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1. NFKBIE mutations are selected by the tumor microenvironment and contribute to immune escape in chronic lymphocytic leukemia

Author

Bonato, Alice, Chakraborty, Supriya, Bomben, Riccardo, Canarutto, Giulia, Felician, Giulia, Martines, Claudio, Zucchetto, Antonella, Pozzo, Federico, Vujovikj, Marija, Polesel, Jerry, Chiarenza, Annalisa, Del Principe, Maria Ilaria, Del Poeta, Giovanni, D’Arena, Giovanni, Marasca, Roberto, Tafuri, Agostino, Laurenti, Luca, Piazza, Silvano, Dimovski, Aleksandar J., Gattei, Valter, and Efremov, Dimitar G.

Published
2024
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6. Constitutive IP3 signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP3 receptor disruptor BIRD-2

Author

Bittremieux, Mart, La Rovere, Rita M., Akl, Haidar, Martines, Claudio, Welkenhuyzen, Kirsten, Dubron, Kathia, Baes, Myriam, Janssens, Ann, Vandenberghe, Peter, Laurenti, Luca, Rietdorf, Katja, Morciano, Giampaolo, Pinton, Paolo, Mikoshiba, Katsuhiko, Bootman, Martin D., Efremov, Dimitar G., De Smedt, Humbert, Parys, Jan B., and Bultynck, Geert

Published
2019
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8. Chronic Lymphocytic Leukemia Cells with Mutated Nfkbie Are Positively Selected By Microenvironmental Signals and Display Reduced Sensitivity to Ibrutinib Treatment

Author

Bonato, Alice, primary, Bomben, Riccardo, additional, Chakraborty, Supriya, additional, Felician, Giulia, additional, Martines, Claudio, additional, Zucchetto, Antonella, additional, Chiarenza, Annalisa, additional, Del Poeta, Giovanni, additional, Marasca, Roberto, additional, Tafuri, Agostino, additional, Laurenti, Luca, additional, Dimovski, Aleksandar J., additional, Gattei, Valter, additional, and Efremov, Dimitar G, additional

Published
2021
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9. CLL-358: Adaptation of Chronic Lymphocytic Leukemia to Ibrutinib Is Mediated by Epigenetic Plasticity of Residual Disease and Bypass Signaling via the MAPK Pathway

Author

Bergamo, Lodovico Terzi di, primary, Forestieri, Gabriela, additional, Loh, Jui Wan, additional, Singh, Amartya, additional, Spina, Valeria, additional, Zucchetto, Antonella, additional, Condoluci, Adalgisa, additional, Faderl, Martin, additional, Koch, Ricardo, additional, Bruscaggin, Alessio, additional, Pini, Katia, additional, Wu, Wei, additional, Piffaretti, Deborah, additional, Bittolo, Tamara, additional, Tissino, Erika, additional, De Paoli, Lorenzo, additional, Deambrogi, Clara, additional, Frustaci, Anna Maria, additional, Autore, Francesco, additional, Merli, Michele, additional, Scarfò, Lydia, additional, Rasi, Silvia, additional, Passweg, Jakob, additional, Moia, Riccardo, additional, Martines, Claudio, additional, Ghia, Paolo, additional, Cavalli, Franco, additional, Zucca, Emanuele, additional, Gerber, Bernhard, additional, Gillessen, Silke, additional, Stüssi, Georg, additional, Montillo, Marco, additional, Passamonti, Francesco, additional, Gregor, Michael, additional, Laurenti, Luca, additional, Tedeschi, Alessandra, additional, Gaidano, Gianluca, additional, Efremov, Dimitar, additional, Gattei, Valter, additional, Khiabanian, Hossein, additional, and Rossi, Davide, additional

Published
2021
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10. Poster: CLL-358: Adaptation of Chronic Lymphocytic Leukemia to Ibrutinib Is Mediated by Epigenetic Plasticity of Residual Disease and Bypass Signaling via the MAPK Pathway

Author

Bergamo, Lodovico Terzi di, primary, Forestieri, Gabriela, additional, Loh, Jui Wan, additional, Singh, Amartya, additional, Spina, Valeria, additional, Zucchetto, Antonella, additional, Condoluci, Adalgisa, additional, Faderl, Martin, additional, Koch, Ricardo, additional, Bruscaggin, Alessio, additional, Pini, Katia, additional, Wu, Wei, additional, Piffaretti, Deborah, additional, Bittolo, Tamara, additional, Tissino, Erika, additional, De Paoli, Lorenzo, additional, Deambrogi, Clara, additional, Frustaci, Anna Maria, additional, Autore, Francesco, additional, Merli, Michele, additional, Scarfò, Lydia, additional, Rasi, Silvia, additional, Passweg, Jakob, additional, Moia, Riccardo, additional, Martines, Claudio, additional, Ghia, Paolo, additional, Cavalli, Franco, additional, Zucca, Emanuele, additional, Gerber, Bernhard, additional, Gillessen, Silke, additional, Stüssi, Georg, additional, Montillo, Marco, additional, Passamonti, Francesco, additional, Gregor, Michael, additional, Laurenti, Luca, additional, Tedeschi, Alessandra, additional, Gaidano, Gianluca, additional, Efremov, Dimitar, additional, Gattei, Valter, additional, Khiabanian, Hossein, additional, and Rossi, Davide, additional

Published
2021
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12. Combined Genetic Lesions in TP53 and CDKN2A/CDKN2B Drive B Cell Receptor-Dependent/Costimulatory Signal-Independent Proliferation in Richter Syndrome

Author

Chakraborty, Supriya, primary, Martines, Claudio, additional, Porro, Fabiola, additional, Fortunati, Ilaria, additional, Bonato, Alice, additional, Dimishkovska, Marija, additional, Yadav, Brijesh, additional, Innocenti, Idanna, additional, Fazio, Rosa, additional, Vaisitti, Tizianna, additional, Deaglio, Silvia, additional, Zamò, Alberto, additional, Dimovski, Aleksandar, additional, Laurenti, Luca, additional, and Efremov, Dimitar G, additional

Published
2020
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13. Combined Genetic Lesions in TP53 and CDKN2A/CDKN2B Drive B Cell Receptor-Dependent/Costimulatory Signal-Independent Proliferation in Richter Syndrome

Author

Chakraborty, Supriya, Martines, Claudio, Porro, Fabiola, Fortunati, Ilaria, Bonato, Alice, Dimishkovska, Marija, Yadav, Brijesh, Innocenti, Idanna, Fazio, Rosa, Vaisitti, Tizianna, Deaglio, Silvia, Zamò, Alberto, Dimovski, Aleksandar, Laurenti, Luca, Efremov, Dimitar G, Laurenti, Luca (ORCID:0000-0002-8327-1396), Chakraborty, Supriya, Martines, Claudio, Porro, Fabiola, Fortunati, Ilaria, Bonato, Alice, Dimishkovska, Marija, Yadav, Brijesh, Innocenti, Idanna, Fazio, Rosa, Vaisitti, Tizianna, Deaglio, Silvia, Zamò, Alberto, Dimovski, Aleksandar, Laurenti, Luca, Efremov, Dimitar G, and Laurenti, Luca (ORCID:0000-0002-8327-1396)

Abstract

n/a

Published
2020

14. A CRISPR/Cas9-Generated Murine Model Reveals Cooperation between BCR Signaling and CDKN2A/2B and TP53 Disruption in Richter Syndrome

Author

Chakraborty, Supriya, primary, Fortunati, Ilaria, additional, Martines, Claudio, additional, Yadav, Brijesh, additional, Dimishkovska, Marija, additional, Innocenti, Idanna, additional, Fazio, Rosa, additional, D'Arena, Giovanni, additional, Dimovski, Aleksandar, additional, Laurenti, Luca, additional, and Efremov, Dimitar G, additional

Published
2019
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15. Serum IgM/Fcmr Interactions Inhibit BCR Signaling and Influence the Cinical Course of CLL

Author

Gobessi, Stefania, primary, Laurenti, Luca, additional, Porro, Fabiola, additional, Martines, Claudio, additional, Fazio, Rosa, additional, Xerxa, Elena, additional, Innocenti, Idanna, additional, Zucchetto, Antonella, additional, Chen, Shih-Shih, additional, Yan, Xiao-Jie, additional, Chiorazzi, Nicholas, additional, Gattei, Valter, additional, and Efremov, Dimitar G, additional

Published
2018
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16. ABT‐199 (Venetoclax), a BH3‐mimetic Bcl‐2 inhibitor, does not cause Ca2+‐signalling dysregulation or toxicity in pancreatic acinar cells

Author

Jakubowska, Monika A, primary, Kerkhofs, Martijn, additional, Martines, Claudio, additional, Efremov, Dimitar G, additional, Gerasimenko, Julia V, additional, Gerasimenko, Oleg V, additional, Petersen, Ole H, additional, Bultynck, Geert, additional, Vervliet, Tim, additional, and Ferdek, Pawel E, additional

Published
2018
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17. Constitutive IP3 signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP3 receptor disruptor BIRD-2

Author

Bittremieux, Mart, primary, La Rovere, Rita M., additional, Akl, Haidar, additional, Martines, Claudio, additional, Welkenhuyzen, Kirsten, additional, Dubron, Kathia, additional, Baes, Myriam, additional, Janssens, Ann, additional, Vandenberghe, Peter, additional, Laurenti, Luca, additional, Rietdorf, Katja, additional, Morciano, Giampaolo, additional, Pinton, Paolo, additional, Mikoshiba, Katsuhiko, additional, Bootman, Martin D., additional, Efremov, Dimitar G., additional, De Smedt, Humbert, additional, Parys, Jan B., additional, and Bultynck, Geert, additional

Published
2018
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18. ABT-199 (Venetoclax), a BH3-mimetic Bcl-2 inhibitor, does not cause Ca2+ -signalling dysregulation or toxicity in pancreatic acinar cells.

Author

Jakubowska, Monika A, Kerkhofs, Martijn, Martines, Claudio, Efremov, Dimitar G, Gerasimenko, Julia V, Gerasimenko, Oleg V, Petersen, Ole H, Bultynck, Geert, Vervliet, Tim, and Ferdek, Pawel E

Subjects
PANCREATIC acinar cells, CELL death, CANCER cells, CELL analysis, PANCREATIC cancer, CANCER cell migration
Abstract

Background and Purpose: Many cancer cells depend on anti-apoptotic B-cell lymphoma 2 (Bcl-2) proteins for their survival. Bcl-2 antagonism through Bcl-2 homology 3 (BH3) mimetics has emerged as a novel anti-cancer therapy. ABT-199 (Venetoclax), a recently developed BH3 mimetic that selectively inhibits Bcl-2, was introduced into the clinic for treatment of relapsed chronic lymphocytic leukaemia. Early generations of Bcl-2 inhibitors evoked sustained Ca2+ responses in pancreatic acinar cells (PACs) inducing cell death. Therefore, BH3 mimetics could potentially be toxic for the pancreas when used to treat cancer. Although ABT-199 was shown to kill Bcl-2-dependent cancer cells without affecting intracellular Ca2+ signalling, its effects on PACs have not yet been determined. Hence, it is essential and timely to assess whether this recently approved anti-leukaemic drug might potentially have pancreatotoxic effects.Experimental Approach: Single-cell Ca2+ measurements and cell death analysis were performed on isolated mouse PACs.Key Results: Inhibition of Bcl-2 via ABT-199 did not elicit intracellular Ca2+ signalling on its own or potentiate Ca2+ signalling induced by physiological/pathophysiological stimuli in PACs. Although ABT-199 did not affect cell death in PACs, under conditions that killed ABT-199-sensitive cancer cells, cytosolic Ca2+ extrusion was slightly enhanced in the presence of ABT-199. In contrast, inhibition of Bcl-xL potentiated pathophysiological Ca2+ responses in PACs, without exacerbating cell death.Conclusion and Implications: Our results demonstrate that apart from having a modest effect on cytosolic Ca2+ extrusion, ABT-199 does not substantially alter intracellular Ca2+ homeostasis in normal PACs and should be safe for the pancreas during cancer treatment.Linked Articles: This article is part of a themed section on Mitochondrial Pharmacology: Featured Mechanisms and Approaches for Therapy Translation. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.22/issuetoc. [ABSTRACT FROM AUTHOR]

Published
2019
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19. Constitutive IP3signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP3receptor disruptor BIRD-2

Author

Bittremieux, Mart, Rovere, Rita, Akl, Haidar, Martines, Claudio, Welkenhuyzen, Kirsten, Dubron, Kathia, Baes, Myriam, Janssens, Ann, Vandenberghe, Peter, Laurenti, Luca, Rietdorf, Katja, Morciano, Giampaolo, Pinton, Paolo, Mikoshiba, Katsuhiko, Bootman, Martin, Efremov, Dimitar, Smedt, Humbert, Parys, Jan, and Bultynck, Geert

Abstract

Anti-apoptotic Bcl-2 proteins are upregulated in different cancers, including diffuse large B-cell lymphoma (DLBCL) and chronic lymphocytic leukemia (CLL), enabling survival by inhibiting pro-apoptotic Bcl-2-family members and inositol 1,4,5-trisphosphate (IP3) receptor (IP3R)-mediated Ca2+-signaling. A peptide tool (Bcl-2/IP3R Disruptor-2; BIRD-2) was developed to abrogate the interaction of Bcl-2 with IP3Rs by targeting Bcl-2′s BH4 domain. BIRD-2 triggers cell death in primary CLL cells and in DLBCL cell lines. Particularly, DLBCL cells with high levels of IP3R2 were sensitive to BIRD-2. Here, we report that BIRD-2-induced cell death in DLBCL cells does not only depend on high IP3R2-expression levels, but also on constitutive IP3signaling, downstream of the tonically active B-cell receptor. The basal Ca2+level in SU-DHL-4 DLBCL cells was significantly elevated due to the constitutive IP3production. This constitutive IP3signaling fulfilled a pro-survival role, since inhibition of phospholipase C (PLC) using U73122 (2.5 µM) caused cell death in SU-DHL-4 cells. Milder inhibition of IP3signaling using a lower U73122 concentration (1 µM) or expression of an IP3sponge suppressed both BIRD-2-induced Ca2+elevation and apoptosis in SU-DHL-4 cells. Basal PLC/IP3signaling also fulfilled a pro-survival role in other DLBCL cell lines, including Karpas 422, RI-1 and SU-DHL-6 cells, whereas PLC inhibition protected these cells against BIRD-2-evoked apoptosis. Finally, U73122 treatment also suppressed BIRD-2-induced cell death in primary CLL, both in unsupported systems and in co-cultures with CD40L-expressing fibroblasts. Thus, constitutive IP3signaling in lymphoma and leukemia cells is not only important for cancer cell survival, but also represents a vulnerability, rendering cancer cells dependent on Bcl-2 to limit IP3R activity. BIRD-2 seems to switch constitutive IP3signaling from pro-survival into pro-death, presenting a plausible therapeutic strategy.

Published
2019
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22. Constitutive IP3 signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP3 receptor disruptor BIRD-2

Author

Bittremieux, Mart, La Rovere, Rita M., Akl, Haidar, Martines, Claudio, Welkenhuyzen, Kirsten, Dubron, Kathia, Baes, Myriam, Janssens, Ann, Vandenberghe, Peter, Laurenti, Luca, Rietdorf, Katja, Morciano, Giampaolo, Pinton, Paolo, Mikoshiba, Katsuhiko, Bootman, Martin D., Efremov, Dimitar G., De Smedt, Humbert, Parys, Jan B., Bultynck, Geert, Bittremieux, Mart, La Rovere, Rita M., Akl, Haidar, Martines, Claudio, Welkenhuyzen, Kirsten, Dubron, Kathia, Baes, Myriam, Janssens, Ann, Vandenberghe, Peter, Laurenti, Luca, Rietdorf, Katja, Morciano, Giampaolo, Pinton, Paolo, Mikoshiba, Katsuhiko, Bootman, Martin D., Efremov, Dimitar G., De Smedt, Humbert, Parys, Jan B., and Bultynck, Geert

Abstract

Anti-apoptotic Bcl-2 proteins are upregulated in different cancers, including diffuse large B-cell lymphoma (DLBCL) and chronic lymphocytic leukemia (CLL), enabling survival by inhibiting pro-apoptotic Bcl-2-family members and inositol 1,4,5-trisphosphate (IP3) receptor (IP3R)-mediated Ca2+-signaling. A peptide tool (Bcl-2/IP3R Disruptor-2; BIRD-2) was developed to abrogate the interaction of Bcl-2 with IP3Rs by targeting Bcl-2′s BH4 domain. BIRD-2 triggers cell death in primary CLL cells and in DLBCL cell lines. Particularly, DLBCL cells with high levels of IP3R2 were sensitive to BIRD-2. Here, we report that BIRD-2-induced cell death in DLBCL cells does not only depend on high IP3R2-expression levels, but also on constitutive IP3 signaling, downstream of the tonically active B-cell receptor. The basal Ca2+ level in SU-DHL-4 DLBCL cells was significantly elevated due to the constitutive IP3 production. This constitutive IP3 signaling fulfilled a pro-survival role, since inhibition of phospholipase C (PLC) using U73122 (2.5 µM) caused cell death in SU-DHL-4 cells. Milder inhibition of IP3 signaling using a lower U73122 concentration (1 µM) or expression of an IP3 sponge suppressed both BIRD-2-induced Ca2+ elevation and apoptosis in SU-DHL-4 cells. Basal PLC/IP3 signaling also fulfilled a pro-survival role in other DLBCL cell lines, including Karpas 422, RI-1 and SU-DHL-6 cells, whereas PLC inhibition protected these cells against BIRD-2-evoked apoptosis. Finally, U73122 treatment also suppressed BIRD-2-induced cell death in primary CLL, both in unsupported systems and in co-cultures with CD40L-expressing fibroblasts. Thus, constitutive IP3 signaling in lymphoma and leukemia cells is not only important for cancer cell survival, but also represents a vulnerability, rendering cancer cells dependent on Bcl-2

23. Constitutive IP3 signaling underlies the sensitivity of B-cell cancers to the Bcl-2/IP3 receptor disruptor BIRD-2

Author

Bittremieux, Mart, La Rovere, Rita M., Akl, Haidar, Martines, Claudio, Welkenhuyzen, Kirsten, Dubron, Kathia, Baes, Myriam, Janssens, Ann, Vandenberghe, Peter, Laurenti, Luca, Rietdorf, Katja, Morciano, Giampaolo, Pinton, Paolo, Mikoshiba, Katsuhiko, Bootman, Martin D., Efremov, Dimitar G., De Smedt, Humbert, Parys, Jan B., Bultynck, Geert, Bittremieux, Mart, La Rovere, Rita M., Akl, Haidar, Martines, Claudio, Welkenhuyzen, Kirsten, Dubron, Kathia, Baes, Myriam, Janssens, Ann, Vandenberghe, Peter, Laurenti, Luca, Rietdorf, Katja, Morciano, Giampaolo, Pinton, Paolo, Mikoshiba, Katsuhiko, Bootman, Martin D., Efremov, Dimitar G., De Smedt, Humbert, Parys, Jan B., and Bultynck, Geert

Abstract

Anti-apoptotic Bcl-2 proteins are upregulated in different cancers, including diffuse large B-cell lymphoma (DLBCL) and chronic lymphocytic leukemia (CLL), enabling survival by inhibiting pro-apoptotic Bcl-2-family members and inositol 1,4,5-trisphosphate (IP3) receptor (IP3R)-mediated Ca2+-signaling. A peptide tool (Bcl-2/IP3R Disruptor-2; BIRD-2) was developed to abrogate the interaction of Bcl-2 with IP3Rs by targeting Bcl-2′s BH4 domain. BIRD-2 triggers cell death in primary CLL cells and in DLBCL cell lines. Particularly, DLBCL cells with high levels of IP3R2 were sensitive to BIRD-2. Here, we report that BIRD-2-induced cell death in DLBCL cells does not only depend on high IP3R2-expression levels, but also on constitutive IP3 signaling, downstream of the tonically active B-cell receptor. The basal Ca2+ level in SU-DHL-4 DLBCL cells was significantly elevated due to the constitutive IP3 production. This constitutive IP3 signaling fulfilled a pro-survival role, since inhibition of phospholipase C (PLC) using U73122 (2.5 µM) caused cell death in SU-DHL-4 cells. Milder inhibition of IP3 signaling using a lower U73122 concentration (1 µM) or expression of an IP3 sponge suppressed both BIRD-2-induced Ca2+ elevation and apoptosis in SU-DHL-4 cells. Basal PLC/IP3 signaling also fulfilled a pro-survival role in other DLBCL cell lines, including Karpas 422, RI-1 and SU-DHL-6 cells, whereas PLC inhibition protected these cells against BIRD-2-evoked apoptosis. Finally, U73122 treatment also suppressed BIRD-2-induced cell death in primary CLL, both in unsupported systems and in co-cultures with CD40L-expressing fibroblasts. Thus, constitutive IP3 signaling in lymphoma and leukemia cells is not only important for cancer cell survival, but also represents a vulnerability, rendering cancer cells dependent on Bcl-2

24. Potassium/sodium cation carriers robustly up-regulate CD20 antigen by targeting MYC, and synergize with anti-CD20 immunotherapies to eliminate malignant B cells.

Author

Torun A, Zdanowicz A, Miazek-Zapala N, Zapala P, Pradhan B, Jedrzejczyk M, Ciechanowicz A, Pilch Z, Skorzynski M, Słabicki M, Rymkiewicz G, Barankiewicz J, Martines C, Laurenti L, Struga M, Winiarska M, Golab J, Kucia M, Ratajczak MZ, Huczynski A, Calado DP, Efremov DG, Zerrouqi A, and Pyrzynska B

Abstract

Our investigation uncovers that nanomolar concentrations of salinomycin, monensin, nigericin, and narasin (a group of potassium/sodium cation carriers) robustly enhance surface expression of CD20 antigen in B-cell-derived tumor cells, including primary malignant cells of chronic lymphocytic leukemia and diffuse large B-cell lymphoma. Experiments in vitro, ex vivo, and animal model reveal a novel approach of combining salinomycin or monensin with therapeutic anti-CD20 monoclonal antibodies or anti-CD20 CAR-T cells, significantly improving non- Hodgkin lymphoma (NHL) therapy. The results of RNA-seq, genetic editing, and chemical inhibition delineate the molecular mechanism of CD20 upregulation, at least partially, to the downregulation of MYC, the transcriptional repressor of the MS4A1 gene encoding CD20. Our findings propose the cation carriers as compounds targeting MYC oncogene, which can be combined with anti-CD20 antibodies or adoptive cellular therapies to treat NHL and mitigate resistance, which frequently depends on the CD20 antigen loss, offering new solutions to improve patient outcomes.

Published
2024
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