER  - 

@article{
author = "Klapproth, Kay and Sander, Sandrine and Marinković, Dragan and Baumann, Bernd and Wirth, Thomas",
year = "2009",
abstract = "Deregulated c-MYC is found in a variety of cancers where it promotes proliferation as well as apoptosis. In many hematologic malignancies, enhanced NF-kappa B exerts prosurvival functions. Here we investigated the role of NF-kappa B in mouse and human c-MYC-transformed lymphomas. The NF-kappa B pathway is extinguished in murine lymphoma cells, and extrinsic stimuli typically inducing NF-kappa B activity fail to activate this pathway. Genetic activation of the NF-kappa B pathway induces apoptosis in these cells, whereas inhibition of NF-kappa B by an I kappa B alpha superrepressor provides a selective advantage in vivo. Furthermore, in human Burkitt lymphoma cells we find that NF-kappa B activation induces apoptosis. NF-kappa B up-regulates Fas and predisposes to Fas-induced cell death, which is caspase-8 mediated and can be prevented by CFLAR overexpression. We conclude that c-MYC overexpression sensitizes cells to NF-kappa B-induced apoptosis, and persistent inactivity of NF-kappa B signaling is a prerequisite for MYC-mediated tumorigenesis. We could also show that low immunogenicity and Fas insensitivity of MYC-driven lymphoma cells are reversed by activation of NF-kappa B. Our observations provide a molecular explanation for the described absence of the NF-kappa B signaling in Burkitt lymphoma and question the applicability of NF-kappa B inhibitors as candidates for treatment of this cancer. (Blood. 2009; 114: 2448-2458)",
publisher = "Amer Soc Hematology, Washington",
journal = "Blood",
title = "The IKK2/NF-kappa B pathway suppresses MYC-induced lymphomagenesis",
pages = "2458-2448",
number = "12",
volume = "114",
doi = "10.1182/blood-2008-09-181008"
}

Klapproth, K., Sander, S., Marinković, D., Baumann, B.,& Wirth, T.. (2009). The IKK2/NF-kappa B pathway suppresses MYC-induced lymphomagenesis. in Blood
Amer Soc Hematology, Washington., 114(12), 2448-2458.
https://doi.org/10.1182/blood-2008-09-181008

Klapproth K, Sander S, Marinković D, Baumann B, Wirth T. The IKK2/NF-kappa B pathway suppresses MYC-induced lymphomagenesis. in Blood. 2009;114(12):2448-2458.
doi:10.1182/blood-2008-09-181008 .

Klapproth, Kay, Sander, Sandrine, Marinković, Dragan, Baumann, Bernd, Wirth, Thomas, "The IKK2/NF-kappa B pathway suppresses MYC-induced lymphomagenesis" in Blood, 114, no. 12 (2009):2448-2458,
https://doi.org/10.1182/blood-2008-09-181008 . .

TY  - JOUR
AU  - Kokai, Enikoe
AU  - Voss, Florian
AU  - Fleischer, Frank
AU  - Kempe, Sybille
AU  - Marinković, Dragan
AU  - Wolburg, Hartwig
AU  - Leithaeuser, Frank
AU  - Schmidt, Volker
AU  - Deutsch, Urban
AU  - Wirth, Thomas
PY  - 2009
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/252
AB  - Previous work has shown that c-Myc is required for adequate vasculogenesis and angiogenesis. To further investigate the contribution of Myc to these processes, we conditionally expressed c-Myc in embryonic endothelial cells using a tetracycline-regulated system. Endothelial Myc overexpression resulted in severe defects in the embryonic vascular system. Myc-expressing embryos undergo widespread edema formation and multiple hemorrhagic lesions. They die between embryonic days 14.5 and 17.5. The changes in vascular permeability are not caused by deficiencies in vascular basement membrane composition or pericyte coverage. However, the overall turnover of endothelial cells is elevated as is revealed by increased levels of both proliferation and apoptosis. Whole-mount immunohistochemical analysis revealed alterations in the architecture of capillary networks. The dermal vasculature of Myc-expressing embryos is characterized by a reduction in vessel branching, which occurs despite upregulation of the proangiogenic factors vascular endothelial growth factor-A and angiopoietin-2. Thus, the net outcome of an excess of vascular endothelial growth factor-A and angiopoietin-2 in the face of an elevated cellular turnover appears to be a defect in vascular integrity. (Circ Res. 2009;104:1151-1159.)
PB  - Lippincott Williams & Wilkins, Philadelphia
T2  - Circulation Research
T1  - Myc Regulates Embryonic Vascular Permeability and Remodeling
EP  - U59
IS  - 10
SP  - 1151
VL  - 104
DO  - 10.1161/CIRCRESAHA.108.191460
ER  - 

@article{
author = "Kokai, Enikoe and Voss, Florian and Fleischer, Frank and Kempe, Sybille and Marinković, Dragan and Wolburg, Hartwig and Leithaeuser, Frank and Schmidt, Volker and Deutsch, Urban and Wirth, Thomas",
year = "2009",
abstract = "Previous work has shown that c-Myc is required for adequate vasculogenesis and angiogenesis. To further investigate the contribution of Myc to these processes, we conditionally expressed c-Myc in embryonic endothelial cells using a tetracycline-regulated system. Endothelial Myc overexpression resulted in severe defects in the embryonic vascular system. Myc-expressing embryos undergo widespread edema formation and multiple hemorrhagic lesions. They die between embryonic days 14.5 and 17.5. The changes in vascular permeability are not caused by deficiencies in vascular basement membrane composition or pericyte coverage. However, the overall turnover of endothelial cells is elevated as is revealed by increased levels of both proliferation and apoptosis. Whole-mount immunohistochemical analysis revealed alterations in the architecture of capillary networks. The dermal vasculature of Myc-expressing embryos is characterized by a reduction in vessel branching, which occurs despite upregulation of the proangiogenic factors vascular endothelial growth factor-A and angiopoietin-2. Thus, the net outcome of an excess of vascular endothelial growth factor-A and angiopoietin-2 in the face of an elevated cellular turnover appears to be a defect in vascular integrity. (Circ Res. 2009;104:1151-1159.)",
publisher = "Lippincott Williams & Wilkins, Philadelphia",
journal = "Circulation Research",
title = "Myc Regulates Embryonic Vascular Permeability and Remodeling",
pages = "U59-1151",
number = "10",
volume = "104",
doi = "10.1161/CIRCRESAHA.108.191460"
}

Kokai, E., Voss, F., Fleischer, F., Kempe, S., Marinković, D., Wolburg, H., Leithaeuser, F., Schmidt, V., Deutsch, U.,& Wirth, T.. (2009). Myc Regulates Embryonic Vascular Permeability and Remodeling. in Circulation Research
Lippincott Williams & Wilkins, Philadelphia., 104(10), 1151-U59.
https://doi.org/10.1161/CIRCRESAHA.108.191460

Kokai E, Voss F, Fleischer F, Kempe S, Marinković D, Wolburg H, Leithaeuser F, Schmidt V, Deutsch U, Wirth T. Myc Regulates Embryonic Vascular Permeability and Remodeling. in Circulation Research. 2009;104(10):1151-U59.
doi:10.1161/CIRCRESAHA.108.191460 .

Kokai, Enikoe, Voss, Florian, Fleischer, Frank, Kempe, Sybille, Marinković, Dragan, Wolburg, Hartwig, Leithaeuser, Frank, Schmidt, Volker, Deutsch, Urban, Wirth, Thomas, "Myc Regulates Embryonic Vascular Permeability and Remodeling" in Circulation Research, 104, no. 10 (2009):1151-U59,
https://doi.org/10.1161/CIRCRESAHA.108.191460 . .

TY  - JOUR
AU  - Schlee, Martin
AU  - Hoelzel, Michael
AU  - Bernard, Sandra
AU  - Mailhammer, Reinhard
AU  - Schuhmacher, Marino
AU  - Reschke, Judith
AU  - Eick, Dirk
AU  - Marinković, Dragan
AU  - Wirth, Thomas
AU  - Rosenwald, Andreas
AU  - Staudt, Louis M.
AU  - Eilers, Martin
AU  - Baran-Marszak, Fanny
AU  - Fagard, Remi
AU  - Feuillard, Jean
AU  - Laux, Gerhard
AU  - Bornkamm, Georg W.
PY  - 2007
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/119
AB  - Deregulation of the proto-oncogene c-myc is a key event in the pathogenesis of many tumors. A paradigm is the activation of the c-myc gene by chromosomal translocations in Burkitt lymphoma (BL). Despite expression of a restricted set of Epstein-Barr viral (EBV) antigens, BL cells are not recognized by antigen-specific cytotoxic T cells (CTLs) because of their inability to process and present HLA class I-restricted antigens. In contrast, cells of EBV-driven posttransplant lymphoproliferative disease (PTLD) are recognized and rejected by EBV-specific CTLs. It is not known whether the poor immunogenicity of BL cells is due to nonexpression of viral antigens, overexpression of c-myc, or both. To understand the basis for immune recognition and escape, we have compared the mRNA expression profiles of BL and EBV-immortalized cells (as PTLD model). Among the genes expressed at low level in BL cells, we have identified many genes involved in the NF-kappa B and interferon response that play a pivotal role in antigen presentation and immune recognition. Using a cell line in which EBNA2 and c-myc can be regulated at will, we show that c-MYC negatively regulates STAT1, the central player linking the Type-I and Type-H interferon response. Switching off c-myc expression leads to STAT1 induction through a direct and indirect mechanism involving induction of Type-I interferons. c-MYC thus masks an interferon-inducing activity in these cells. Our findings imply that immune escape of tumor cells is not only a matter of in vivo selection but may be additionally promoted by activation of a cellular oncogene.
PB  - Wiley-Liss, Hoboken
T2  - International Journal of Cancer
T1  - c-MYC activation impairs the NF-kappa B and the interferon response: Implications for the pathogenesis of Burkitt's lymphoma
EP  - 1395
IS  - 7
SP  - 1387
VL  - 120
DO  - 10.1002/ijc.22372
ER  - 

@article{
author = "Schlee, Martin and Hoelzel, Michael and Bernard, Sandra and Mailhammer, Reinhard and Schuhmacher, Marino and Reschke, Judith and Eick, Dirk and Marinković, Dragan and Wirth, Thomas and Rosenwald, Andreas and Staudt, Louis M. and Eilers, Martin and Baran-Marszak, Fanny and Fagard, Remi and Feuillard, Jean and Laux, Gerhard and Bornkamm, Georg W.",
year = "2007",
abstract = "Deregulation of the proto-oncogene c-myc is a key event in the pathogenesis of many tumors. A paradigm is the activation of the c-myc gene by chromosomal translocations in Burkitt lymphoma (BL). Despite expression of a restricted set of Epstein-Barr viral (EBV) antigens, BL cells are not recognized by antigen-specific cytotoxic T cells (CTLs) because of their inability to process and present HLA class I-restricted antigens. In contrast, cells of EBV-driven posttransplant lymphoproliferative disease (PTLD) are recognized and rejected by EBV-specific CTLs. It is not known whether the poor immunogenicity of BL cells is due to nonexpression of viral antigens, overexpression of c-myc, or both. To understand the basis for immune recognition and escape, we have compared the mRNA expression profiles of BL and EBV-immortalized cells (as PTLD model). Among the genes expressed at low level in BL cells, we have identified many genes involved in the NF-kappa B and interferon response that play a pivotal role in antigen presentation and immune recognition. Using a cell line in which EBNA2 and c-myc can be regulated at will, we show that c-MYC negatively regulates STAT1, the central player linking the Type-I and Type-H interferon response. Switching off c-myc expression leads to STAT1 induction through a direct and indirect mechanism involving induction of Type-I interferons. c-MYC thus masks an interferon-inducing activity in these cells. Our findings imply that immune escape of tumor cells is not only a matter of in vivo selection but may be additionally promoted by activation of a cellular oncogene.",
publisher = "Wiley-Liss, Hoboken",
journal = "International Journal of Cancer",
title = "c-MYC activation impairs the NF-kappa B and the interferon response: Implications for the pathogenesis of Burkitt's lymphoma",
pages = "1395-1387",
number = "7",
volume = "120",
doi = "10.1002/ijc.22372"
}

Schlee, M., Hoelzel, M., Bernard, S., Mailhammer, R., Schuhmacher, M., Reschke, J., Eick, D., Marinković, D., Wirth, T., Rosenwald, A., Staudt, L. M., Eilers, M., Baran-Marszak, F., Fagard, R., Feuillard, J., Laux, G.,& Bornkamm, G. W.. (2007). c-MYC activation impairs the NF-kappa B and the interferon response: Implications for the pathogenesis of Burkitt's lymphoma. in International Journal of Cancer
Wiley-Liss, Hoboken., 120(7), 1387-1395.
https://doi.org/10.1002/ijc.22372

Schlee M, Hoelzel M, Bernard S, Mailhammer R, Schuhmacher M, Reschke J, Eick D, Marinković D, Wirth T, Rosenwald A, Staudt LM, Eilers M, Baran-Marszak F, Fagard R, Feuillard J, Laux G, Bornkamm GW. c-MYC activation impairs the NF-kappa B and the interferon response: Implications for the pathogenesis of Burkitt's lymphoma. in International Journal of Cancer. 2007;120(7):1387-1395.
doi:10.1002/ijc.22372 .

Schlee, Martin, Hoelzel, Michael, Bernard, Sandra, Mailhammer, Reinhard, Schuhmacher, Marino, Reschke, Judith, Eick, Dirk, Marinković, Dragan, Wirth, Thomas, Rosenwald, Andreas, Staudt, Louis M., Eilers, Martin, Baran-Marszak, Fanny, Fagard, Remi, Feuillard, Jean, Laux, Gerhard, Bornkamm, Georg W., "c-MYC activation impairs the NF-kappa B and the interferon response: Implications for the pathogenesis of Burkitt's lymphoma" in International Journal of Cancer, 120, no. 7 (2007):1387-1395,
https://doi.org/10.1002/ijc.22372 . .

TY  - JOUR
AU  - Samanta, DN
AU  - Palmetshofer, A
AU  - Marinković, Dragan
AU  - Wirth, Thomas
AU  - Serfling, E
AU  - Nitschke, L.
PY  - 2005
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/37
AB  - Marginal zone (MZ) B cells and peritoneal B-I cells provide a first defense system of thymus-independent Ab responses against foreign pathogens and therefore share a number of functional properties. Recently, development of B-1a cells was shown to be controlled by the transcription factor NFATc1. We show here that mice deficient for NFATc2 and c3 display a distinct lower representation of MZ B cells, which is correlated with a reduced capturing of trinitrophenyl-Ficoll. In contrast, mature follicular B cells from NFATc2/c3(-/-) mice are strongly increased in number. NFATc2/c3-/- B cells exhibit a marked increase in BCR-induced intracellular Ca(2+) mobilization and proliferation. However, trinitrophenyl-Ficoll-specific IgM and IgG3 responses of NFATc2/c3-deficient mice are intact, and chimeric mice reconstituted with NFATc2/3-deficient B cells show a normal number of MZ B cells and normal BCR responses. These observations suggest that the strongly elevated Th2 cytokine milieu in NFATc2/c3-deficient mice leads to a hyperactivation of mature, follicular B cells, whereas MZ B cells are less responsive to these signals.
PB  - Amer Assoc Immunologists, Bethesda
T2  - Journal of Immunology
T1  - B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice
EP  - 4802
IS  - 8
SP  - 4797
VL  - 174
DO  - 10.4049/jimmunol.174.8.4797
ER  - 

@article{
author = "Samanta, DN and Palmetshofer, A and Marinković, Dragan and Wirth, Thomas and Serfling, E and Nitschke, L.",
year = "2005",
abstract = "Marginal zone (MZ) B cells and peritoneal B-I cells provide a first defense system of thymus-independent Ab responses against foreign pathogens and therefore share a number of functional properties. Recently, development of B-1a cells was shown to be controlled by the transcription factor NFATc1. We show here that mice deficient for NFATc2 and c3 display a distinct lower representation of MZ B cells, which is correlated with a reduced capturing of trinitrophenyl-Ficoll. In contrast, mature follicular B cells from NFATc2/c3(-/-) mice are strongly increased in number. NFATc2/c3-/- B cells exhibit a marked increase in BCR-induced intracellular Ca(2+) mobilization and proliferation. However, trinitrophenyl-Ficoll-specific IgM and IgG3 responses of NFATc2/c3-deficient mice are intact, and chimeric mice reconstituted with NFATc2/3-deficient B cells show a normal number of MZ B cells and normal BCR responses. These observations suggest that the strongly elevated Th2 cytokine milieu in NFATc2/c3-deficient mice leads to a hyperactivation of mature, follicular B cells, whereas MZ B cells are less responsive to these signals.",
publisher = "Amer Assoc Immunologists, Bethesda",
journal = "Journal of Immunology",
title = "B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice",
pages = "4802-4797",
number = "8",
volume = "174",
doi = "10.4049/jimmunol.174.8.4797"
}

Samanta, D., Palmetshofer, A., Marinković, D., Wirth, T., Serfling, E.,& Nitschke, L.. (2005). B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice. in Journal of Immunology
Amer Assoc Immunologists, Bethesda., 174(8), 4797-4802.
https://doi.org/10.4049/jimmunol.174.8.4797

Samanta D, Palmetshofer A, Marinković D, Wirth T, Serfling E, Nitschke L. B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice. in Journal of Immunology. 2005;174(8):4797-4802.
doi:10.4049/jimmunol.174.8.4797 .

Samanta, DN, Palmetshofer, A, Marinković, Dragan, Wirth, Thomas, Serfling, E, Nitschke, L., "B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice" in Journal of Immunology, 174, no. 8 (2005):4797-4802,
https://doi.org/10.4049/jimmunol.174.8.4797 . .

TY  - JOUR
AU  - Marinković, Dragan
AU  - Marinković, Tatjana
AU  - Mahr, B
AU  - Hess, J
AU  - Wirth, Thomas
PY  - 2004
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/35
AB  - It is well documented that deregulation of MYC leads to tumor development, yet many aspects of this process are only partially understood. We have established a transgenic mouse model in which c-MYC is conditionally expressed in lymphoid cells using the tetracycline-regulated system of gene regulation. Mice with continuously expressed transgenic c-MYC died of invasive T- or B-cell lymphomas within 4 months. Lymphomas developing in transgenic mice were c-MYC dependent since doxycycline treatment led to tumor regression. Using transplantation of established tumor cell lines labeled with GFP, we followed the fate of neoplastic cells in recipients upon MYC inactivation. This approach allowed us to elucidate both apoptosis and differentiation as mechanisms of tumor elimination. Comparative genomic hybridization (CGH) and FISH analyses were performed in order to analyze possible chromosomal aberrations induced by c-MYC. We observed that overexpression of c-MYC is sufficient to induce recurrent patterns of genomic instability. The main observation was a gain of genomic material that corresponded to chromosome 15 in several T-cell tumors, which could be identified as trisomy.
PB  - Wiley, Hoboken
T2  - International Journal of Cancer
T1  - Reversible lymphomagenesis in conditionally c-MYC expressing mice
EP  - 342
IS  - 3
SP  - 336
VL  - 110
DO  - 10.1002/ijc.20099
ER  - 

@article{
author = "Marinković, Dragan and Marinković, Tatjana and Mahr, B and Hess, J and Wirth, Thomas",
year = "2004",
abstract = "It is well documented that deregulation of MYC leads to tumor development, yet many aspects of this process are only partially understood. We have established a transgenic mouse model in which c-MYC is conditionally expressed in lymphoid cells using the tetracycline-regulated system of gene regulation. Mice with continuously expressed transgenic c-MYC died of invasive T- or B-cell lymphomas within 4 months. Lymphomas developing in transgenic mice were c-MYC dependent since doxycycline treatment led to tumor regression. Using transplantation of established tumor cell lines labeled with GFP, we followed the fate of neoplastic cells in recipients upon MYC inactivation. This approach allowed us to elucidate both apoptosis and differentiation as mechanisms of tumor elimination. Comparative genomic hybridization (CGH) and FISH analyses were performed in order to analyze possible chromosomal aberrations induced by c-MYC. We observed that overexpression of c-MYC is sufficient to induce recurrent patterns of genomic instability. The main observation was a gain of genomic material that corresponded to chromosome 15 in several T-cell tumors, which could be identified as trisomy.",
publisher = "Wiley, Hoboken",
journal = "International Journal of Cancer",
title = "Reversible lymphomagenesis in conditionally c-MYC expressing mice",
pages = "342-336",
number = "3",
volume = "110",
doi = "10.1002/ijc.20099"
}

Marinković, D., Marinković, T., Mahr, B., Hess, J.,& Wirth, T.. (2004). Reversible lymphomagenesis in conditionally c-MYC expressing mice. in International Journal of Cancer
Wiley, Hoboken., 110(3), 336-342.
https://doi.org/10.1002/ijc.20099

Marinković D, Marinković T, Mahr B, Hess J, Wirth T. Reversible lymphomagenesis in conditionally c-MYC expressing mice. in International Journal of Cancer. 2004;110(3):336-342.
doi:10.1002/ijc.20099 .

Marinković, Dragan, Marinković, Tatjana, Mahr, B, Hess, J, Wirth, Thomas, "Reversible lymphomagenesis in conditionally c-MYC expressing mice" in International Journal of Cancer, 110, no. 3 (2004):336-342,
https://doi.org/10.1002/ijc.20099 . .

TY  - JOUR
AU  - Marinković, Dragan
AU  - Marinković, Tatjana
AU  - Kokai, Enikoe
AU  - Barth, T.
AU  - Moller, P.
AU  - Wirth, Thomas
PY  - 2004
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/33
AB  - The c-Myc transcription factor regulates a wide set of genes involved in processes such as proliferation, differentiation and apoptosis. Therefore, altered expression of Myc leads to deregulation of a large number of target genes and, as a consequence, to tumorigenesis. For understanding Myc-induced transformation, identification of these target genes is essential. In this study, we searched for Myc target genes involved in lymphomagenesis using different mouse T and B cell lymphoma cell lines transformed by a conditional Myc-allele. Target genes obtained by microarray experiments were further subjected to a kinetic analysis of mRNA expression upon Myc inactivation/reactivation, bioinformatic examination of Myc binding sites and chromatin immunoprecipitation. This approach allowed us to define targets whose activation is a direct consequence of Myc binding. Among the 38 novel Myc targets, we identified several genes implicated in the tumor development. These genes are not only relevant for mouse lymphomas because we observed their upregulation in human lymphomas as well. Our findings further the understanding of Myc-induced lymphomagenesis and help toward developing more efficient antitumor strategies.
PB  - Oxford Univ Press, Oxford
T2  - Nucleic Acids Research
T1  - Identification of novel Myc target genes with a potential role in lymphomagenesis
EP  - 5378
IS  - 18
SP  - 5368
VL  - 32
DO  - 10.1093/nar/gkh877
ER  - 

@article{
author = "Marinković, Dragan and Marinković, Tatjana and Kokai, Enikoe and Barth, T. and Moller, P. and Wirth, Thomas",
year = "2004",
abstract = "The c-Myc transcription factor regulates a wide set of genes involved in processes such as proliferation, differentiation and apoptosis. Therefore, altered expression of Myc leads to deregulation of a large number of target genes and, as a consequence, to tumorigenesis. For understanding Myc-induced transformation, identification of these target genes is essential. In this study, we searched for Myc target genes involved in lymphomagenesis using different mouse T and B cell lymphoma cell lines transformed by a conditional Myc-allele. Target genes obtained by microarray experiments were further subjected to a kinetic analysis of mRNA expression upon Myc inactivation/reactivation, bioinformatic examination of Myc binding sites and chromatin immunoprecipitation. This approach allowed us to define targets whose activation is a direct consequence of Myc binding. Among the 38 novel Myc targets, we identified several genes implicated in the tumor development. These genes are not only relevant for mouse lymphomas because we observed their upregulation in human lymphomas as well. Our findings further the understanding of Myc-induced lymphomagenesis and help toward developing more efficient antitumor strategies.",
publisher = "Oxford Univ Press, Oxford",
journal = "Nucleic Acids Research",
title = "Identification of novel Myc target genes with a potential role in lymphomagenesis",
pages = "5378-5368",
number = "18",
volume = "32",
doi = "10.1093/nar/gkh877"
}

Marinković, D., Marinković, T., Kokai, E., Barth, T., Moller, P.,& Wirth, T.. (2004). Identification of novel Myc target genes with a potential role in lymphomagenesis. in Nucleic Acids Research
Oxford Univ Press, Oxford., 32(18), 5368-5378.
https://doi.org/10.1093/nar/gkh877

Marinković D, Marinković T, Kokai E, Barth T, Moller P, Wirth T. Identification of novel Myc target genes with a potential role in lymphomagenesis. in Nucleic Acids Research. 2004;32(18):5368-5378.
doi:10.1093/nar/gkh877 .

Marinković, Dragan, Marinković, Tatjana, Kokai, Enikoe, Barth, T., Moller, P., Wirth, Thomas, "Identification of novel Myc target genes with a potential role in lymphomagenesis" in Nucleic Acids Research, 32, no. 18 (2004):5368-5378,
https://doi.org/10.1093/nar/gkh877 . .

TY  - CONF
AU  - Samanta, Depriya
AU  - Marinković, Dragan
AU  - Palmetshofer, Alois
AU  - Wirth, Thomas
AU  - Nitschke, Lars
AU  - Serfling, Edgar
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/1461
C3  - Book of abstracts
T1  - Deficiency of NFATc2+c3 impairs generation of marginal zone B cell compartment
EP  - 1068
UR  - https://hdl.handle.net/21.15107/rcub_rfasper_1461
ER  - 

@conference{
author = "Samanta, Depriya and Marinković, Dragan and Palmetshofer, Alois and Wirth, Thomas and Nitschke, Lars and Serfling, Edgar",
year = "2003",
journal = "Book of abstracts",
title = "Deficiency of NFATc2+c3 impairs generation of marginal zone B cell compartment",
pages = "1068",
url = "https://hdl.handle.net/21.15107/rcub_rfasper_1461"
}

Samanta, D., Marinković, D., Palmetshofer, A., Wirth, T., Nitschke, L.,& Serfling, E.. (2003). Deficiency of NFATc2+c3 impairs generation of marginal zone B cell compartment. in Book of abstracts.
https://hdl.handle.net/21.15107/rcub_rfasper_1461

Samanta D, Marinković D, Palmetshofer A, Wirth T, Nitschke L, Serfling E. Deficiency of NFATc2+c3 impairs generation of marginal zone B cell compartment. in Book of abstracts. 2003;:null-1068.
https://hdl.handle.net/21.15107/rcub_rfasper_1461 .

Samanta, Depriya, Marinković, Dragan, Palmetshofer, Alois, Wirth, Thomas, Nitschke, Lars, Serfling, Edgar, "Deficiency of NFATc2+c3 impairs generation of marginal zone B cell compartment" in Book of abstracts (2003),
https://hdl.handle.net/21.15107/rcub_rfasper_1461 .

TY  - CONF
AU  - Marinković, Dragan
AU  - Samardžić, Tatjana
AU  - Betina, Schreiner
AU  - Hess, Jochen
AU  - Hameister, Harold
AU  - Wirth, Thomas
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/1459
C3  - Book of abstracts
T1  - Analysis of genomic instability in lymphomas induced by conditional Myc expression
EP  - 109
UR  - https://hdl.handle.net/21.15107/rcub_rfasper_1459
ER  - 

@conference{
author = "Marinković, Dragan and Samardžić, Tatjana and Betina, Schreiner and Hess, Jochen and Hameister, Harold and Wirth, Thomas",
year = "2003",
journal = "Book of abstracts",
title = "Analysis of genomic instability in lymphomas induced by conditional Myc expression",
pages = "109",
url = "https://hdl.handle.net/21.15107/rcub_rfasper_1459"
}

Marinković, D., Samardžić, T., Betina, S., Hess, J., Hameister, H.,& Wirth, T.. (2003). Analysis of genomic instability in lymphomas induced by conditional Myc expression. in Book of abstracts.
https://hdl.handle.net/21.15107/rcub_rfasper_1459

Marinković D, Samardžić T, Betina S, Hess J, Hameister H, Wirth T. Analysis of genomic instability in lymphomas induced by conditional Myc expression. in Book of abstracts. 2003;:null-109.
https://hdl.handle.net/21.15107/rcub_rfasper_1459 .

Marinković, Dragan, Samardžić, Tatjana, Betina, Schreiner, Hess, Jochen, Hameister, Harold, Wirth, Thomas, "Analysis of genomic instability in lymphomas induced by conditional Myc expression" in Book of abstracts (2003),
https://hdl.handle.net/21.15107/rcub_rfasper_1459 .

TY  - CONF
AU  - Samardžić, Tatjana
AU  - Marinković, Dragan
AU  - Nielsen, Peter
AU  - Nitschke, Lars
AU  - Wirth, Thomas
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/1450
C3  - Book of abstracts
T1  - BOB.1/OBF.1 deficiency leads to reduction of the marginal zone B cell compartment
EP  - 107
UR  - https://hdl.handle.net/21.15107/rcub_rfasper_1450
ER  - 

@conference{
author = "Samardžić, Tatjana and Marinković, Dragan and Nielsen, Peter and Nitschke, Lars and Wirth, Thomas",
year = "2003",
journal = "Book of abstracts",
title = "BOB.1/OBF.1 deficiency leads to reduction of the marginal zone B cell compartment",
pages = "107",
url = "https://hdl.handle.net/21.15107/rcub_rfasper_1450"
}

Samardžić, T., Marinković, D., Nielsen, P., Nitschke, L.,& Wirth, T.. (2003). BOB.1/OBF.1 deficiency leads to reduction of the marginal zone B cell compartment. in Book of abstracts.
https://hdl.handle.net/21.15107/rcub_rfasper_1450

Samardžić T, Marinković D, Nielsen P, Nitschke L, Wirth T. BOB.1/OBF.1 deficiency leads to reduction of the marginal zone B cell compartment. in Book of abstracts. 2003;:null-107.
https://hdl.handle.net/21.15107/rcub_rfasper_1450 .

Samardžić, Tatjana, Marinković, Dragan, Nielsen, Peter, Nitschke, Lars, Wirth, Thomas, "BOB.1/OBF.1 deficiency leads to reduction of the marginal zone B cell compartment" in Book of abstracts (2003),
https://hdl.handle.net/21.15107/rcub_rfasper_1450 .

TY  - JOUR
AU  - Amano, H.
AU  - Amano, E.
AU  - Moll, T.
AU  - Marinković, Dragan
AU  - Ibnou-Zekri, N
AU  - Martinez-Soria, E.
AU  - Semac, I
AU  - Wirth, Thomas
AU  - Nitschke, L.
AU  - Izui, S
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/32
AB  - The accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of an as yet unidentified mutant gene, Yaa (Y-linked autoimmune acceleration). In view of a possible role of marginal zone (MZ) B cells in murine SLE, we have explored whether the expression of the Yaa mutation affects the differentiation of MZ and follicular B cells, thereby implicating the acceleration of the disease. In this study, we show that both BXSB and C57BL/6 Yaa mice, including two different substrains of BXSB Yaa males that are protected from SLE, displayed an impaired development of MZ B cells early in life. Studies in bone marrow chimeras revealed that the loss of MZ B cells resulted from a defect intrinsic to B cells expressing the Yaa mutation. The lack of selective expansion of MZ B cells in diseased BXSB Yaa males strongly argues against a major role of MZ B cells in the generation of pathogenic autoantibodies in the BXSB model of SLE. Furthermore, a comparative analysis with mice deficient in CD22 or expressing an IgM anti-trinitrophenyl/DNA transgene suggests that the hyperreactive phenotype of Yaa B cells, as judged by a markedly increased spontaneous IgM secretion, is likely to contribute to the enhanced maturation toward follicular B cells and the block in the MZ B cell generation.
PB  - Amer Assoc Immunologists, Bethesda
T2  - Journal of Immunology
T1  - The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells
EP  - 2301
IS  - 5
SP  - 2293
VL  - 170
DO  - 10.4049/jimmunol.170.5.2293
ER  - 

@article{
author = "Amano, H. and Amano, E. and Moll, T. and Marinković, Dragan and Ibnou-Zekri, N and Martinez-Soria, E. and Semac, I and Wirth, Thomas and Nitschke, L. and Izui, S",
year = "2003",
abstract = "The accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of an as yet unidentified mutant gene, Yaa (Y-linked autoimmune acceleration). In view of a possible role of marginal zone (MZ) B cells in murine SLE, we have explored whether the expression of the Yaa mutation affects the differentiation of MZ and follicular B cells, thereby implicating the acceleration of the disease. In this study, we show that both BXSB and C57BL/6 Yaa mice, including two different substrains of BXSB Yaa males that are protected from SLE, displayed an impaired development of MZ B cells early in life. Studies in bone marrow chimeras revealed that the loss of MZ B cells resulted from a defect intrinsic to B cells expressing the Yaa mutation. The lack of selective expansion of MZ B cells in diseased BXSB Yaa males strongly argues against a major role of MZ B cells in the generation of pathogenic autoantibodies in the BXSB model of SLE. Furthermore, a comparative analysis with mice deficient in CD22 or expressing an IgM anti-trinitrophenyl/DNA transgene suggests that the hyperreactive phenotype of Yaa B cells, as judged by a markedly increased spontaneous IgM secretion, is likely to contribute to the enhanced maturation toward follicular B cells and the block in the MZ B cell generation.",
publisher = "Amer Assoc Immunologists, Bethesda",
journal = "Journal of Immunology",
title = "The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells",
pages = "2301-2293",
number = "5",
volume = "170",
doi = "10.4049/jimmunol.170.5.2293"
}

Amano, H., Amano, E., Moll, T., Marinković, D., Ibnou-Zekri, N., Martinez-Soria, E., Semac, I., Wirth, T., Nitschke, L.,& Izui, S.. (2003). The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells. in Journal of Immunology
Amer Assoc Immunologists, Bethesda., 170(5), 2293-2301.
https://doi.org/10.4049/jimmunol.170.5.2293

Amano H, Amano E, Moll T, Marinković D, Ibnou-Zekri N, Martinez-Soria E, Semac I, Wirth T, Nitschke L, Izui S. The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells. in Journal of Immunology. 2003;170(5):2293-2301.
doi:10.4049/jimmunol.170.5.2293 .

Amano, H., Amano, E., Moll, T., Marinković, Dragan, Ibnou-Zekri, N, Martinez-Soria, E., Semac, I, Wirth, Thomas, Nitschke, L., Izui, S, "The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells" in Journal of Immunology, 170, no. 5 (2003):2293-2301,
https://doi.org/10.4049/jimmunol.170.5.2293 . .

TY  - JOUR
AU  - Brunner, C
AU  - Marinković, Dragan
AU  - Klein, J
AU  - Samardžić, T.
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/31
AB  - Mice deficient for the transcriptional coactivator BOB.1/OBF.1 show several defects in B cell differentiation. Numbers of immature transitional B cells in the bone marrow are reduced and fewer B cells reach the periphery. Furthermore, germinal center B cells are absent and marginal zone (MZ) B lymphocytes are markedly reduced. Increased levels of B cell apoptosis in these mice prompted us to analyze expression and function of antiapoptotic proteins. Bcl2 expression is strongly reduced in BOB.1/OBF.1-deficient pre-B cells. When BOB.1/OBF.1-deficient mice were crossed with Bcl2-transgenic mice, B cell development in the bone marrow and numbers of B cells in peripheral lymphoid organs were normalized. However, neither germinal center B cells nor MZ B cells were rescued. Additionally, Bcl2 did not rescue the defects in signaling and affinity maturation found in BOB.1/OBF.1-deficient mice. Interestingly, Bcl2-transgenic mice by themselves show an MZ B cell defect. Virtually no functional MZ B cells were detected in these mice. In contrast, mice deficient for Bcl2 show a relative increase in MZ B cell numbers, indicating a previously undetected function of Bcl2 for this B cell compartment.
PB  - Rockefeller Univ Press, New York
T2  - Journal of Experimental Medicine
T1  - B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice
EP  - 1211
IS  - 9
SP  - 1205
VL  - 197
DO  - 10.1084/jem.20022014
ER  - 

@article{
author = "Brunner, C and Marinković, Dragan and Klein, J and Samardžić, T. and Nitschke, L. and Wirth, Thomas",
year = "2003",
abstract = "Mice deficient for the transcriptional coactivator BOB.1/OBF.1 show several defects in B cell differentiation. Numbers of immature transitional B cells in the bone marrow are reduced and fewer B cells reach the periphery. Furthermore, germinal center B cells are absent and marginal zone (MZ) B lymphocytes are markedly reduced. Increased levels of B cell apoptosis in these mice prompted us to analyze expression and function of antiapoptotic proteins. Bcl2 expression is strongly reduced in BOB.1/OBF.1-deficient pre-B cells. When BOB.1/OBF.1-deficient mice were crossed with Bcl2-transgenic mice, B cell development in the bone marrow and numbers of B cells in peripheral lymphoid organs were normalized. However, neither germinal center B cells nor MZ B cells were rescued. Additionally, Bcl2 did not rescue the defects in signaling and affinity maturation found in BOB.1/OBF.1-deficient mice. Interestingly, Bcl2-transgenic mice by themselves show an MZ B cell defect. Virtually no functional MZ B cells were detected in these mice. In contrast, mice deficient for Bcl2 show a relative increase in MZ B cell numbers, indicating a previously undetected function of Bcl2 for this B cell compartment.",
publisher = "Rockefeller Univ Press, New York",
journal = "Journal of Experimental Medicine",
title = "B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice",
pages = "1211-1205",
number = "9",
volume = "197",
doi = "10.1084/jem.20022014"
}

Brunner, C., Marinković, D., Klein, J., Samardžić, T., Nitschke, L.,& Wirth, T.. (2003). B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice. in Journal of Experimental Medicine
Rockefeller Univ Press, New York., 197(9), 1205-1211.
https://doi.org/10.1084/jem.20022014

Brunner C, Marinković D, Klein J, Samardžić T, Nitschke L, Wirth T. B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice. in Journal of Experimental Medicine. 2003;197(9):1205-1211.
doi:10.1084/jem.20022014 .

Brunner, C, Marinković, Dragan, Klein, J, Samardžić, T., Nitschke, L., Wirth, Thomas, "B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice" in Journal of Experimental Medicine, 197, no. 9 (2003):1205-1211,
https://doi.org/10.1084/jem.20022014 . .

TY  - JOUR
AU  - Samardžić, T.
AU  - Marinković, Dragan
AU  - Danzer, CP
AU  - Gerlach, J
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/30
AB  - CD22 is a B cell-specific member of the immunoglobulin superfamily and binds to sialic acid. CD22 inhibits B cell receptor signaling. Mice deficient for CD22 show a largely normal B cell development. Here, we have performed a detailed analysis of the splenic B cell population and found that the subset of marginal zone (MZ) B cells was selectively reduced in CD22-deficient mice. CD22-deficient mice showed a lack of TNP-ficoll capturing cells in the MZ and a reduced response to TNP-ficoll, particularly when the antigen was applied intravenously. CD22-deficient B cells showed both enhanced motility as well as enhanced chemotaxis to certain chemokines. The altered chemokine responsiveness or the higher signaling capacity of CD22-deficient B cells may lead to the compromised MZ B cell compartment, as both processes have previously been shown to affect MZ composition.
PB  - Wiley-V C H Verlag Gmbh, Weinheim
T2  - European Journal of Immunology
T1  - Reduction of marginal zone B cells in CD22-deficient mice
EP  - 567
IS  - 2
SP  - 561
VL  - 32
DO  - 10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H
ER  - 

@article{
author = "Samardžić, T. and Marinković, Dragan and Danzer, CP and Gerlach, J and Nitschke, L. and Wirth, Thomas",
year = "2002",
abstract = "CD22 is a B cell-specific member of the immunoglobulin superfamily and binds to sialic acid. CD22 inhibits B cell receptor signaling. Mice deficient for CD22 show a largely normal B cell development. Here, we have performed a detailed analysis of the splenic B cell population and found that the subset of marginal zone (MZ) B cells was selectively reduced in CD22-deficient mice. CD22-deficient mice showed a lack of TNP-ficoll capturing cells in the MZ and a reduced response to TNP-ficoll, particularly when the antigen was applied intravenously. CD22-deficient B cells showed both enhanced motility as well as enhanced chemotaxis to certain chemokines. The altered chemokine responsiveness or the higher signaling capacity of CD22-deficient B cells may lead to the compromised MZ B cell compartment, as both processes have previously been shown to affect MZ composition.",
publisher = "Wiley-V C H Verlag Gmbh, Weinheim",
journal = "European Journal of Immunology",
title = "Reduction of marginal zone B cells in CD22-deficient mice",
pages = "567-561",
number = "2",
volume = "32",
doi = "10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H"
}

Samardžić, T., Marinković, D., Danzer, C., Gerlach, J., Nitschke, L.,& Wirth, T.. (2002). Reduction of marginal zone B cells in CD22-deficient mice. in European Journal of Immunology
Wiley-V C H Verlag Gmbh, Weinheim., 32(2), 561-567.
https://doi.org/10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H

Samardžić T, Marinković D, Danzer C, Gerlach J, Nitschke L, Wirth T. Reduction of marginal zone B cells in CD22-deficient mice. in European Journal of Immunology. 2002;32(2):561-567.
doi:10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H .

Samardžić, T., Marinković, Dragan, Danzer, CP, Gerlach, J, Nitschke, L., Wirth, Thomas, "Reduction of marginal zone B cells in CD22-deficient mice" in European Journal of Immunology, 32, no. 2 (2002):561-567,
https://doi.org/10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H . .

TY  - CONF
AU  - Samardžić, Tatjana
AU  - Marinković, Dragan
AU  - Nielsen, Peter
AU  - Nitschke, Lars
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/1406
C3  - Book of abstracts
T1  - Role of the B cell specific co-activator BOB.1/OBF.1 in regulating BCR-signaling and development of peripheral B cell populations
EP  - 37
UR  - https://hdl.handle.net/21.15107/rcub_rfasper_1406
ER  - 

@conference{
author = "Samardžić, Tatjana and Marinković, Dragan and Nielsen, Peter and Nitschke, Lars and Wirth, Thomas",
year = "2002",
journal = "Book of abstracts",
title = "Role of the B cell specific co-activator BOB.1/OBF.1 in regulating BCR-signaling and development of peripheral B cell populations",
pages = "37",
url = "https://hdl.handle.net/21.15107/rcub_rfasper_1406"
}

Samardžić, T., Marinković, D., Nielsen, P., Nitschke, L.,& Wirth, T.. (2002). Role of the B cell specific co-activator BOB.1/OBF.1 in regulating BCR-signaling and development of peripheral B cell populations. in Book of abstracts.
https://hdl.handle.net/21.15107/rcub_rfasper_1406

Samardžić T, Marinković D, Nielsen P, Nitschke L, Wirth T. Role of the B cell specific co-activator BOB.1/OBF.1 in regulating BCR-signaling and development of peripheral B cell populations. in Book of abstracts. 2002;:null-37.
https://hdl.handle.net/21.15107/rcub_rfasper_1406 .

Samardžić, Tatjana, Marinković, Dragan, Nielsen, Peter, Nitschke, Lars, Wirth, Thomas, "Role of the B cell specific co-activator BOB.1/OBF.1 in regulating BCR-signaling and development of peripheral B cell populations" in Book of abstracts (2002),
https://hdl.handle.net/21.15107/rcub_rfasper_1406 .

TY  - CONF
AU  - Samardžić, Tatjana
AU  - Marinković, Dragan
AU  - Nielsen, Peter
AU  - Nitschke, Lars
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/1404
C3  - Book of abstracts
T1  - BOB.1/OBF.1 deficient mice show a dramatically reduced Marginal Zone B cell compartment
EP  - 23
UR  - https://hdl.handle.net/21.15107/rcub_rfasper_1404
ER  - 

@conference{
author = "Samardžić, Tatjana and Marinković, Dragan and Nielsen, Peter and Nitschke, Lars and Wirth, Thomas",
year = "2002",
journal = "Book of abstracts",
title = "BOB.1/OBF.1 deficient mice show a dramatically reduced Marginal Zone B cell compartment",
pages = "23",
url = "https://hdl.handle.net/21.15107/rcub_rfasper_1404"
}

Samardžić, T., Marinković, D., Nielsen, P., Nitschke, L.,& Wirth, T.. (2002). BOB.1/OBF.1 deficient mice show a dramatically reduced Marginal Zone B cell compartment. in Book of abstracts.
https://hdl.handle.net/21.15107/rcub_rfasper_1404

Samardžić T, Marinković D, Nielsen P, Nitschke L, Wirth T. BOB.1/OBF.1 deficient mice show a dramatically reduced Marginal Zone B cell compartment. in Book of abstracts. 2002;:null-23.
https://hdl.handle.net/21.15107/rcub_rfasper_1404 .

Samardžić, Tatjana, Marinković, Dragan, Nielsen, Peter, Nitschke, Lars, Wirth, Thomas, "BOB.1/OBF.1 deficient mice show a dramatically reduced Marginal Zone B cell compartment" in Book of abstracts (2002),
https://hdl.handle.net/21.15107/rcub_rfasper_1404 .

TY  - CONF
AU  - Marinković, Dragan
AU  - Samardžić, Tatjana
AU  - Shreiner, Bettina
AU  - Hess, Jochen
AU  - Hameister, Harold
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/1402
T1  - Analysis of genomic instability in lymphomas induced by conditional Myc expression
EP  - 132
UR  - https://hdl.handle.net/21.15107/rcub_rfasper_1402
ER  - 

@conference{
author = "Marinković, Dragan and Samardžić, Tatjana and Shreiner, Bettina and Hess, Jochen and Hameister, Harold and Wirth, Thomas",
year = "2002",
title = "Analysis of genomic instability in lymphomas induced by conditional Myc expression",
pages = "132",
url = "https://hdl.handle.net/21.15107/rcub_rfasper_1402"
}

Marinković, D., Samardžić, T., Shreiner, B., Hess, J., Hameister, H.,& Wirth, T.. (2002). Analysis of genomic instability in lymphomas induced by conditional Myc expression. .
https://hdl.handle.net/21.15107/rcub_rfasper_1402

Marinković D, Samardžić T, Shreiner B, Hess J, Hameister H, Wirth T. Analysis of genomic instability in lymphomas induced by conditional Myc expression. 2002;:null-132.
https://hdl.handle.net/21.15107/rcub_rfasper_1402 .

Marinković, Dragan, Samardžić, Tatjana, Shreiner, Bettina, Hess, Jochen, Hameister, Harold, Wirth, Thomas, "Analysis of genomic instability in lymphomas induced by conditional Myc expression" (2002),
https://hdl.handle.net/21.15107/rcub_rfasper_1402 .

TY  - JOUR
AU  - Samardžić, T.
AU  - Gerlach, J
AU  - Muller, K
AU  - Marinković, Dragan
AU  - Hess, J
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/29
AB  - BOB.1/OBF1 (also called OCA-B), a B lymphocyte-specific transcriptional coactivator, is recruited to octamer-containing promoters by interacting with the Oct-1 or Oct-2 proteins. BOB.1/OBF.1-deficient mice show impaired secondary immunoglobulin isotype secretion and complete absence of germinal centers. Furthermore, numbers of splenic B cells are reduced due to a developmental block at the transitional B cell stage in the bone marrow. We found that surface expression of CD22 is selectively increased on B lineage cells in the bone marrow of BOB.1/OBF.1-deficient mice. CD22 is known as a negative regulator of B cell receptor signaling. We therefore investigated whether defects in B cell development in the BOB.1/OBF1-deficient mice might be due to CD22 up-regulation. Mice were generated lacking both genes. In BOB.1/OBF.1 xCD22 double-deficient mice, numbers of transitional B cells in the bone marrow were normal. Consequently, double-deficient mice also had normal B to T cell ratios in the spleen. We show that BOB.1/OBF.1(-/-) B cells were incapable to induce BCR-triggered Ca2+ mobilization. This Ca2+-signalling defect was restored in BOBA/ OBF1 xCD22 double-deficient B cells. Nevertheless, double-deficient animals were unable to mount humoral immune responses and to form germinal centers. Finally, we demonstrate that CD22(-/-) splenic B cells proliferate independently of BOB.1/OBF1 upon stimulation with LPS. These studies suggest that the B cell differentiation defect observed in BOB.1/OBF.1(-/-) mice is BCR-signal dependent. However, the impairment in germinal center formation is caused by a different mechanism.
PB  - Wiley-V C H Verlag Gmbh, Weinheim
T2  - European Journal of Immunology
T1  - CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice
EP  - 2489
IS  - 9
SP  - 2481
VL  - 32
DO  - 10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C
ER  - 

@article{
author = "Samardžić, T. and Gerlach, J and Muller, K and Marinković, Dragan and Hess, J and Nitschke, L. and Wirth, Thomas",
year = "2002",
abstract = "BOB.1/OBF1 (also called OCA-B), a B lymphocyte-specific transcriptional coactivator, is recruited to octamer-containing promoters by interacting with the Oct-1 or Oct-2 proteins. BOB.1/OBF.1-deficient mice show impaired secondary immunoglobulin isotype secretion and complete absence of germinal centers. Furthermore, numbers of splenic B cells are reduced due to a developmental block at the transitional B cell stage in the bone marrow. We found that surface expression of CD22 is selectively increased on B lineage cells in the bone marrow of BOB.1/OBF.1-deficient mice. CD22 is known as a negative regulator of B cell receptor signaling. We therefore investigated whether defects in B cell development in the BOB.1/OBF1-deficient mice might be due to CD22 up-regulation. Mice were generated lacking both genes. In BOB.1/OBF.1 xCD22 double-deficient mice, numbers of transitional B cells in the bone marrow were normal. Consequently, double-deficient mice also had normal B to T cell ratios in the spleen. We show that BOB.1/OBF.1(-/-) B cells were incapable to induce BCR-triggered Ca2+ mobilization. This Ca2+-signalling defect was restored in BOBA/ OBF1 xCD22 double-deficient B cells. Nevertheless, double-deficient animals were unable to mount humoral immune responses and to form germinal centers. Finally, we demonstrate that CD22(-/-) splenic B cells proliferate independently of BOB.1/OBF1 upon stimulation with LPS. These studies suggest that the B cell differentiation defect observed in BOB.1/OBF.1(-/-) mice is BCR-signal dependent. However, the impairment in germinal center formation is caused by a different mechanism.",
publisher = "Wiley-V C H Verlag Gmbh, Weinheim",
journal = "European Journal of Immunology",
title = "CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice",
pages = "2489-2481",
number = "9",
volume = "32",
doi = "10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C"
}

Samardžić, T., Gerlach, J., Muller, K., Marinković, D., Hess, J., Nitschke, L.,& Wirth, T.. (2002). CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. in European Journal of Immunology
Wiley-V C H Verlag Gmbh, Weinheim., 32(9), 2481-2489.
https://doi.org/10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C

Samardžić T, Gerlach J, Muller K, Marinković D, Hess J, Nitschke L, Wirth T. CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. in European Journal of Immunology. 2002;32(9):2481-2489.
doi:10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C .

Samardžić, T., Gerlach, J, Muller, K, Marinković, Dragan, Hess, J, Nitschke, L., Wirth, Thomas, "CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice" in European Journal of Immunology, 32, no. 9 (2002):2481-2489,
https://doi.org/10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C . .

TY  - JOUR
AU  - Samardžić, T.
AU  - Marinković, Dragan
AU  - Nielsen, P.J.
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/28
AB  - Marginal-zone (MZ) B cells represent a first line of defense against particulate blood-borne antigens. Together with the B1 cells, they are responsible for the early response against type It T-independent antigens. The molecular pathways controlling the development of MZ B cells are only poorly understood. We found that these cells are virtually absent in mice deficient in the BOB.1/OBF.1 coactivator. Loss of these B cells was demonstrated by the lack. of cells showing the appropriate cell surface phenotype but also by histological analyses and tri-nitro-phenol-Ficoll capturing. The lack of these cells is a B-cell-intrinsic defect, as shown by bone marrow complementation experiments. We also show that the expression of BOB.1/OBF.1 in peripheral B cells is required for the development of MZ B lymphocytes. Our analysis of BOB.1/OBF.1-deficient splenic B cells reveals alterations in cell motility, tumor necrosis factor receptor expression, and B-cell receptor (BCR) signaling. These changes could contribute to the loss of MZ B lymphocytes by altering the maturation of the cells. Interestingly, development of and BCR signaling in B1 B cells are completely normal in BOB.1/OBF.1 mutant mice.
PB  - Amer Soc Microbiology, Washington
T2  - Molecular and Cellular Biology
T1  - BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment
EP  - 8331
IS  - 23
SP  - 8320
VL  - 22
DO  - 10.1128/MCB.22.23.8320-8331.2002
ER  - 

@article{
author = "Samardžić, T. and Marinković, Dragan and Nielsen, P.J. and Nitschke, L. and Wirth, Thomas",
year = "2002",
abstract = "Marginal-zone (MZ) B cells represent a first line of defense against particulate blood-borne antigens. Together with the B1 cells, they are responsible for the early response against type It T-independent antigens. The molecular pathways controlling the development of MZ B cells are only poorly understood. We found that these cells are virtually absent in mice deficient in the BOB.1/OBF.1 coactivator. Loss of these B cells was demonstrated by the lack. of cells showing the appropriate cell surface phenotype but also by histological analyses and tri-nitro-phenol-Ficoll capturing. The lack of these cells is a B-cell-intrinsic defect, as shown by bone marrow complementation experiments. We also show that the expression of BOB.1/OBF.1 in peripheral B cells is required for the development of MZ B lymphocytes. Our analysis of BOB.1/OBF.1-deficient splenic B cells reveals alterations in cell motility, tumor necrosis factor receptor expression, and B-cell receptor (BCR) signaling. These changes could contribute to the loss of MZ B lymphocytes by altering the maturation of the cells. Interestingly, development of and BCR signaling in B1 B cells are completely normal in BOB.1/OBF.1 mutant mice.",
publisher = "Amer Soc Microbiology, Washington",
journal = "Molecular and Cellular Biology",
title = "BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment",
pages = "8331-8320",
number = "23",
volume = "22",
doi = "10.1128/MCB.22.23.8320-8331.2002"
}

Samardžić, T., Marinković, D., Nielsen, P.J., Nitschke, L.,& Wirth, T.. (2002). BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment. in Molecular and Cellular Biology
Amer Soc Microbiology, Washington., 22(23), 8320-8331.
https://doi.org/10.1128/MCB.22.23.8320-8331.2002

Samardžić T, Marinković D, Nielsen P, Nitschke L, Wirth T. BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment. in Molecular and Cellular Biology. 2002;22(23):8320-8331.
doi:10.1128/MCB.22.23.8320-8331.2002 .

Samardžić, T., Marinković, Dragan, Nielsen, P.J., Nitschke, L., Wirth, Thomas, "BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment" in Molecular and Cellular Biology, 22, no. 23 (2002):8320-8331,
https://doi.org/10.1128/MCB.22.23.8320-8331.2002 . .