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Giulia Petroni

Researcher at Cornell University

Publications -  21
Citations -  1378

Giulia Petroni is an academic researcher from Cornell University. The author has contributed to research in topics: Autophagy & Cancer cell. The author has an hindex of 8, co-authored 21 publications receiving 303 citations. Previous affiliations of Giulia Petroni include University of Florence.

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Autophagy in major human diseases

Daniel J. Klionsky, +71 more
- 01 Oct 2021 - 
TL;DR: In this paper, preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.
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Detection of immunogenic cell death and its relevance for cancer therapy

TL;DR: Qualitative approaches for measuring ICD markers in vitro and ex vivo for the discovery of next-generation antineoplastic agents, the development of personalized anticancer regimens, and the identification of optimal therapeutic combinations for the clinical management of cancer are outlined.
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Mitochondrial DNA drives abscopal responses to radiation that are inhibited by autophagy.

TL;DR: It is shown that tumor cell autophagy opposes inflammatory cell death following radiation therapy and can be inhibited to enhance antitumor responses, suggesting that mitochondrial outer membrane permeabilization may represent a valid target for boosting radiation therapy immunogenicity in patients with breast cancer.
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Immunomodulation by targeted anticancer agents

TL;DR: The main immunomodulatory effects of targeted anticancer agents are discussed and potential avenues to harness them in support of superior clinical efficacy are explored.
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Apoptotic caspases inhibit abscopal responses to radiation and identify a new prognostic biomarker for breast cancer patients

TL;DR: It is reported that mouse mammary carcinoma TSA cells lacking Casp3 or subjected to chemical caspase inhibition were as sensitive to the cytostatic and cytotoxic effects of radiation therapy in vitro as their control counterparts, yet secreted increased levels of type I IFN.