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  1. Article ; Online: A new mechanism for autophagy regulation of anti-tumor immune responses.

    Thorburn, Andrew

    Autophagy

    2020  Volume 16, Issue 12, Page(s) 2282–2284

    Abstract: In this commentary I discuss a recent paper that describes a new mechanism for how macroautophagy/autophagy regulates the immune response to cancer, and relate it to other recent studies in this area. These recent developments may allow more effective ... ...

    Abstract In this commentary I discuss a recent paper that describes a new mechanism for how macroautophagy/autophagy regulates the immune response to cancer, and relate it to other recent studies in this area. These recent developments may allow more effective strategies to manipulate autophagy to improve cancer therapy.
    MeSH term(s) Autophagy ; Humans ; Immune System/metabolism ; Immune System/pathology ; Immunity ; Neoplasms/immunology ; Neoplasms/pathology
    Language English
    Publishing date 2020-09-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2020.1817286
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  2. Article ; Online: Crosstalk between autophagy and apoptosis: Mechanisms and therapeutic implications.

    Thorburn, Andrew

    Progress in molecular biology and translational science

    2020  Volume 172, Page(s) 55–65

    Abstract: The cellular recycling process of macroautophagy, which is the mechanism by which cellular material is delivered to lysosomes via double membraned vesicles called autophagosomes, is intimately connected to programmed cell death pathways, especially ... ...

    Abstract The cellular recycling process of macroautophagy, which is the mechanism by which cellular material is delivered to lysosomes via double membraned vesicles called autophagosomes, is intimately connected to programmed cell death pathways, especially apoptosis. In this article, I discuss some underlying mechanisms and their implications for improving cancer therapy and propose that the approaches that have been taken to understand the autophagy-apoptosis connection to enhance cancer drug action can serve as a model for the kinds of information that should be developed to understand how autophagy controls other biological processes as well.
    Language English
    Publishing date 2020-05-18
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2471995-X
    ISSN 1878-0814 ; 0079-6603 ; 1877-1173
    ISSN (online) 1878-0814
    ISSN 0079-6603 ; 1877-1173
    DOI 10.1016/bs.pmbts.2020.04.023
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  3. Article ; Online: Enhancing anti-tumor immunity by autophagy inhibition.

    Thorburn, Andrew / Towers, Christina G

    Nature cancer

    2021  Volume 2, Issue 5, Page(s) 484–486

    MeSH term(s) Autophagy/immunology ; Humans ; Neoplasms/drug therapy
    Language English
    Publishing date 2021-05-03
    Publishing country England
    Document type Journal Article ; Comment
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-021-00214-8
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  4. Article ; Online: Autophagy and disease.

    Thorburn, Andrew

    The Journal of biological chemistry

    2017  Volume 293, Issue 15, Page(s) 5425–5430

    Abstract: As outlined in the accompanying Minireviews, autophagy is a complicated and highly regulated process that delivers cellular material to lysosomes for degrading, recycling, and generating molecules that fuel cellular metabolism. Autophagy is important for ...

    Abstract As outlined in the accompanying Minireviews, autophagy is a complicated and highly regulated process that delivers cellular material to lysosomes for degrading, recycling, and generating molecules that fuel cellular metabolism. Autophagy is important for normal cellular and organismal physiology, and both increased and decreased autophagy has been associated with disease. Importantly, these connections are already being exploited to treat patients with dozens of clinical trials that aim to manipulate autophagy to treat (or prevent) disease. This Minireview discusses some of the important issues and problems to be solved if these efforts are to be successful.
    MeSH term(s) Animals ; Autophagy ; Clinical Trials as Topic ; Humans
    Language English
    Publishing date 2017-11-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.R117.810739
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  5. Article ; Online: Autophagy and organelle homeostasis in cancer.

    Miller, Dannah R / Thorburn, Andrew

    Developmental cell

    2021  Volume 56, Issue 7, Page(s) 906–918

    Abstract: Beginning with the earliest studies of autophagy in cancer, there have been indications that autophagy can both promote and inhibit cancer growth and progression; autophagy regulation of organelle homeostasis is similarly complicated. In this review we ... ...

    Abstract Beginning with the earliest studies of autophagy in cancer, there have been indications that autophagy can both promote and inhibit cancer growth and progression; autophagy regulation of organelle homeostasis is similarly complicated. In this review we discuss pro- and antitumor effects of organelle-targeted autophagy and how this contributes to several hallmarks of cancer, such as evading cell death, genomic instability, and altered metabolism. Typically, the removal of damaged or dysfunctional organelles prevents tumor development but can also aid in proliferation or drug resistance in established tumors. By better understanding how organelle-specific autophagy takes place and can be manipulated, it may be possible to go beyond the brute-force approach of trying to manipulate all autophagy in order to improve therapeutic targeting of this process in cancer.
    MeSH term(s) Autophagy ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Homeostasis ; Humans ; Macroautophagy ; Mitophagy ; Neoplasms/metabolism
    Language English
    Publishing date 2021-03-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2021.02.010
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  6. Article ; Online: Autophagy and its effects: making sense of double-edged swords.

    Thorburn, Andrew

    PLoS biology

    2014  Volume 12, Issue 10, Page(s) e1001967

    Abstract: Autophagy is the mechanism by which cellular material is delivered to lysosomes and degraded. This process has become a major focus of biological and biomedical research with thousands of papers published each year and rapidly growing appreciation that ... ...

    Abstract Autophagy is the mechanism by which cellular material is delivered to lysosomes and degraded. This process has become a major focus of biological and biomedical research with thousands of papers published each year and rapidly growing appreciation that autophagy affects many normal and pathological processes. However, as we learn more about this evolutionarily ancient process, we are discovering that autophagy's effects may work for both the good and the bad of an organism. Here, I discuss some of these context-dependent findings and how, as we make sense of them, we can try to apply our knowledge for practical purposes.
    MeSH term(s) Animals ; Autophagy ; Bacterial Infections/physiopathology ; Humans ; Neoplasms/physiopathology
    Language English
    Publishing date 2014-10-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2126776-5
    ISSN 1545-7885 ; 1544-9173
    ISSN (online) 1545-7885
    ISSN 1544-9173
    DOI 10.1371/journal.pbio.1001967
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  7. Article ; Online: Autophagy inhibition improves anti-cancer drugs

    Fitzwalter, Brent E / Thorburn, Andrew

    Oncotarget

    2018  Volume 9, Issue 39, Page(s) 25384–25385

    Language English
    Publishing date 2018-05-22
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.25366
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  8. Article ; Online: Regulation of Apoptosis by Autophagy to Enhance Cancer Therapy.

    Tompkins, Kenneth D / Thorburn, Andrew

    The Yale journal of biology and medicine

    2019  Volume 92, Issue 4, Page(s) 707–718

    Abstract: In cancer therapy, a principle goal is to kill cancer cells while minimizing death of normal cells. Traditional cytotoxic therapies and the newer agents that target specific signaling proteins that are critical for cancer cell growth do this by ... ...

    Abstract In cancer therapy, a principle goal is to kill cancer cells while minimizing death of normal cells. Traditional cytotoxic therapies and the newer agents that target specific signaling proteins that are critical for cancer cell growth do this by activating a specific type of programmed cell death - apoptosis. However, it has been well established that cancer cells have varying levels of responses to apoptotic stimuli, with some being close to an "apoptotic threshold" and others being further away and that this ultimately determines whether cancer therapy is successful or not. In this review, we will highlight how the underlying mechanisms that control apoptosis thresholds relate to another important homeostatic process in cell survival and cell death, autophagy, and discuss recent evidence suggesting how inhibition of autophagy can enhance the action of anti-cancer drugs by modulating the apoptotic response.
    MeSH term(s) Animals ; Apoptosis ; Autophagy ; Clinical Trials as Topic ; Humans ; Models, Biological ; Molecular Targeted Therapy ; Neoplasms/pathology ; Neoplasms/therapy
    Language English
    Publishing date 2019-12-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 200515-3
    ISSN 1551-4056 ; 0044-0086
    ISSN (online) 1551-4056
    ISSN 0044-0086
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  9. Article ; Online: Circumventing autophagy inhibition.

    Towers, Christina G / Thorburn, Andrew

    Cell cycle (Georgetown, Tex.)

    2019  Volume 18, Issue 24, Page(s) 3421–3431

    Abstract: Autophagy is cellular recycling process that plays a complex role in cancer. Pre-clinical studies indicating a pro-tumorigenic role of autophagy have led to the launch of dozens of clinical trials combining autophagy inhibition with other standard of ... ...

    Abstract Autophagy is cellular recycling process that plays a complex role in cancer. Pre-clinical studies indicating a pro-tumorigenic role of autophagy have led to the launch of dozens of clinical trials combining autophagy inhibition with other standard of care therapies in different tumor types. A recent publication utilized a novel, acute, CRISPR/Cas9 assay to identify cancer cell lines that are exquisitely sensitive to loss of core autophagy genes within the first 7 days. However, weeks later, rare populations of originally autophagy dependent cells were found that could circumvent autophagy inhibition. Analysis of these rare clones revealed that in the process of circumventing loss of autophagy, the cells upregulated NRF2 signaling to maintain protein homeostasis and consequently become more sensitive to proteasome inhibition as well as knock down of NRF2. This review highlights recent publications regarding the role of autophagy in cancer and potential mechanisms cancer cells may be able to commandeer to circumvent autophagy inhibition. We hope to make significant clinical advances by understanding if and when cancer cells will become resistant to autophagy inhibition, and pre-clinical studies may be able to provide insight into the best combinatorial therapies to prevent tumor relapse while on autophagy inhibitors.
    MeSH term(s) Autophagy/genetics ; CRISPR-Cas Systems/genetics ; Carcinogenesis/genetics ; Cell Lineage/genetics ; Clonal Evolution/genetics ; Humans ; NF-E2-Related Factor 2/genetics ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/therapy ; Signal Transduction/genetics
    Chemical Substances NF-E2-Related Factor 2 ; NFE2L2 protein, human
    Language English
    Publishing date 2019-11-18
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2019.1692483
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  10. Article ; Online: Mitochondrial-derived vesicles compensate for loss of LC3-mediated mitophagy.

    Towers, Christina G / Wodetzki, Darya K / Thorburn, Jacqueline / Smith, Katharine R / Caino, M Cecilia / Thorburn, Andrew

    Developmental cell

    2021  Volume 56, Issue 14, Page(s) 2029–2042.e5

    Abstract: Mitochondria are critical metabolic and signaling hubs, and dysregulated mitochondrial homeostasis is implicated in many diseases. Degradation of damaged mitochondria by selective GABARAP/LC3-dependent macro-autophagy (mitophagy) is critical for ... ...

    Abstract Mitochondria are critical metabolic and signaling hubs, and dysregulated mitochondrial homeostasis is implicated in many diseases. Degradation of damaged mitochondria by selective GABARAP/LC3-dependent macro-autophagy (mitophagy) is critical for maintaining mitochondrial homeostasis. To identify alternate forms of mitochondrial quality control that functionally compensate if mitophagy is inactive, we selected for autophagy-dependent cancer cells that survived loss of LC3-dependent autophagosome formation caused by inactivation of ATG7 or RB1CC1/FIP200. We discovered rare surviving autophagy-deficient clones that adapted to maintain mitochondrial homeostasis after gene inactivation and identified two enhanced mechanisms affecting mitochondria including mitochondrial dynamics and mitochondrial-derived vesicles (MDVs). To further understand these mechanisms, we quantified MDVs via flow cytometry and confirmed an SNX9-mediated mechanism necessary for flux of MDVs to lysosomes. We show that the autophagy-dependent cells acquire unique dependencies on these processes, indicating that these alternate forms of mitochondrial homeostasis compensate for loss of autophagy to maintain mitochondrial health.
    MeSH term(s) Autophagy ; Autophagy-Related Protein 7/genetics ; Autophagy-Related Protein 7/metabolism ; Autophagy-Related Proteins/genetics ; Autophagy-Related Proteins/metabolism ; Endosomes/metabolism ; Humans ; Lysosomes ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Dynamics ; Mitophagy ; Sorting Nexins/genetics ; Sorting Nexins/metabolism ; Transport Vesicles/physiology
    Chemical Substances Autophagy-Related Proteins ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; RB1CC1 protein, human ; SNX9 protein, human ; Sorting Nexins ; ATG7 protein, human (EC 6.2.1.45) ; Autophagy-Related Protein 7 (EC 6.2.1.45)
    Language English
    Publishing date 2021-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2021.06.003
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