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  1. Article ; Online: Something Old and Something New to Unleash the Power of Natural Killer Cells against Metastases.

    Demaria, Sandra

    Cancer immunology research

    2021  Volume 10, Issue 1, Page(s) 3

    Abstract: Single-agent immunotherapy has improved outcomes for patients with cancer, but only a minority of patients respond, necessitating investigation of combinations of immunotherapy agents. In this issue ... ...

    Abstract Single-agent immunotherapy has improved outcomes for patients with cancer, but only a minority of patients respond, necessitating investigation of combinations of immunotherapy agents. In this issue of
    MeSH term(s) Animals ; Humans ; Immunotherapy ; Killer Cells, Natural ; Lung Neoplasms ; Mice ; Neoadjuvant Therapy ; Triple Negative Breast Neoplasms
    Language English
    Publishing date 2021-11-23
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2732489-8
    ISSN 2326-6074 ; 2326-6066
    ISSN (online) 2326-6074
    ISSN 2326-6066
    DOI 10.1158/2326-6066.CIR-21-0948
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7022: Show issues Location:
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  2. Article ; Online: Mammary pilar metaplasia.

    Stephan, Carla / Demaria, Sandra / Hoda, Syed A

    American journal of clinical pathology

    2024  

    Language English
    Publishing date 2024-03-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 2944-0
    ISSN 1943-7722 ; 0002-9173
    ISSN (online) 1943-7722
    ISSN 0002-9173
    DOI 10.1093/ajcp/aqae026
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  3. Article ; Online: CD40 agonism improves anti-tumor T cell priming induced by the combination of radiation therapy plus CTLA4 inhibition and enhances tumor response.

    Charpentier, Maud / Formenti, Silvia / Demaria, Sandra

    Oncoimmunology

    2023  Volume 12, Issue 1, Page(s) 2258011

    Abstract: Radiation therapy (RT) combined with CTLA4 blockers converts immunosuppressed (cold) mouse triple negative breast cancers (TNBCs) into immune infiltrated (hot) lesions. We have recently shown that targeting the myeloid compartment to improve dendritic ... ...

    Abstract Radiation therapy (RT) combined with CTLA4 blockers converts immunosuppressed (cold) mouse triple negative breast cancers (TNBCs) into immune infiltrated (hot) lesions. We have recently shown that targeting the myeloid compartment to improve dendritic cell activation is required for most TNBC-bearing mice to achieve superior therapeutic responses to RT plus CTLA4 inhibitors.
    MeSH term(s) Animals ; Mice ; Humans ; CTLA-4 Antigen ; Immune Checkpoint Inhibitors ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/radiotherapy ; T-Lymphocytes
    Chemical Substances CTLA-4 Antigen ; Immune Checkpoint Inhibitors ; CTLA4 protein, human
    Language English
    Publishing date 2023-09-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2645309-5
    ISSN 2162-402X ; 2162-402X
    ISSN (online) 2162-402X
    ISSN 2162-402X
    DOI 10.1080/2162402X.2023.2258011
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  4. Article ; Online: The interplay between the DNA damage response and ectonucleotidases modulates tumor response to therapy.

    Stagg, John / Golden, Encouse / Wennerberg, Erik / Demaria, Sandra

    Science immunology

    2023  Volume 8, Issue 85, Page(s) eabq3015

    Abstract: The extracellular nucleoside adenosine reduces tissue inflammation and is generated by irreversible dephosphorylation of adenosine monophosphate (AMP) mediated by the ectonucleotidase CD73. The pro-inflammatory nucleotides adenosine triphosphate, ... ...

    Abstract The extracellular nucleoside adenosine reduces tissue inflammation and is generated by irreversible dephosphorylation of adenosine monophosphate (AMP) mediated by the ectonucleotidase CD73. The pro-inflammatory nucleotides adenosine triphosphate, nicotinamide adenine dinucleotide, and cyclic guanosine -monophosphate-AMP (cGAMP), which are produced in the tumor microenvironment (TME) during therapy-induced immunogenic cell death and activation of innate immune signaling, can be converted into AMP by ectonucleotidases CD39, CD38, and CD203a/ENPP1. Thus, ectonucleotidases shape the TME by converting immune-activating signals into an immunosuppressive one. Ectonucleotidases also hinder the ability of therapies including radiation therapy, which enhance the release of pro-inflammatory nucleotides in the extracellular milieu, to induce immune-mediated tumor rejection. Here, we review the immunosuppressive effects of adenosine and the role of different ectonucleotidases in modulating antitumor immune responses. We discuss emerging opportunities to target adenosine generation and/or its ability to signal via adenosine receptors expressed by immune and cancer cells in the context of combination immunotherapy and radiotherapy.
    MeSH term(s) Humans ; Neoplasms/therapy ; Adenosine ; Adenosine Triphosphate ; Adenosine Monophosphate ; DNA Damage ; Tumor Microenvironment
    Chemical Substances Adenosine (K72T3FS567) ; Adenosine Triphosphate (8L70Q75FXE) ; Adenosine Monophosphate (415SHH325A)
    Language English
    Publishing date 2023-07-07
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abq3015
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  5. Article ; Online: Liver Metastasis Irradiation Can Restore Immunotherapeutic Responsiveness.

    Demaria, Sandra / Formenti, Silvia C

    Trends in immunology

    2021  Volume 42, Issue 4, Page(s) 275–277

    Abstract: Allogeneic liver transplants tolerize the immune system, preventing organ rejection from the same donor. A recent article by Yu et al. shows that liver metastases can likewise prevent tumor rejection in immunotherapy-treated murine and human hosts. ... ...

    Abstract Allogeneic liver transplants tolerize the immune system, preventing organ rejection from the same donor. A recent article by Yu et al. shows that liver metastases can likewise prevent tumor rejection in immunotherapy-treated murine and human hosts. Furthermore, radiation can reprogram the liver microenvironment to restore systemic tumor rejection.
    MeSH term(s) Animals ; Humans ; Immunotherapy ; Liver Neoplasms/therapy ; Macrophages ; Mice ; T-Lymphocytes ; Tumor Microenvironment
    Language English
    Publishing date 2021-02-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2021.02.007
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1601: Show issues Location:
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  6. Article: TREX1 is a checkpoint for innate immune sensing of DNA damage that fosters cancer immune resistance.

    Demaria, Sandra / Vanpouille-Box, Claire

    Emerging topics in life sciences

    2021  Volume 1, Issue 5, Page(s) 509–515

    Abstract: Genomic instability is a hallmark of neoplastic transformation that leads to the accumulation of mutations, and generates a state of replicative stress in neoplastic cells associated with dysregulated DNA damage repair (DDR) responses. The importance of ... ...

    Abstract Genomic instability is a hallmark of neoplastic transformation that leads to the accumulation of mutations, and generates a state of replicative stress in neoplastic cells associated with dysregulated DNA damage repair (DDR) responses. The importance of increasing mutations in driving cancer progression is well established, whereas relatively little attention has been devoted to the DNA displaced to the cytosol of cancer cells, a byproduct of genomic instability and of the ensuing DDR response. The presence of DNA in the cytosol promotes the activation of viral defense pathways in all cells, leading to activation of innate and adaptive immune responses. In fact, the improper accumulation of cytosolic DNA in normal cells is known to drive severe autoimmune pathology. Thus, cancer cells must evade cytoplasmic DNA detection pathways to avoid immune-mediated destruction. The main sensor for cytoplasmic DNA is the cyclic GMP-AMP synthase, cGAS. Upon activation by cytosolic DNA, cGAS catalyzes the formation of the second messenger cGAMP, which activates STING (stimulator of IFN genes), leading to the production of type I interferon (IFN-I). IFN-I is a critical effector of cell-mediated antiviral and antitumor immunity, and its production by cancer cells can be subverted by several mechanisms. However, the key upstream regulator of cytosolic DNA-mediated immune stimulation is the DNA exonuclease 3'-repair exonuclease 1 (TREX1). Here, we will discuss evidence in support of a role of TREX1 as an immune checkpoint that, when up-regulated, hinders the development of antitumor immune responses.
    Language English
    Publishing date 2021-01-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 2882721-1
    ISSN 2397-8554 ; 2397-8554 ; 2397-8562
    ISSN (online) 2397-8554
    ISSN 2397-8554 ; 2397-8562
    DOI 10.1042/ETLS20170063
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Live Imaging to Quantify Cellular Radiosensitivity in Patient-Derived Tumor Organoids.

    Charpentier, Maud / Bloy, Norma / Formenti, Silvia C / Galluzzi, Lorenzo / Demaria, Sandra

    Journal of visualized experiments : JoVE

    2024  , Issue 206

    Abstract: Radiation therapy (RT) is one of the mainstays of modern clinical cancer management. However, not all cancer types are equally sensitive to irradiation, often (but not always) because of differences in the ability of malignant cells to repair oxidative ... ...

    Abstract Radiation therapy (RT) is one of the mainstays of modern clinical cancer management. However, not all cancer types are equally sensitive to irradiation, often (but not always) because of differences in the ability of malignant cells to repair oxidative DNA damage as elicited by ionizing rays. Clonogenic assays have been employed for decades to assess the sensitivity of cultured cancer cells to ionizing irradiation, largely because irradiated cancer cells often die in a delayed manner that is difficult to quantify with short-term flow cytometry- or microscopy-assisted techniques. Unfortunately, clonogenic assays cannot be employed as such for more complex tumor models, such as patient-derived tumor organoids (PDTOs). Indeed, irradiating established PDTOs may not necessarily abrogate their growth as multicellular units, unless their stem-like compartment is completely eradicated. Moreover, irradiating PDTO-derived single-cell suspensions may not properly recapitulate the sensitivity of malignant cells to RT in the context of established PDTOs. Here, we detail an adaptation of conventional clonogenic assays that involves exposure of established PDTOs to ionizing radiation, followed by single-cell dissociation, replating in suitable culture conditions and live imaging. Non-irradiated (control) PDTO-derived stem-like cells reform growing PDTOs with a PDTO-specific efficiency, which is negatively influenced by irradiation in a dose-dependent manner. In these conditions, PDTO-forming efficiency and growth rate can be quantified as a measure of radiosensitivity on time-lapse images collected until control PDTOs achieve a predefined space occupancy.
    Language English
    Publishing date 2024-04-05
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/66680
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  8. Article ; Online: Future of Radiation and Immunotherapy.

    Formenti, Silvia C / Demaria, Sandra

    International journal of radiation oncology, biology, physics

    2020  Volume 108, Issue 1, Page(s) 3–5

    MeSH term(s) Humans ; Immunotherapy ; Neoplasms/immunology ; Neoplasms/radiotherapy ; Radiotherapy
    Language English
    Publishing date 2020-08-20
    Publishing country United States
    Document type Editorial
    ZDB-ID 197614-x
    ISSN 1879-355X ; 0360-3016
    ISSN (online) 1879-355X
    ISSN 0360-3016
    DOI 10.1016/j.ijrobp.2020.04.034
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    Zs.A 1218: Show issues Location:
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  9. Article: Pipeline to identify neoantigens exposed by radiation.

    Lhuillier, Claire / Van Nest, Samantha J / Rudqvist, Nils-Petter / Demaria, Sandra

    Methods in cell biology

    2023  Volume 180, Page(s) 25–37

    Abstract: Mutation-associated neoantigens are key targets of tumor-specific T cells and thus play a major role in driving responses to immune checkpoint blockade (ICB) therapy in tumors with high mutational burden. However, only a small number of mutated peptides ... ...

    Abstract Mutation-associated neoantigens are key targets of tumor-specific T cells and thus play a major role in driving responses to immune checkpoint blockade (ICB) therapy in tumors with high mutational burden. However, only a small number of mutated peptides are actually presented by MHC molecules and only a minority can induce T cell responses. In addition, the recognition of these neoantigens by T cells is limited by the level of expression of the mutated gene product in the tumor cells. Preclinical studies have shown that radiation can convert the irradiated tumor into an in situ vaccine, leading to the priming of tumor-specific T cells and to the rejection of otherwise ICB-resistant tumors. There is now preclinical and clinical evidence that radiation can upregulate the expression of genes containing immunogenic mutations and expose them to the immune system. Therefore, the identification of neoantigens upregulated by radiation could help to predict which patients might benefit from treatment with combinations of radiotherapy and ICB and could also be incorporated into personalized neoantigen vaccination strategies. In this chapter, we present the pipeline that we used to identify relevant radiation-upregulated neoantigens in a poorly immunogenic mouse model of metastatic breast cancer.
    MeSH term(s) Animals ; Mice ; Humans ; Antigens, Neoplasm/genetics ; Antigens, Neoplasm/chemistry ; Neoplasms/genetics ; Neoplasms/radiotherapy ; T-Lymphocytes ; Mutation ; Peptides
    Chemical Substances Antigens, Neoplasm ; Peptides
    Language English
    Publishing date 2023-04-06
    Publishing country United States
    Document type Journal Article
    ISSN 0091-679X
    ISSN 0091-679X
    DOI 10.1016/bs.mcb.2023.02.010
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  10. Article ; Online: Tumor-Associated Lymphocytes and Breast Cancer Survival in Black and White Women.

    Newman, Lisa A / Chen, Yalei / Martini, Rachel / Demaria, Sandra / Formenti, Silvia / Elemento, Olivier / Davis, Melissa B

    JAMA surgery

    2024  

    Language English
    Publishing date 2024-03-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2701841-6
    ISSN 2168-6262 ; 2168-6254
    ISSN (online) 2168-6262
    ISSN 2168-6254
    DOI 10.1001/jamasurg.2023.8024
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