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Your search keyword '"Maiuri, Maria Chiara"' showing total 25 results
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25 results on '"Maiuri, Maria Chiara"'

1. Mammary carcinoma: toward a realistic mouse model of incurable cancers.

Author

Pérez-Lanzón, Maria, Maiuri, Maria Chiara, Lopez-Otin, Carlos, and Kroemer, Guido

Subjects
*LABORATORY mice, *ANIMAL disease models, *CARCINOMA, *IMMUNE response, *CELL lines
Abstract

As long as breast cancer (BC) stays under immunosurveillance, it can be controlled by treatments eliciting anticancer immune responses. However, once BC escapes immunosurveillance, it becomes therapeutically uncontrollable. A paper in the Journal for ImmunoTherapy of Cancer describes a new hormone receptor-positive BC cell line generating incurable tumors in C57BL/6 mice. [ABSTRACT FROM AUTHOR]

Published
2023
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5. Coffee induces autophagy in vivo.

Author

Pietrocola, Federico, Malik, Shoaib Ahmad, Mariño, Guillermo, Vacchelli, Eerika, Senovilla, Laura, Chaba, Kariman, Niso-Santano, Mireia, Maiuri, Maria Chiara, Madeo, Frank, and Kroemer, Guido

Published
2014
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7. Targeting autophagy as a novel strategy for facilitating the therapeutic action of potentiators on ΔF508 cystic fibrosis transmembrane conductance regulator.

Author

Luciani, Alessandro, Villella, Valeria Rachela, Esposito, Speranza, Gavina, Manuela, Russo, Ilaria, Silano, Marco, Guido, Stefano, Pettoello-Mantovani, Massimo, Carnuccio, Rosa, Scholte, Bob, De Matteis, Antonella, Maiuri, Maria Chiara, Raia, Valeria, Luini, Alberto, Kroemer, Guido, and Maiuri, Luigi

Published
2012
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20. Longevity-relevant regulation of autophagy at the level of the acetylproteome.

Author

Mariño, Guillermo, Morselli, Eugenia, Bennetzen, Martin V., Eisenberg, Tobias, Megalou, Evgenia, Schroeder, Sabrina, Cabrera, Sandra, Bénit, Paule, Rustin, Pierre, Criollo, Alfredo, Kepp, Oliver, Galluzzi, Lorenzo, Shen, Shensi, Malik, Shoaib A., Maiuri, Maria Chiara, Horio, Yoshiyuki, López-Otín, Carlos, Andersen, Jens S., Tavernarakis, Nektarios, and Madeo, Frank

Published
2011
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22. IKK connects autophagy to major stress pathways.

Author

Criollo, Alfredo, Senovilla, Laura, Authier, Hélène, Maiuri, Maria Chiara, Morselli, Eugenia, Vitale, Ilio, Kepp, Oliver, Tasdemir, Ezgi, Galluzzi, Lorenzo, Shensi Shen, Tailler, Maximilien, Delahaye, Nicolas, Tesniere, Antoine, De Stefano, Daniela, Younes, Aména Ben, Harper, Francis, Pierron, Gérard, Lavandero, Sergio, Zitvogel, Laurence, and Israel, Alain

Published
2010
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23. Aspirin--another caloric-restriction mimetic.

Author

Pietrocola, Federico, Castoldi, Francesca, Maiuri, Maria Chiara, and Kroemer, Guido

Abstract

The capacity of cells and organisms to sustain, and to eventually adapt to, environmental and genetic insults declines with age. Because macroautophagy/autophagy is regarded as one of the major determinants of cellular fitness in vitro and in vivo, maneuvers that aim at promoting autophagy may slow down aging and promote health span. Caloric restriction (CR), a reduction in caloric intake without malnutrition, efficiently counteracts aging-associated features, yet is difficult to be applied to humans. Caloric-restriction mimetics (CRMs) are pharmacological agents that recapitulate the main biochemical properties of CR, namely a global reduction of protein acetylation and the induction of autophagy. We found that the ancient drug aspirin and its active metabolite salicylate stimulate autophagic flux by virtue of their inhibitory action on acetyltransferase EP300. The inhibition of EP300 results from a direct competition between salicylate and acetyl coenzyme A for binding to the catalytic domain of the enzyme. This mode of action appears to be conserved across evolution as it accounts for the induction of autophagy by aspirin in various mouse models and in the nematode Caenorhabditis elegans. In sum, aspirin acts as a CRM. [ABSTRACT FROM AUTHOR]

Published
2018
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24. Systemic autophagy in the therapeutic response to anthracycline-based chemotherapy.

Author

Castoldi, Francesca, Vacchelli, Erika, Zitvogel, Laurence, Maiuri, Maria Chiara, Pietrocola, Federico, and Kroemer, Guido

Subjects
CELL death, TUMOR growth, CANCER cells, IMMUNE response, FASTING, MITOXANTRONE, AUTOPHAGY
Abstract

The success of chemotherapy largely depends on the anticancer immune response triggered by tumor cells that succumb to immunogenic cell death (ICD). One of the hallmarks of ICD is premortem autophagy that facilitates the release of adenosine triphosphate from dying cancer cells and acts as a chemoattractant for dendritic cell precursors. Here, we show that the immune response induced by inoculation of cancer cells undergoing ICD in response to the anthracycline mitoxantrone (MTX) can be improved by a short-term fasting regimen (48 hours of starvation) and that this effect is reversed by systemic administration of the autophagy inhibitor dimethyl α-ketoglutarate. Tumor growth reduction by MTX treatment is known to depend on autophagy induction in cancer cells as well as on an intact immune system. We compared the antitumor effects of MTX on autophagy-competent cancers implanted in wild type (WT) or partially autophagy-deficient (Becn1± or Atg4b−/-) mice. While there was no difference in the tumor growth reducing effects of MTX on tumors evolving in WT, Becn1+/- and Atg4b−/- mice, we observed an increase in the toxicity of MTX on Atg4b−/- mice. These results suggest that autophagy in cancer cells (but less so in host cells) is rate-limiting for therapeutically relevant anticancer immune responses, yet has a major role in blunting the life-threatening toxicity of chemotherapy. [ABSTRACT FROM AUTHOR]

Published
2019
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