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30 results on '"Sukkurwala, Abdul Qader"'

1. Data from Cisplatin Resistance Associated with PARP Hyperactivation

Author

Michels, Judith, primary, Vitale, Ilio, primary, Galluzzi, Lorenzo, primary, Adam, Julien, primary, Olaussen, Ken André, primary, Kepp, Oliver, primary, Senovilla, Laura, primary, Talhaoui, Ibtissam, primary, Guegan, Justine, primary, Enot, David Pierre, primary, Talbot, Monique, primary, Robin, Angélique, primary, Girard, Philippe, primary, Oréar, Cédric, primary, Lissa, Delphine, primary, Sukkurwala, Abdul Qader, primary, Garcia, Pauline, primary, Behnam-Motlagh, Parviz, primary, Kohno, Kimitoshi, primary, Wu, Gen Sheng, primary, Brenner, Catherine, primary, Dessen, Philippe, primary, Saparbaev, Murat, primary, Soria, Jean-Charles, primary, Castedo, Maria, primary, and Kroemer, Guido, primary

Published
2023
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2. Supplementary Table 1, Figures 1 - 8 from Cisplatin Resistance Associated with PARP Hyperactivation

Author

Michels, Judith, primary, Vitale, Ilio, primary, Galluzzi, Lorenzo, primary, Adam, Julien, primary, Olaussen, Ken André, primary, Kepp, Oliver, primary, Senovilla, Laura, primary, Talhaoui, Ibtissam, primary, Guegan, Justine, primary, Enot, David Pierre, primary, Talbot, Monique, primary, Robin, Angélique, primary, Girard, Philippe, primary, Oréar, Cédric, primary, Lissa, Delphine, primary, Sukkurwala, Abdul Qader, primary, Garcia, Pauline, primary, Behnam-Motlagh, Parviz, primary, Kohno, Kimitoshi, primary, Wu, Gen Sheng, primary, Brenner, Catherine, primary, Dessen, Philippe, primary, Saparbaev, Murat, primary, Soria, Jean-Charles, primary, Castedo, Maria, primary, and Kroemer, Guido, primary

Published
2023
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4. Anticancer Chemotherapy-Induced Intratumoral Recruitment and Differentiation of Antigen-Presenting Cells

Author

Ma, Yuting, Adjemian, Sandy, Mattarollo, Stephen R., Yamazaki, Takahiro, Aymeric, Laetitia, Yang, Heng, Portela Catani, João Paulo, Hannani, Dalil, Duret, Helene, Steegh, Kim, Martins, Isabelle, Schlemmer, Frederic, Michaud, Mickaël, Kepp, Oliver, Sukkurwala, Abdul Qader, Menger, Laurie, Vacchelli, Erika, Droin, Nathalie, Galluzzi, Lorenzo, Krzysiek, Roman, Gordon, Siamon, Taylor, Philip R., Van Endert, Peter, Solary, Eric, Smyth, Mark J., Zitvogel, Laurence, and Kroemer, Guido

Published
2013
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5. Autophagy-Dependent Anticancer Immune Responses Induced by Chemotherapeutic Agents in Mice

Author

Michaud, Mickaël, Martins, Isabelle, Sukkurwala, Abdul Qader, Adjemian, Sandy, Ma, Yuting, Pellegatti, Patrizia, Shen, Shensi, Kepp, Oliver, Scoazec, Marie, Mignot, Grégoire, Rello-Varona, Santiago, Tailler, Maximilien, Menger, Laurie, Vacchelli, Erika, Galluzzi, Lorenzo, Ghiringhelli, François, di Virgilio, Francesco, Zitvogel, Laurence, and Kroemer, Guido

Published
2011
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7. Fluorescent Biosensors for the Detection of HMGB1 Release

Author

Martins, Isabelle, primary, Kepp, Oliver, additional, Menger, Laurie, additional, Michaud, Mickäel, additional, Adjemian, Sandy, additional, Sukkurwala, Abdul Qader, additional, Vacchelli, Erika, additional, Galluzzi, Lorenzo, additional, and Kroemer, Guido, additional

Published
2013
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8. Quantification of Cell Cycle-Arresting Proteins

Author

Kepp, Oliver, primary, Martins, Isabelle, additional, Menger, Laurie, additional, Michaud, Mickaël, additional, Adjemian, Sandy, additional, Sukkurwala, Abdul Qader, additional, Galluzzi, Lorenzo, additional, and Kroemer, Guido, additional

Published
2012
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9. Consensus guidelines for the detection of immunogenic cell death

Author

Kepp, Oliver, primary, Senovilla, Laura, additional, Vitale, Ilio, additional, Vacchelli, Erika, additional, Adjemian, Sandy, additional, Agostinis, Patrizia, additional, Apetoh, Lionel, additional, Aranda, Fernando, additional, Barnaba, Vincenzo, additional, Bloy, Norma, additional, Bracci, Laura, additional, Breckpot, Karine, additional, Brough, David, additional, Buqué, Aitziber, additional, Castro, Maria G., additional, Cirone, Mara, additional, Colombo, Maria I., additional, Cremer, Isabelle, additional, Demaria, Sandra, additional, Dini, Luciana, additional, Eliopoulos, Aristides G., additional, Faggioni, Alberto, additional, Formenti, Silvia C., additional, Fučíková, Jitka, additional, Gabriele, Lucia, additional, Gaipl, Udo S., additional, Galon, Jérôme, additional, Garg, Abhishek, additional, Ghiringhelli, François, additional, Giese, Nathalia A., additional, Guo, Zong Sheng, additional, Hemminki, Akseli, additional, Herrmann, Martin, additional, Hodge, James W., additional, Holdenrieder, Stefan, additional, Honeychurch, Jamie, additional, Hu, Hong-Min, additional, Huang, Xing, additional, Illidge, Tim M., additional, Kono, Koji, additional, Korbelik, Mladen, additional, Krysko, Dmitri V., additional, Loi, Sherene, additional, Lowenstein, Pedro R., additional, Lugli, Enrico, additional, Ma, Yuting, additional, Madeo, Frank, additional, Manfredi, Angelo A., additional, Martins, Isabelle, additional, Mavilio, Domenico, additional, Menger, Laurie, additional, Merendino, Nicolò, additional, Michaud, Michael, additional, Mignot, Gregoire, additional, Mossman, Karen L., additional, Multhoff, Gabriele, additional, Oehler, Rudolf, additional, Palombo, Fabio, additional, Panaretakis, Theocharis, additional, Pol, Jonathan, additional, Proietti, Enrico, additional, Ricci, Jean-Ehrland, additional, Riganti, Chiara, additional, Rovere-Querini, Patrizia, additional, Rubartelli, Anna, additional, Sistigu, Antonella, additional, Smyth, Mark J., additional, Sonnemann, Juergen, additional, Spisek, Radek, additional, Stagg, John, additional, Sukkurwala, Abdul Qader, additional, Tartour, Eric, additional, Thorburn, Andrew, additional, Thorne, Stephen H., additional, Vandenabeele, Peter, additional, Velotti, Francesca, additional, Workenhe, Samuel T., additional, Yang, Haining, additional, Zong, Wei-Xing, additional, Zitvogel, Laurence, additional, Kroemer, Guido, additional, and Galluzzi, Lorenzo, additional

Published
2014
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11. Cisplatin Resistance Associated with PARP Hyperactivation

Author

Michels, Judith, Vitale, Ilio, Galluzzi, Lorenzo, Adam, Julien, Olaussen, Ken Andre, Kepp, Oliver, Senovilla, Laura, Talhaoui, Ibtissam, Guegan, Justine, Enot, David Pierre, Talbot, Monique, Robin, Angelique, Girard, Philippe, Orear, Cedric, Lissa, Delphine, Sukkurwala, Abdul Qader, Garcia, Pauline, Behnam Motlagh, Parviz, Kohno, Kimitoshi, Wu, Gen Sheng, Brenner, Catherine, Dessen, Philippe, Saparbaev, Murat, Soria, Jean-Charles, Castedo, Maria, Kroemer, Guido, Michels, Judith, Vitale, Ilio, Galluzzi, Lorenzo, Adam, Julien, Olaussen, Ken Andre, Kepp, Oliver, Senovilla, Laura, Talhaoui, Ibtissam, Guegan, Justine, Enot, David Pierre, Talbot, Monique, Robin, Angelique, Girard, Philippe, Orear, Cedric, Lissa, Delphine, Sukkurwala, Abdul Qader, Garcia, Pauline, Behnam Motlagh, Parviz, Kohno, Kimitoshi, Wu, Gen Sheng, Brenner, Catherine, Dessen, Philippe, Saparbaev, Murat, Soria, Jean-Charles, Castedo, Maria, and Kroemer, Guido

Abstract

Non-small cell lung carcinoma patients are frequently treated with cisplatin (CDDP), most often yielding temporary clinical responses. Here, we show that PARP1 is highly expressed and constitutively hyperactivated in a majority of human CDDP-resistant cancer cells of distinct histologic origin. Cells manifesting elevated intracellular levels of poly(ADP-ribosyl)ated proteins (PAR(high)) responded to pharmacologic PARP inhibitors as well as to PARP1-targeting siRNAs by initiating a DNA damage response that translated into cell death following the activation of the intrinsic pathway of apoptosis. Moreover, PARP1-overexpressing tumor cells and xenografts displayed elevated levels of PAR, which predicted the response to PARP inhibitors in vitro and in vivo more accurately than PARP1 expression itself. Thus, a majority of CDDP-resistant cancer cells appear to develop a dependency to PARP1, becoming susceptible to PARP inhibitor-induced apoptosis. Cancer Res; 73(7); 2271-80.

Published
2013
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14. ATP-dependent recruitment, survival and differentiation of dendritic cell precursors in the tumor bed after anticancer chemotherapy

Author

Ma, Yuting, primary, Adjemian, Sandy, additional, Yang, Heng, additional, Catani, João Paulo Portela, additional, Hannani, Dalil, additional, Martins, Isabelle, additional, Michaud, Mickaël, additional, Kepp, Oliver, additional, Sukkurwala, Abdul Qader, additional, Vacchelli, Erika, additional, Galluzzi, Lorenzo, additional, Zitvogel, Laurence, additional, and Kroemer, Guido, additional

Published
2013
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15. Cisplatin Resistance Associated with PARP Hyperactivation

Author

Michels, Judith, primary, Vitale, Ilio, additional, Galluzzi, Lorenzo, additional, Adam, Julien, additional, Olaussen, Ken André, additional, Kepp, Oliver, additional, Senovilla, Laura, additional, Talhaoui, Ibtissam, additional, Guegan, Justine, additional, Enot, David Pierre, additional, Talbot, Monique, additional, Robin, Angélique, additional, Girard, Philippe, additional, Oréar, Cédric, additional, Lissa, Delphine, additional, Sukkurwala, Abdul Qader, additional, Garcia, Pauline, additional, Behnam-Motlagh, Parviz, additional, Kohno, Kimitoshi, additional, Wu, Gen Sheng, additional, Brenner, Catherine, additional, Dessen, Philippe, additional, Saparbaev, Murat, additional, Soria, Jean-Charles, additional, Castedo, Maria, additional, and Kroemer, Guido, additional

Published
2013
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16. Anticancer activity of cardiac glycosides

Author

Kepp, Oliver, primary, Menger, Laurie, additional, Vacchelli, Erika, additional, Adjemian, Sandy, additional, Martins, Isabelle, additional, Ma, Yuting, additional, Sukkurwala, Abdul Qader, additional, Michaud, Mickaël, additional, Galluzzi, Lorenzo, additional, Zitvogel, Laurence, additional, and Kroemer, Guido, additional

Published
2012
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17. Immunohistochemical detection of cytoplasmic LC3 puncta in human cancer specimens

Author

Ladoire, Sylvain, primary, Chaba, Kariman, additional, Martins, Isabelle, additional, Sukkurwala, Abdul Qader, additional, Adjemian, Sandy, additional, Michaud, Mickaël, additional, Poirier-Colame, Vichnou, additional, Andreiuolo, Felipe, additional, Galluzzi, Lorenzo, additional, White, Eileen, additional, Rosenfeldt, Mathias, additional, Ryan, Kevin M., additional, Zitvogel, Laurence, additional, and Kroemer, Guido, additional

Published
2012
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18. Cardiac Glycosides Exert Anticancer Effects by Inducing Immunogenic Cell Death

Author

Menger, Laurie, primary, Vacchelli, Erika, additional, Adjemian, Sandy, additional, Martins, Isabelle, additional, Ma, Yuting, additional, Shen, Shensi, additional, Yamazaki, Takahiro, additional, Sukkurwala, Abdul Qader, additional, Michaud, Mickaël, additional, Mignot, Grégoire, additional, Schlemmer, Frederic, additional, Sulpice, Eric, additional, Locher, Clara, additional, Gidrol, Xavier, additional, Ghiringhelli, François, additional, Modjtahedi, Nazanine, additional, Galluzzi, Lorenzo, additional, André, Fabrice, additional, Zitvogel, Laurence, additional, Kepp, Oliver, additional, and Kroemer, Guido, additional

Published
2012
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19. Loss-of-function alleles ofP2RX7andTLR4fail to affect the response to chemotherapy in non-small cell lung cancer

Author

Vacchelli, Erika, primary, Galluzzi, Lorenzo, additional, Rousseau, Vanessa, additional, Rigoni, Alice, additional, Tesniere, Antoine, additional, Delahaye, Nicolas, additional, Schlemmer, Fre´de´ric, additional, Menger, Laurie, additional, Sukkurwala, Abdul Qader, additional, Adjemian, Sandy, additional, Martins, Isabelle, additional, Michaud, Mickaël, additional, Dunant, Ariane, additional, Kepp, Oliver, additional, Brambilla, Elisabeth, additional, Soria, Jean-Charles, additional, Zitvogel, Laurence, additional, and Kroemer, Guido, additional

Published
2012
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25. Loss-of-function alleles of P2RX7and TLR4fail to affect the response to chemotherapy in non-small cell lung cancer

Author

Vacchelli, Erika, Galluzzi, Lorenzo, Rousseau, Vanessa, Rigoni, Alice, Tesniere, Antoine, Delahaye, Nicolas, Schlemmer, Fre´de´ric, Menger, Laurie, Sukkurwala, Abdul Qader, Adjemian, Sandy, Martins, Isabelle, Michaud, Mickaël, Dunant, Ariane, Kepp, Oliver, Brambilla, Elisabeth, Soria, Jean-Charles, Zitvogel, Laurence, and Kroemer, Guido

Abstract

The success of anticancer chemotherapy relies at least in part on the induction of an immune response against tumor cells. Thus, tumors growing on mice that lack the pattern recognition receptor TLR4 or the purinergic receptor P2RX7 fail to respond to chemotherapy with anthracyclins or oxaliplatin in conditions in which the same neoplasms growing on immunocompetent mice would do so. Similarly, the therapeutic efficacy (measured as progression-free survival) of adjuvant chemotherapy with anthracyclins is reduced in breast cancer patients bearing loss-of-function alleles of TLR4or P2RX7. TLR4loss-of-function alleles also have a negative impact on the therapeutic outcome of oxaliplatin in colorectal cancer patients. Here, we report that loss-of-function TLR4and P2RX7alleles do not affect overall survival in non-small cell lung cancer (NSCLC) patients, irrespective of the administration and type of chemotherapy. The intrinsic characteristics of NSCLC (which near-to-always is chemoresistant and associated with poor prognosis) and/or the type of therapy that is employed to treat this malignancy (which near-to-always is based on cisplatin) may explain why two genes that affect the immune response to dying cells fail to influence the clinical progression of NSCLC patients.

Published
2012
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27. Quantification of cell cycle-arresting proteins.

Author

Kepp O, Martins I, Menger L, Michaud M, Adjemian S, Sukkurwala AQ, Galluzzi L, and Kroemer G

Subjects
Cellular Senescence, Cyclin-Dependent Kinase Inhibitor Proteins isolation & purification, Electrophoresis, Gene Expression Regulation, HeLa Cells, Humans, Cell Cycle Checkpoints, Cyclin-Dependent Kinase Inhibitor Proteins metabolism, Immunoblotting methods
Abstract

Cellular senescence, which can be defined as a stress response preventing the propagation of cells that have accumulated potentially oncogenic alterations, is invariably associated with a permanent cell cycle arrest. Such an irreversible blockage is mainly mediated by the persistent upregulation of one or more cyclin-dependent kinase inhibitors (CKIs), including (though not limited to) p16( INK4A ) and p21( CIP1 ) and p27( KIP1 ). CKIs operate by binding to cyclin-dependent kinases (CDKs), de facto inhibiting their enzymatic activity. Here, we provide an immunoblotting-based method for the detection and quantification of CKIs in vitro and ex vivo, together with a set of guidelines for the interpretation of results.

Published
2013
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28. Fluorescent biosensors for the detection of HMGB1 release.

Author

Martins I, Kepp O, Menger L, Michaud M, Adjemian S, Sukkurwala AQ, Vacchelli E, Galluzzi L, and Kroemer G

Subjects
Cell Death, Cells, Cultured, Green Fluorescent Proteins metabolism, Humans, Image Processing, Computer-Assisted, Microscopy, Fluorescence, Recombinant Fusion Proteins metabolism, Biosensing Techniques methods, HMGB1 Protein analysis, HMGB1 Protein metabolism
Abstract

During necrosis and following some instances of apoptosis (in particular in the absence of a proficient phagocytic system), the nonhistone chromatin component high-mobility group box 1 (HMGB1) is released in the extracellular space. In vivo, extracellular HMGB1 can bind Toll-like receptor 4 on the surface of dendritic cells, de facto operating as a danger-associated molecular pattern and alarming the organism to the presence of stressful conditions. Recent results indicate that the release of HMGB1 is one of the key features for cell death to be perceived as immunogenic, i.e., to be capable of triggering a cognate immune response in vivo. Thus, only anticancer agents that-among other features-allow for the release of HMGB1 as they induce cell death are expected to stimulate anticancer immune responses. To investigate the immunogenic potential of conventional anticancer agents and novel cell death inducers on a high-throughput scale, we engineered human osteosarcoma U2OS cells to express HMGB1 fused at the N-terminus of the green fluorescent protein (GFP). Coupled to fluorescence microscopy workstations for automated image acquisition and analysis, this HMGB1-GFP-based biosensor is amenable for the identification of potential inducers of immunogenic cell death among large chemical libraries.

Published
2013
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29. Loss-of-function alleles of P2RX7 and TLR4 fail to affect the response to chemotherapy in non-small cell lung cancer.

Author

Vacchelli E, Galluzzi L, Rousseau V, Rigoni A, Tesniere A, Delahaye N, Schlemmer FD, Menger L, Sukkurwala AQ, Adjemian S, Martins I, Michaud M, Dunant A, Kepp O, Brambilla E, Soria JC, Zitvogel L, and Kroemer G

Abstract

The success of anticancer chemotherapy relies at least in part on the induction of an immune response against tumor cells. Thus, tumors growing on mice that lack the pattern recognition receptor TLR4 or the purinergic receptor P2RX7 fail to respond to chemotherapy with anthracyclins or oxaliplatin in conditions in which the same neoplasms growing on immunocompetent mice would do so. Similarly, the therapeutic efficacy (measured as progression-free survival) of adjuvant chemotherapy with anthracyclins is reduced in breast cancer patients bearing loss-of-function alleles of TLR4 or P2RX7. TLR4 loss-of-function alleles also have a negative impact on the therapeutic outcome of oxaliplatin in colorectal cancer patients. Here, we report that loss-of-function TLR4 and P2RX7 alleles do not affect overall survival in non-small cell lung cancer (NSCLC) patients, irrespective of the administration and type of chemotherapy. The intrinsic characteristics of NSCLC (which near-to-always is chemoresistant and associated with poor prognosis) and/or the type of therapy that is employed to treat this malignancy (which near-to-always is based on cisplatin) may explain why two genes that affect the immune response to dying cells fail to influence the clinical progression of NSCLC patients.

Published
2012
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30. [Contributions of immunogenic cell death to the efficacy of anticancer chemotherapy].

Author

Kroemer G, Adjemian S, Michaud M, Martins I, Kepp O, Sukkurwala AQ, Menger L, Vacchelli E, Ma Y, and Zitvogel L

Subjects
Antineoplastic Agents therapeutic use, Humans, Antineoplastic Agents pharmacology, Cell Death immunology, Drug Resistance, Neoplasm immunology, Neoplasms drug therapy, Neoplasms immunology
Abstract

Immunogenic cell death, characterized by calreticulin exposure on the surface of the dying cell, release of the nuclear protein high mobility group box 1 (HMGB1), and release of ATP, enables stimulation of the immune system. We outlined the importance of this kind of cell death for the success of some anticancer chemotherapies. However, defects in the immunogenic cell death signalling pathway can lead to therapeutic failure, apparently because anticancer immune responses must contribute to the efficacy of chemotherapeutic regimens. These defects can be related to the therapy, the tumour cell, the host or the tumour-host interface. It is necessary to characterize these defects to restore and improve the efficacy of anticancer chemotherapies.

Published
2011

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