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19 results on '"Malka, Yuval"'

1. Adoptive T cell therapy targeting an inducible and broadly shared product of aberrant mRNA translation

Author

Champagne, Julien, Nielsen, Morten M., Feng, Xiaodong, Montenegro Navarro, Jasmine, Pataskar, Abhijeet, Voogd, Rhianne, Giebel, Lisanne, Nagel, Remco, Berenst, Nadine, Fumagalli, Amos, Kochavi, Adva, Lovecchio, Domenica, Valcanover, Lorenzo, Malka, Yuval, Yang, Weiwen, Laos, Maarja, Li, Yingqian, Proost, Natalie, van de Ven, Marieke, van Tellingen, Olaf, Bleijerveld, Onno B., Haanen, John B.A.G., Olweus, Johanna, and Agami, Reuven

Published
2025
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2. P-stalk ribosomes act as master regulators of cytokine-mediated processes

Author

Dopler, Anna, Alkan, Ferhat, Malka, Yuval, van der Kammen, Rob, Hoefakker, Kelly, Taranto, Daniel, Kocabay, Naz, Mimpen, Iris, Ramirez, Christel, Malzer, Elke, Isaeva, Olga I., Kerkhoff, Mandy, Gangaev, Anastasia, Silva, Joana, Ramalho, Sofia, Hoekman, Liesbeth, Altelaar, Maarten, Beijersbergen, Roderick, Akkari, Leila, Yewdell, Jonathan Wilson, Kvistborg, Pia, and Faller, William James

Published
2024
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3. Multimodal stimulation screens reveal unique and shared genes limiting T cell fitness

Author

Lin, Chun-Pu, Levy, Pierre L., Alflen, Astrid, Apriamashvili, Georgi, Ligtenberg, Maarten A., Vredevoogd, David W., Bleijerveld, Onno B., Alkan, Ferhat, Malka, Yuval, Hoekman, Liesbeth, Markovits, Ettai, George, Austin, Traets, Joleen J.H., Krijgsman, Oscar, van Vliet, Alex, Poźniak, Joanna, Pulido-Vicuña, Carlos Ariel, de Bruijn, Beaunelle, van Hal-van Veen, Susan E., Boshuizen, Julia, van der Helm, Pim W., Díaz-Gómez, Judit, Warda, Hamdy, Behrens, Leonie M., Mardesic, Paula, Dehni, Bilal, Visser, Nils L., Marine, Jean-Christophe, Markel, Gal, Faller, William J., Altelaar, Maarten, Agami, Reuven, Besser, Michal J., and Peeper, Daniel S.

Published
2024
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6. Multimodal stimulation screens reveal unique and shared genes limiting T cell fitness

Author

Lin, Chun Pu, Levy, Pierre L., Alflen, Astrid, Apriamashvili, Georgi, Ligtenberg, Maarten A., Vredevoogd, David W., Bleijerveld, Onno B., Alkan, Ferhat, Malka, Yuval, Hoekman, Liesbeth, Markovits, Ettai, George, Austin, Traets, Joleen J.H., Krijgsman, Oscar, van Vliet, Alex, Poźniak, Joanna, Pulido-Vicuña, Carlos Ariel, de Bruijn, Beaunelle, van Hal-van Veen, Susan E., Boshuizen, Julia, van der Helm, Pim W., Díaz-Gómez, Judit, Warda, Hamdy, Behrens, Leonie M., Mardesic, Paula, Dehni, Bilal, Visser, Nils L., Marine, Jean Christophe, Markel, Gal, Faller, William J., Altelaar, Maarten, Agami, Reuven, Besser, Michal J., Peeper, Daniel S., Lin, Chun Pu, Levy, Pierre L., Alflen, Astrid, Apriamashvili, Georgi, Ligtenberg, Maarten A., Vredevoogd, David W., Bleijerveld, Onno B., Alkan, Ferhat, Malka, Yuval, Hoekman, Liesbeth, Markovits, Ettai, George, Austin, Traets, Joleen J.H., Krijgsman, Oscar, van Vliet, Alex, Poźniak, Joanna, Pulido-Vicuña, Carlos Ariel, de Bruijn, Beaunelle, van Hal-van Veen, Susan E., Boshuizen, Julia, van der Helm, Pim W., Díaz-Gómez, Judit, Warda, Hamdy, Behrens, Leonie M., Mardesic, Paula, Dehni, Bilal, Visser, Nils L., Marine, Jean Christophe, Markel, Gal, Faller, William J., Altelaar, Maarten, Agami, Reuven, Besser, Michal J., and Peeper, Daniel S.

Abstract

Genes limiting T cell antitumor activity may serve as therapeutic targets. It has not been systematically studied whether there are regulators that uniquely or broadly contribute to T cell fitness. We perform genome-scale CRISPR-Cas9 knockout screens in primary CD8 T cells to uncover genes negatively impacting fitness upon three modes of stimulation: (1) intense, triggering activation-induced cell death (AICD); (2) acute, triggering expansion; (3) chronic, causing dysfunction. Besides established regulators, we uncover genes controlling T cell fitness either specifically or commonly upon differential stimulation. Dap5 ablation, ranking highly in all three screens, increases translation while enhancing tumor killing. Loss of Icam1-mediated homotypic T cell clustering amplifies cell expansion and effector functions after both acute and intense stimulation. Lastly, Ctbp1 inactivation induces functional T cell persistence exclusively upon chronic stimulation. Our results functionally annotate fitness regulators based on their unique or shared contribution to traits limiting T cell antitumor activity.

Published
2024

7. DNA damage induces p53-independent apoptosis through ribosome stalling

Author

CMM Groep Snippert, Cancer, Onderzoek Medische Oncologie, MS Medische Oncologie, Boon, Nicolaas J, Oliveira, Rafaela A, Körner, Pierré-René, Kochavi, Adva, Mertens, Sander, Malka, Yuval, Voogd, Rhianne, van der Horst, Suzanne E M, Huismans, Maarten A, Smabers, Lidwien P, Draper, Jonne M, Wessels, Lodewyk F A, Haahr, Peter, Roodhart, Jeanine M L, Schumacher, Ton N M, Snippert, Hugo J, Agami, Reuven, Brummelkamp, Thijn R, CMM Groep Snippert, Cancer, Onderzoek Medische Oncologie, MS Medische Oncologie, Boon, Nicolaas J, Oliveira, Rafaela A, Körner, Pierré-René, Kochavi, Adva, Mertens, Sander, Malka, Yuval, Voogd, Rhianne, van der Horst, Suzanne E M, Huismans, Maarten A, Smabers, Lidwien P, Draper, Jonne M, Wessels, Lodewyk F A, Haahr, Peter, Roodhart, Jeanine M L, Schumacher, Ton N M, Snippert, Hugo J, Agami, Reuven, and Brummelkamp, Thijn R

Published
2024

8. Multimodal stimulation screens reveal unique and shared genes limiting T cell fitness

Author

Sub Biomol.Mass Spect. and Proteomics, Afd Biomol.Mass Spect. and Proteomics, Biomolecular Mass Spectrometry and Proteomics, Lin, Chun Pu, Levy, Pierre L., Alflen, Astrid, Apriamashvili, Georgi, Ligtenberg, Maarten A., Vredevoogd, David W., Bleijerveld, Onno B., Alkan, Ferhat, Malka, Yuval, Hoekman, Liesbeth, Markovits, Ettai, George, Austin, Traets, Joleen J.H., Krijgsman, Oscar, van Vliet, Alex, Poźniak, Joanna, Pulido-Vicuña, Carlos Ariel, de Bruijn, Beaunelle, van Hal-van Veen, Susan E., Boshuizen, Julia, van der Helm, Pim W., Díaz-Gómez, Judit, Warda, Hamdy, Behrens, Leonie M., Mardesic, Paula, Dehni, Bilal, Visser, Nils L., Marine, Jean Christophe, Markel, Gal, Faller, William J., Altelaar, Maarten, Agami, Reuven, Besser, Michal J., Peeper, Daniel S., Sub Biomol.Mass Spect. and Proteomics, Afd Biomol.Mass Spect. and Proteomics, Biomolecular Mass Spectrometry and Proteomics, Lin, Chun Pu, Levy, Pierre L., Alflen, Astrid, Apriamashvili, Georgi, Ligtenberg, Maarten A., Vredevoogd, David W., Bleijerveld, Onno B., Alkan, Ferhat, Malka, Yuval, Hoekman, Liesbeth, Markovits, Ettai, George, Austin, Traets, Joleen J.H., Krijgsman, Oscar, van Vliet, Alex, Poźniak, Joanna, Pulido-Vicuña, Carlos Ariel, de Bruijn, Beaunelle, van Hal-van Veen, Susan E., Boshuizen, Julia, van der Helm, Pim W., Díaz-Gómez, Judit, Warda, Hamdy, Behrens, Leonie M., Mardesic, Paula, Dehni, Bilal, Visser, Nils L., Marine, Jean Christophe, Markel, Gal, Faller, William J., Altelaar, Maarten, Agami, Reuven, Besser, Michal J., and Peeper, Daniel S.

Published
2024

10. An “alert state” ribosome population acts as a master regulator of cytokine-mediated processes

Author

Dopler, Anna, primary, Alkan, Ferhat, additional, Malka, Yuval, additional, Hoefakker, Kelly, additional, Isaeva, Olga I., additional, Kerkhoff, Mandy, additional, Gangaev, Anastasia, additional, Silva, Joana, additional, Ramalho, Sofia, additional, Hoekman, Liesbeth, additional, Altelaar, Maarten, additional, van der Kammen, Rob, additional, Yewdell, Jonathan Wilson, additional, Kvistborg, Pia, additional, and Faller, William James, additional

Published
2023
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11. DNA damage induces p53-independent apoptosis through ribosome stalling.

Author

Boon, Nicolaas J., Oliveira, Rafaela A., Körner, Pierré-René, Kochavi, Adva, Mertens, Sander, Malka, Yuval, Voogd, Rhianne, van der Horst, Suzanne E. M., Huismans, Maarten A., Smabers, Lidwien P., Draper, Jonne M., Wessels, Lodewyk F. A., Haahr, Peter, Roodhart, Jeanine M. L., Schumacher, Ton N. M., Snippert, Hugo J., Agami, Reuven, and Brummelkamp, Thijn R.

Published
2024

12. MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer

Author

Bhin, Jinhyuk, primary, Yemelyanenko, Julia, additional, Chao, Xue, additional, Klarenbeek, Sjoerd, additional, Opdam, Mark, additional, Malka, Yuval, additional, Hoekman, Liesbeth, additional, Kruger, Dinja, additional, Bleijerveld, Onno, additional, Brambillasca, Chiara S., additional, Sprengers, Justin, additional, Siteur, Bjørn, additional, Annunziato, Stefano, additional, van Haren, Matthijs J., additional, Martin, Nathaniel I., additional, van de Ven, Marieke, additional, Peters, Dennis, additional, Agami, Reuven, additional, Linn, Sabine C., additional, Boven, Epie, additional, Altelaar, Maarten, additional, Jonkers, Jos, additional, Zingg, Daniel, additional, and Wessels, Lodewyk F.A., additional

Published
2023
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13. MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer

Author

Bhin, Jinhyuk, Yemelyanenko, Julia, Chao, Xue, Klarenbeek, Sjoerd, Opdam, Mark, Malka, Yuval, Hoekman, Liesbeth, Kruger, Dinja, Bleijerveld, Onno, Brambillasca, Chiara S., Sprengers, Justin, Siteur, Bjørn, Annunziato, Stefano, van Haren, Matthijs J., Martin, Nathaniel I., van de Ven, Marieke, Peters, Dennis, Agami, Reuven, Linn, Sabine C., Boven, Epie, Altelaar, Maarten, Jonkers, Jos, Zingg, Daniel, Wessels, Lodewyk F.A., Bhin, Jinhyuk, Yemelyanenko, Julia, Chao, Xue, Klarenbeek, Sjoerd, Opdam, Mark, Malka, Yuval, Hoekman, Liesbeth, Kruger, Dinja, Bleijerveld, Onno, Brambillasca, Chiara S., Sprengers, Justin, Siteur, Bjørn, Annunziato, Stefano, van Haren, Matthijs J., Martin, Nathaniel I., van de Ven, Marieke, Peters, Dennis, Agami, Reuven, Linn, Sabine C., Boven, Epie, Altelaar, Maarten, Jonkers, Jos, Zingg, Daniel, and Wessels, Lodewyk F.A.

Abstract

Targeting the PI3K–AKT–mTOR pathway is a promising therapeutic strategy for breast cancer treatment. However, low response rates and development of resistance to PI3K–AKT–mTOR inhibitors remain major clinical challenges. Here, we show that MYC activation drives resistance to mTOR inhibitors (mTORi) in breast cancer. Multiomic profiling of mouse invasive lobular carcinoma (ILC) tumors revealed recurrent Myc amplifications in tumors that acquired resistance to the mTORi AZD8055. MYC activation was associated with biological processes linked to mTORi response and counteracted mTORi-induced translation inhibition by promoting translation of ribosomal proteins. In vitro and in vivo induction of MYC conferred mTORi resistance in mouse and human breast cancer models. Conversely, AZD8055-resistant ILC cells depended on MYC, as demonstrated by the synergistic effects of mTORi and MYCi combination treatment. Notably, MYC status was significantly associated with poor response to everolimus therapy in metastatic breast cancer patients. Thus, MYC is a clinically relevant driver of mTORi resistance that may stratify breast cancer patients for mTOR-targeted therapies.

Published
2023

14. MYC is a clinically significant driver of mTOR inhibitor resistance in breast cancer

Author

Afd Biomol.Mass Spect. and Proteomics, Biomolecular Mass Spectrometry and Proteomics, Chemical Biology and Drug Discovery, Bhin, Jinhyuk, Yemelyanenko, Julia, Chao, Xue, Klarenbeek, Sjoerd, Opdam, Mark, Malka, Yuval, Hoekman, Liesbeth, Kruger, Dinja, Bleijerveld, Onno, Brambillasca, Chiara S., Sprengers, Justin, Siteur, Bjørn, Annunziato, Stefano, van Haren, Matthijs J., Martin, Nathaniel I., van de Ven, Marieke, Peters, Dennis, Agami, Reuven, Linn, Sabine C., Boven, Epie, Altelaar, Maarten, Jonkers, Jos, Zingg, Daniel, Wessels, Lodewyk F.A., Afd Biomol.Mass Spect. and Proteomics, Biomolecular Mass Spectrometry and Proteomics, Chemical Biology and Drug Discovery, Bhin, Jinhyuk, Yemelyanenko, Julia, Chao, Xue, Klarenbeek, Sjoerd, Opdam, Mark, Malka, Yuval, Hoekman, Liesbeth, Kruger, Dinja, Bleijerveld, Onno, Brambillasca, Chiara S., Sprengers, Justin, Siteur, Bjørn, Annunziato, Stefano, van Haren, Matthijs J., Martin, Nathaniel I., van de Ven, Marieke, Peters, Dennis, Agami, Reuven, Linn, Sabine C., Boven, Epie, Altelaar, Maarten, Jonkers, Jos, Zingg, Daniel, and Wessels, Lodewyk F.A.

Published
2023

18. Synergistic Interactions between the Molecular and Neuronal Circadian Networks Drive Robust Behavioral Circadian Rhythms in Drosophila melanogaster.

Author

Weiss, Ron, Bartok, Osnat, Mezan, Shaul, Malka, Yuval, and Kadener, Sebastian

Subjects
DROSOPHILA melanogaster, GENE targeting, NEURONS, NEUROPEPTIDE genetics, GENETICS of biological rhythms
Abstract

Most organisms use 24-hr circadian clocks to keep temporal order and anticipate daily environmental changes. In Drosophila melanogaster CLOCK (CLK) and CYCLE (CYC) initiates the circadian system by promoting rhythmic transcription of hundreds of genes. However, it is still not clear whether high amplitude transcriptional oscillations are essential for circadian timekeeping. In order to address this issue, we generated flies in which the amplitude of CLK-driven transcription can be reduced partially (approx. 60%) or strongly (90%) without affecting the average levels of CLK-target genes. The impaired transcriptional oscillations lead to low amplitude protein oscillations that were not sufficient to drive outputs of peripheral oscillators. However, circadian rhythms in locomotor activity were resistant to partial reduction in transcriptional and protein oscillations. We found that the resilience of the brain oscillator is depending on the neuronal communication among circadian neurons in the brain. Indeed, the capacity of the brain oscillator to overcome low amplitude transcriptional oscillations depends on the action of the neuropeptide PDF and on the pdf-expressing cells having equal or higher amplitude of molecular rhythms than the rest of the circadian neuronal groups in the fly brain. Therefore, our work reveals the importance of high amplitude transcriptional oscillations for cell-autonomous circadian timekeeping. Moreover, we demonstrate that the circadian neuronal network is an essential buffering system that protects against changes in circadian transcription in the brain. [ABSTRACT FROM AUTHOR]

Published
2014
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19. Synergistic Interactions between the Molecular and Neuronal Circadian Networks Drive Robust Behavioral Circadian Rhythms in Drosophila melanogaster.

Author

Weiss, Ron, Bartok, Osnat, Mezan, Shaul, Malka, Yuval, and Kadener, Sebastian

Subjects
*DROSOPHILA melanogaster, *GENE targeting, *NEURONS, *NEUROPEPTIDE genetics, *GENETICS of biological rhythms
Abstract

Most organisms use 24-hr circadian clocks to keep temporal order and anticipate daily environmental changes. In Drosophila melanogaster CLOCK (CLK) and CYCLE (CYC) initiates the circadian system by promoting rhythmic transcription of hundreds of genes. However, it is still not clear whether high amplitude transcriptional oscillations are essential for circadian timekeeping. In order to address this issue, we generated flies in which the amplitude of CLK-driven transcription can be reduced partially (approx. 60%) or strongly (90%) without affecting the average levels of CLK-target genes. The impaired transcriptional oscillations lead to low amplitude protein oscillations that were not sufficient to drive outputs of peripheral oscillators. However, circadian rhythms in locomotor activity were resistant to partial reduction in transcriptional and protein oscillations. We found that the resilience of the brain oscillator is depending on the neuronal communication among circadian neurons in the brain. Indeed, the capacity of the brain oscillator to overcome low amplitude transcriptional oscillations depends on the action of the neuropeptide PDF and on the pdf-expressing cells having equal or higher amplitude of molecular rhythms than the rest of the circadian neuronal groups in the fly brain. Therefore, our work reveals the importance of high amplitude transcriptional oscillations for cell-autonomous circadian timekeeping. Moreover, we demonstrate that the circadian neuronal network is an essential buffering system that protects against changes in circadian transcription in the brain. [ABSTRACT FROM AUTHOR]

Published
2014
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