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Artículos de revistas sobre el tema "Immunité antitumorale"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 25 de enero de 2025

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1

de Guillebon, E. y E. Tartour. "Immunité antitumorale (mécanismes, immunoediting, immunosurveillance)". Oncologie 17, n.º 9 (septiembre de 2015): 337–44. http://dx.doi.org/10.1007/s10269-015-2542-z.

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2

Kaplon, Hélène y Marie-Caroline Dieu-Nosjean. "Quel avenir pour les lymphocytes B infiltrant les tumeurs solides". médecine/sciences 34, n.º 1 (enero de 2018): 72–78. http://dx.doi.org/10.1051/medsci/20183401016.

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Le rôle des lymphocytes B (LB) dans l’immuno-surveillance des tumeurs a longtemps été négligé car il a été souvent considéré comme peu efficace, voire pro-tumoral. Des études approfondies du microenvironnement immunitaire, notamment dans les cancers humains, ont permis de préciser la nature des interactions entre le LB et ses partenaires cellulaires. Cette revue examine un certain nombre de paramètres qui dictent le devenir du LB vers une fonction pro-ou anti-tumorale. Ainsi, la capacité à élaborer une immunité antitumorale qui repose sur les lymphocytes B, et/ ou des anticorps qu’ils sécrètent, fait appel à une palette très variée de mécanismes moléculaires et cellulaires dont certains pourraient représenter de nouvelles cibles thérapeutiques en oncologie.
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3

Ladjemi Maha, Z., T. Chardès, S. Corgnac, V. Garambois, S. Morisseau, B. Robert, C. Bascoul-Mollevi et al. "R109: Vaccination à l’aide de scFv humains anti-trastuzumab : réversion de la tolérance immunologique vis-à-vis de HER2 et induction d’une immunité antitumorale dans les souris MMTV. f.huHER2(Fo5)". Bulletin du Cancer 97, n.º 4 (octubre de 2010): S58. http://dx.doi.org/10.1016/s0007-4551(15)31028-6.

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4

von Kieseritzky, Kathrin. "Antitumorale Immunität beim fortgeschrittenen Mammakarzinom". Im Focus Onkologie 20, n.º 4 (abril de 2017): 28. http://dx.doi.org/10.1007/s15015-017-3237-7.

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5

Sankawa, Yuri. "Das Immunsystem - wie entsteht antitumorale Immunität?" Oncology Research and Treatment 37, n.º 4 (2014): 2–5. http://dx.doi.org/10.1159/000366431.

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6

Kozlova, A. I., E. V. Voropayev y A. I. Konoplya. "THE ROLE OF DENDRITIC CELLS IN FORMATION OF ANTITUMORAL IMMUNITY (literature review)". Health and Ecology Issues, n.º 4 (28 de diciembre de 2014): 19–24. http://dx.doi.org/10.51523/2708-6011.2014-11-4-3.

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At present, dendritic cells are thought to be the main «professional» antigenpresenting cells. They play the leading role in the triggering of the adaptive immune response and its integration with inborn immunity. These properties of dendritic cells determine significant interest for their possible use as a base for making antitumoral vaccines. The results of the study testify about the amplification of the lymphocytes antitumoral activity in relation to the types of tumors against which DC-vaccination was carried out.
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7

Dmitrievskaya, M., D. Ibragimova, A. Useinova y A. Rebik. "THE ROLE OF IMMUNE CHECKPOINT INHIBITORS IN ANTITUMORAL IMMUNITY". Crimea Journal of Experimental and Clinical Medicine 11, n.º 3 (8 de noviembre de 2022): 93–99. http://dx.doi.org/10.29039/2224-6444-2021-11-3-93-99.

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Currently immunotherapy is becoming a fairly effective approach in the fight against various forms of malignant neoplasms. This is due to the discovery and use in clinical practice immune checkpoint inhibitors, which antitumoral effect is associated with blockage the signaling pathways CTLA-4 (cytotoxic T-lymphocyte associated protein 4), PD-1 (programmed cell death protein 1), PD-L1 (programmed cell death ligand 1). The physiological role of immune points is to prevent autoimmune tissue damage by suppressing effectors. How- ever, cancer cells have adapted for using this mechanism to avoid elimination by escape mechanisms from immuno- logical surveillance. This gave impetus to the development of drugs that can inhibit checkpoints, enabling the immune system to destroy tumor cells. Actually, 7 drugs have been registered, which can be divided into three groups according to the mechanism of action: CTLA-4 (pilimumab), PD-1 (nivolumab, pembrolizumab, prolgolimab) and PD-L1 (atezoli- zumab, avelumab, durvalumab) inhibitors. The medicine of the first group inhibits the cellular response at the stage of its activation. The mechanism of action of the second and third groups medicines is aimed at blocking the binding of the PD-1 receptor of lymphocytes and monocytes with PD-L1 ligands and vice versa. The use of immune checkpoint inhibitors can lead to the occurrence of immune-mediated adverse reactions, the nature and frequency of which differ depending on the class of inhibitors. In this regard, timely diagnosis and treatment of complications is the key to the success of anticancer therapy.
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8

Riachi, Mansour E., Carolina G. Alcantara Hirsch, Anthony Sorrentino, Erica Ma, Beny Shapiro, Christopher L. Wolfgang y Dafna Bar-Sagi. "681 EXERCISE STIMULATES ANTITUMORAL IMMUNITY IN PANCREATIC DUCTAL ADENOCARCINOMA". Gastroenterology 166, n.º 5 (mayo de 2024): S—1809—S—1810. http://dx.doi.org/10.1016/s0016-5085(24)04639-0.

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9

Hernández, Ángela-Patricia, Pablo Juanes-Velasco, Alicia Landeira-Viñuela, Halin Bareke, Enrique Montalvillo, Rafael Góngora y Manuel Fuentes. "Restoring the Immunity in the Tumor Microenvironment: Insights into Immunogenic Cell Death in Onco-Therapies". Cancers 13, n.º 11 (5 de junio de 2021): 2821. http://dx.doi.org/10.3390/cancers13112821.

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Immunogenic cell death (ICD) elicited by cancer therapy reshapes the tumor immune microenvironment. A long-term adaptative immune response can be initiated by modulating cell death by therapeutic approaches. Here, the major hallmarks of ICD, endoplasmic reticulum (ER) stress, and damage-associated molecular patterns (DAMPs) are correlated with ICD inducers used in clinical practice to enhance antitumoral activity by suppressing tumor immune evasion. Approaches to monitoring the ICD triggered by antitumoral therapeutics in the tumor microenvironment (TME) and novel perspective in this immune system strategy are also reviewed to give an overview of the relevance of ICD in cancer treatment.
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10

Baleydier, Frederic, Fanette Bernard y Marc Ansari. "The Possibilities of Immunotherapy for Children with Primary Immunodeficiencies Associated with Cancers". Biomolecules 10, n.º 8 (28 de julio de 2020): 1112. http://dx.doi.org/10.3390/biom10081112.

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Many primary immunodeficiencies (PIDs) are recognised as being associated with malignancies, particularly lymphoid malignancies, which represent the highest proportion of cancers occurring in conjunction with this underlying condition. When patients present with genetic errors of immunity, clinicians must often reflect on whether to manage antitumoral treatment conventionally or to take a more personalised approach, considering possible existing comorbidities and the underlying status of immunodeficiency. Recent advances in antitumoral immunotherapies, such as monoclonal antibodies, antigen-specific adoptive cell therapies or compounds with targeted effects, potentially offer significant opportunities for optimising treatment for those patients, especially with lymphoid malignancies. In cases involving PIDs, variable oncogenic mechanisms exist, and opportunities for antitumoral immunotherapies can be considered accordingly. In cases involving a DNA repair defect or genetic instability, monoclonal antibodies can be proposed instead of chemotherapy to avoid severe toxicity. Malignancies secondary to uncontrolled virus-driven proliferation or the loss of antitumoral immunosurveillance may benefit from antivirus cell therapies or allogeneic stem cell transplantation in order to restore the immune antitumoral caretaker function. A subset of PIDs is caused by gene defects affecting targetable signalling pathways directly involved in the oncogenic process, such as the constitutive activation of phosphoinositol 3-kinase/protein kinase B (PI3K/AKT) in activated phosphoinositide 3-kinase delta syndrome (APDS), which can be settled with PI3K/AKT inhibitors. Therefore, immunotherapy provides clinicians with interesting antitumoral therapeutic weapons to treat malignancies when there is an underlying PID.
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11

Martsenyuk, V. P. "Construction and study of stability of an antitumoral immunity model". Cybernetics and Systems Analysis 40, n.º 5 (septiembre de 2004): 778–83. http://dx.doi.org/10.1007/s10559-005-0017-8.

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12

Min, Daniel, Jacob Fiedler y Niroshana Anandasabapathy. "Tissue-resident memory cells in antitumoral immunity and cancer immunotherapy". Current Opinion in Immunology 91 (diciembre de 2024): 102499. http://dx.doi.org/10.1016/j.coi.2024.102499.

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13

Urzúa S., Cristhian A., Mercedes López N., Andrea Pardo Q., Ana Adélia Ribeiro D., Fabián Tempio S., Sergio Abuauad A. y Darío H. Vásquez Z. "Inmunidad antitumoral en neoplasias intraoculares". Revista Hospital Clínico Universidad de Chile 24, n.º 3 (1 de septiembre de 2013): 221–34. http://dx.doi.org/10.5354/2735-7996.2013.73292.

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A physiological function of the immune system is to recognize and destroy cells transformed clones before they become tumors and eliminate tumors after they are formed. This is accomplished by innate and adaptive immune responses, however is a complex task considering the mechanisms of evasion by tumors. Particularly, intraocular neoplasms (ION) would have an advantage against the immune system because the eye is considered a site of immune privilege that through anatomical, physiological and immunoregulatory mechanisms restrict the immune response. Regulatory T lymphocytes(Treg) subtype CD4 + CD25 + Foxp3 + and IL-10 producers, would be crucial in induction of self-tolerance .The loss of balance between proinflammatory profile given by LTh1 and LTh17 and its production of IFN-g and IL-17 versus the modulating function of Treg secreting IL-10 and TGF-β determines a faster tumor growth or not. There is still no conclusive evidence determining the specific mechanisms of immune imbalance in the ION. In this review we updated an overview of antitumor immunity, its particularities to intraocular level and current evidence about echanisms of immune evasion in most common primary malignant ION in adults: uveal melanoma and primary intraocular lymphoma.
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14

Schmidt, Nathalie y Robert Thimme. "Role of Immunity in Pathogenesis and Treatment of Hepatocellular Carcinoma". Digestive Diseases 34, n.º 4 (2016): 429–37. http://dx.doi.org/10.1159/000444558.

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Background: Hepatocellular carcinoma (HCC) is the sixth most common malignancy worldwide with a high mortality. The available treatment options are limited, thus the development of new therapeutic approaches is of a high clinical significance. Key Messages: The immune system plays a central role in the pathogenesis of HCC by supporting tumor growth, tumor survival, angiogenesis and the development of vascular infiltration and metastasis. In contrast, the immune system also exhibits a protective role in tumor surveillance, and specific CD8+ T-cells can be detected for various tumor-associated antigens. However, antitumoral potential of the immune system is limited by various inhibitory mechanisms, for example, an impaired priming and activation of CD8+ T-cells, inhibitory cells (e.g., regulatory T-cells) or the expression of inhibitory receptors (e.g., programmed cell death-1 and cytotoxic T-lymphocyte antigen-4). Immunotherapeutic strategies addressing these inhibitory mechanisms, for example, by providing a source of tumor antigens, depleting immunosuppressive cells or blocking inhibitory receptors, aim to induce and boost naturally occurring antitumoral immune responses. Conclusion: HCC is a tumor with a high incidence and mortality in developing countries as well as in the Western world. Due to the immune system's central role in the pathogenesis and surveillance of HCC, immunotherapy is a new treatment option that has yielded first promising results.
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15

Todaro, Biagio, Silvia Achilli, Benjamin Liet, Eugénie Laigre, Claire Tiertant, David Goyard, Nathalie Berthet y Olivier Renaudet. "Structural influence of antibody recruiting glycodendrimers (ARGs) on antitumoral cytotoxicity". Biomaterials Science 9, n.º 11 (2021): 4076–85. http://dx.doi.org/10.1039/d1bm00485a.

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A series of Antibody Recruiting Glycodendrimer (ARG) was screened against the melanoma cell line M21. We identified lead ARGs that promote up to 57% of selective cytotoxicity in the presence of human serum as the unique source of immunity effectors.
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16

Anfray, Clément, Francesco Mainini, Elisabeth Digifico, Akihiro Maeda, Marina Sironi, Marco Erreni, Achille Anselmo et al. "Intratumoral combination therapy with poly(I:C) and resiquimod synergistically triggers tumor-associated macrophages for effective systemic antitumoral immunity". Journal for ImmunoTherapy of Cancer 9, n.º 9 (septiembre de 2021): e002408. http://dx.doi.org/10.1136/jitc-2021-002408.

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BackgroundTumor-associated macrophages (TAMs) play a key immunosuppressive role that limits the ability of the immune system to fight cancer and hinder the antitumoral efficacy of most treatments currently applied in the clinic. Previous studies have evaluated the antitumoral immune response triggered by (TLR) agonists, such as poly(I:C), imiquimod (R837) or resiquimod (R848) as monotherapies; however, their combination for the treatment of cancer has not been explored. This study investigates the antitumoral efficacy and the macrophage reprogramming triggered by poly(I:C) combined with R848 or with R837, versus single treatments.MethodsTLR agonist treatments were evaluated in vitro for toxicity and immunostimulatory activity by Alamar Blue, ELISA and flow cytometry using primary human and murine M-CSF-differentiated macrophages. Cytotoxic activity of TLR-treated macrophages toward cancer cells was evaluated with an in vitro functional assay by flow cytometry. For in vivo experiments, the CMT167 lung cancer model and the MN/MCA1 fibrosarcoma model metastasizing to lungs were used; tumor-infiltrating leukocytes were evaluated by flow cytometry, RT-qPCR, multispectral immunophenotyping, quantitative proteomic experiments, and protein–protein interaction analysis.ResultsResults demonstrated the higher efficacy of poly(I:C) combined with R848 versus single treatments or combined with R837 to polarize macrophages toward M1-like antitumor effectors in vitro. In vivo, the intratumoral synergistic combination of poly(I:C)+R848 significantly prevented tumor growth and metastasis in lung cancer and fibrosarcoma immunocompetent murine models. Regressing tumors showed increased infiltration of macrophages with a higher M1:M2 ratio, recruitment of CD4+ and CD8+ T cells, accompanied by a reduction of immunosuppressive CD206+ TAMs and FOXP3+/CD4+ T cells. The depletion of both CD4+ and CD8+ T cells resulted in complete loss of treatment efficacy. Treated mice acquired systemic antitumoral response and resistance to tumor rechallenge mediated by boosted macrophage cytotoxic activity and T-cell proliferation. Proteomic experiments validate the superior activation of innate immunity by poly(I:C)+R848 combination versus single treatments or poly(I:C)+R837, and protein–protein-interaction network analysis reveal the key activation of the STAT1 pathway.DiscussionThese findings demonstrate the antitumor immune responses mediated by macrophage activation on local administration of poly(I:C)+R848 combination and support the intratumoral application of this therapy to patients with solid tumors in the clinic.
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17

Pérez, Marina, Berta Buey, Pilar Corral, David Giraldos y Eva Latorre. "Microbiota-Derived Short-Chain Fatty Acids Boost Antitumoral Natural Killer Cell Activity". Journal of Clinical Medicine 13, n.º 13 (2 de julio de 2024): 3885. http://dx.doi.org/10.3390/jcm13133885.

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Background: The intestinal microbiota can regulate numerous host functions, including the immune response. Through fermentation, the microbiota produces and releases microbial metabolites such as short-chain fatty acids (SCFAs), which can affect host homeostasis. There is growing evidence that the gut microbiome can have a major impact on cancer. Specific gut microbial composition and metabolites are associated with tumor status in the host. However, their effects on the antitumor response have scarcely been investigated. Natural killer (NK) cells play an important role in antitumor immunity due to their ability to directly identify and eliminate tumor cells. Methods: The aim of this study was to investigate the effects of SCFAs on antitumoral NK cell activity, using NK-92 cell line. Results: Here, we describe how SCFAs can boost antitumoral NK cell activity. The SCFAs induced the release of NK extracellular vesicles and reduced the secretion of the anti-inflammatory cytokine IL-10. The SCFAs also increased the cytotoxicity of the NK cells against multiple myeloma cells. Conclusions: Our results indicate, for the first time, the enormous potential of SCFAs in regulating antitumoral NK cell defense, where modulation of the SCFAs’ production could play a fundamental role in cancer immunotherapy.
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18

Schürch, Christian M., Salil S. Bhate, Graham L. Barlow, Darci J. Phillips, Luca Noti, Inti Zlobec, Pauline Chu et al. "Coordinated Cellular Neighborhoods Orchestrate Antitumoral Immunity at the Colorectal Cancer Invasive Front". Cell 182, n.º 5 (septiembre de 2020): 1341–59. http://dx.doi.org/10.1016/j.cell.2020.07.005.

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19

Schürch, Christian M., Salil S. Bhate, Graham L. Barlow, Darci J. Phillips, Luca Noti, Inti Zlobec, Pauline Chu et al. "Coordinated Cellular Neighborhoods Orchestrate Antitumoral Immunity at the Colorectal Cancer Invasive Front". Cell 183, n.º 3 (octubre de 2020): 838. http://dx.doi.org/10.1016/j.cell.2020.10.021.

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20

Mustafa, Abdul Rehman, Dominie Miyasato y Eric Wehrenberg-Klee. "Synergizing Thermal Ablation Modalities with Immunotherapy: Enough to Induce Systemic Antitumoral Immunity?" Journal of Vascular and Interventional Radiology 35, n.º 2 (febrero de 2024): 185–97. http://dx.doi.org/10.1016/j.jvir.2023.10.033.

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21

Kovalovsky, Damian, Satish Noonepalle, Manasa Suresh, Dileep Kumar, Michael Berrigan, Anelia Horvath, Allen Kim, David Quiceno-Torres, Karthik Musunuri y Alejandro Villagra. "Abstract 1421: The HDAC6-specific inhibitor AVS100 (SS208) blocks M2 polarization of tumor associated macrophages and potentiates immunotherapy in preclinical tumor models". Cancer Research 84, n.º 6_Supplement (22 de marzo de 2024): 1421. http://dx.doi.org/10.1158/1538-7445.am2024-1421.

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Abstract Inhibition of HDAC6 was associated with an increased proinflammatory tumor microenvironment and an antitumoral response. Here, we show that a highly specific HDAC6 inhibitor AVS100 (SS208), blocks M2 polarization in murine and human macrophages while partially affecting M1 polarization. AVS100 effects were observed as blocked upregulation of M2-related gene signature under M2 polarizing conditions and blocked generation of CD206+ and Arg1+ macrophages. Oral administration of AVS100 had an antitumoral effect in SM1 melanoma and CT26 colon cancer models and increased the efficacy of anti-PD1 treatment, leading to complete remission in melanoma and increased response in colon cancer. Flow cytometry and scRNAseq analysis of tumor-infiltrating immune cells revealed an increase of proinflammatory/anti-inflammatory ratio in tumor-associated macrophages as well as an increase of intratumoral CD8 effector T-cells after AVS100 treatment. Interestingly, cured mice didn’t relapse and became resistant to a subsequent tumor challenge, suggesting acquired antitumoral T-cell immunity. T-cell repertoire analysis of effector/memory T-cells in cured mice revealed a higher number of immunodominant T-cell clones after AVS100 treatment, indicating increased T-cell expansion. Finally, AVS100 has demonstrated no mutagenicity and a strong safety profile in rats and dogs, leading to its recent U.S. FDA clearance of an Investigational New Drug (IND) application and planned initiation of Phase Ia/b clinical trials targeting locally advanced or metastatic solid tumors in the first half of 2024. Altogether, we have performed the preclinical characterization of a novel small molecule inhibitor targeting HDAC6 for solid cancers. AVS100 had an antitumoral effect as single agent and improved the efficacy of immune checkpoint inhibition by blocking the immunoregulatory tumor microenvironment and increasing T-cell immunity. Citation Format: Damian Kovalovsky, Satish Noonepalle, Manasa Suresh, Dileep Kumar, Michael Berrigan, Anelia Horvath, Allen Kim, David Quiceno-Torres, Karthik Musunuri, Alejandro Villagra. The HDAC6-specific inhibitor AVS100 (SS208) blocks M2 polarization of tumor associated macrophages and potentiates immunotherapy in preclinical tumor models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1421.
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22

Dong, Haidong. "Targeting molecular and cellular inhibitory mechanisms for improvement in anti-tumor memory responses reactivated by tumor cell vaccine (50.17)". Journal of Immunology 178, n.º 1_Supplement (1 de abril de 2007): S93. http://dx.doi.org/10.4049/jimmunol.178.supp.50.17.

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Abstract Development of effective vaccination approaches to treat established tumors represents a focus of intensive research because such approaches offer the promise of enhancing immune system priming against tumor antigens via re-stimulation of pre-existing (memory) antitumoral helper and effector immune cells. However, inhibitory mechanisms which function to limit the recall responses of tumor-specific immunity exist remain poorly understood and interfere with therapies anticipated to induce protective immunity. The mouse renal cell carcinoma (RENCA) tumor model was used to investigate variables affecting vaccination outcomes. We demonstrate that although a whole cell irradiated tumor cell vaccine can trigger a functional anti-tumor memory response in the bone marrows of mice with established tumors, these responses do not culminate in the regression of established tumors. In addition, a CD103+ regulatory T (Treg) cell subset accumulates within the draining lymph nodes of tumor-bearing mice. We also show that B7-H1 (CD274, PD-L1), a negative costimulatory ligand, and CD4+ Treg cells collaborate to impair the recall responses of tumor-specific memory T cells. Specifically, mice bearing large established RENCA tumors were treated with tumor cell vaccination in combination with B7-H1 blockade and CD4+ T cell depletion (triple therapy treatment) and monitored for tumor growth and survivability. Triple treatment therapy induced complete regression of large established RENCA tumors and raised long-lasting protective immunity. These results have implications for developing clinical antitumoral vaccination regimens in the setting where tumors express elevated levels of B7-H1 in the presence of abundant Treg cells.
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23

Mattiola, Irene. "Immune Circuits to Shape Natural Killer Cells in Cancer". Cancers 13, n.º 13 (28 de junio de 2021): 3225. http://dx.doi.org/10.3390/cancers13133225.

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Natural killer (NK) cells are innate lymphoid cells playing an important role in anti-cancer immunity. NK cells are efficient in controlling the spreading of metastasis but are not very powerful in fighting against primary tumors. The NK cell capability to infiltrate and persist in the tumor microenvironment and to exert their antitumoral functions is often limited by tumor escape mechanisms. These tumor-mediated strategies not only induce NK cell tolerance but also interfere with the NK cell-dependent immune networking. This review will provide an overview of the tumor escape mechanisms impacting NK cells, identify the immune circuits regulating the NK cell-dependent antitumor immunity and revise the emerging therapeutic approaches to unleash NK cells in cancer.
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24

Jutzy, Jessica M. S., Jeffrey M. Lemons, Jason J. Luke y Steven J. Chmura. "The Evolution of Radiation Therapy in Metastatic Breast Cancer: From Local Therapy to Systemic Agent". International Journal of Breast Cancer 2018 (2018): 1–7. http://dx.doi.org/10.1155/2018/4786819.

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Radiation therapy is a mainstay of treatment in early and locally advanced breast cancer but is typically reserved for palliation of symptomatic lesions in patients with metastatic breast cancer. With new advances in the field of tumor biology and immunology, the role of radiation in the metastatic setting is evolving to harness its immune-enhancing properties. Through the release of tumor antigens, tumor DNA, and cytokines into the tumor microenvironment, radiation augments the antitumoral immune response to affect both the targeted lesion and distant sites of metastatic disease. The use of immunotherapeutics to promote antitumoral immunity has resulted in improved treatment responses in patients with metastatic disease and the combination of radiation therapy and immunotherapy has become an area of intense investigation. In this article, we will review the emerging role of radiation in the treatment of metastatic disease and discuss the current state of the science and clinical trials investigating the combination of radiation and immunotherapy.
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25

Bourquin, Carole, David Anz, Klaus Zwiorek, Anna-Lisa Lanz, Sebastian Fuchs, Sarah Weigel, Cornelia Wurzenberger et al. "Targeting CpG Oligonucleotides to the Lymph Node by Nanoparticles Elicits Efficient Antitumoral Immunity". Journal of Immunology 181, n.º 5 (19 de agosto de 2008): 2990–98. http://dx.doi.org/10.4049/jimmunol.181.5.2990.

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Reis-Sobreiro, Mariana, Afonso Teixeira da Mota, Carolina Jardim y Karine Serre. "Bringing Macrophages to the Frontline against Cancer: Current Immunotherapies Targeting Macrophages". Cells 10, n.º 9 (9 de septiembre de 2021): 2364. http://dx.doi.org/10.3390/cells10092364.

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Macrophages are found in all tissues and display outstanding functional diversity. From embryo to birth and throughout adult life, they play critical roles in development, homeostasis, tissue repair, immunity, and, importantly, in the control of cancer growth. In this review, we will briefly detail the multi-functional, protumoral, and antitumoral roles of macrophages in the tumor microenvironment. Our objective is to focus on the ever-growing therapeutic opportunities, with promising preclinical and clinical results developed in recent years, to modulate the contribution of macrophages in oncologic diseases. While the majority of cancer immunotherapies target T cells, we believe that macrophages have a promising therapeutic potential as tumoricidal effectors and in mobilizing their surroundings towards antitumor immunity to efficiently limit cancer progression.
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Kaymak, D., T. Shekarian, M. Ritz, N. Ferrari, R. Kälin, R. Glass y G. Hutter. "P12.15.A THE IMPACT OF MICROGLIA MODULATION ON THE IMMUNE TUMOR MICROENVIRONMENT IN SYNGENEIC GLIOBLASTOMA MOUSE MODELS". Neuro-Oncology 25, Supplement_2 (1 de septiembre de 2023): ii100. http://dx.doi.org/10.1093/neuonc/noad137.334.

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Abstract BACKGROUND Glioblastoma is exceptionally resistant to T-cell targeting immunotherapies for which the immunosuppressive myeloid compartment is held responsible. As influencer and instructor of antitumoral T-cell-immunity this compartment mainly consists of Monocyte-derived Cells (MdCs) and tissue-resident (TR) macrophages called microglia (MG). Since the response to immunotherapies depend on antigen presenting cells at the tumor site, we aim to investigate this compartment and its individual role in tumor progression by genetically depleting/activating the TR MG. METHODS We made use of two MG-specific and tamoxifen inducible knockout mouse models in which 1) we activate MG by excision of the activation-repressing transcription factor Sall1 (Sall1CreERT2/wt x Sall1fl/wt) and 2) deplete MG by deleting the “survival-receptor” Csf1r on MG (Sall1CreERT2/wt x Csf1rfl/fl). To investigate the effect of MG activation and depletion on the immune tumor microenvironment (iTME), immunocompetent mice were engrafted with syngeneic glioma cells (CT-2A, GL261) and the iTME subsequently characterized by scRNAseq, spectral flow cytometry and immunofluorescence imaging. RESULTS Upon Sall1-KO MG demonstrate a morphologically reactive phenotype reminiscent of activated MG. The MG-specific deletion of Csf1r effectively depletes the brain parenchyma of TR MG which rapidly gets repopulated by a morphologically distinct microglia-(like) population. Genetic activation of MG leads to a survival benefit in Gl261-engrafted mice compared to Cre-negative littermates. In contrast, depletion of MG significantly reduces the survival in Gl261 and CT-2A engrafted mice. ScRNAseq confirms the effective depletion of MG and the subsequent emergence of a microglia-like cell population that despite microscopical resemblance to MG, transcriptionally remains distinct. The iTME in MG-depleted mice is characterized by a decreased abundance of exhausted and naïve CD8-Tcells and an increased infiltration of MdCs. Gene set enrichment analysis demonstrate a dampened inflammatory immune profile of infiltrating MdCs highlighted by a downregulation of hallmark gene sets of “interferon-α and γ response” and “TNFα-signaling via NF-κB”. CONCLUSION The presence of MG orchestrate the development towards a more antitumorigenic iTME by shaping the antitumoral response of incoming myeloid cells and furthermore directly or indirectly influencing T-cell immunity. Understanding this interplay of MG and MdCs in cancer and its impact on instruction of antitumoral T-cell immunity could help guiding the development of novel immunotherapeutic strategies in GBM.
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28

Kreiter, Sebastian, Abderraouf Selmi, Mustafa Diken, Michael Koslowski, Cedrik M. Britten, Christoph Huber, Özlem Türeci y Ugur Sahin. "Intranodal Vaccination with Naked Antigen-Encoding RNA Elicits Potent Prophylactic and Therapeutic Antitumoral Immunity". Cancer Research 70, n.º 22 (2 de noviembre de 2010): 9031–40. http://dx.doi.org/10.1158/0008-5472.can-10-0699.

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29

Erlach, Katja C., Verena Böhm, Christof K. Seckert, Matthias J. Reddehase y Jürgen Podlech. "Lymphoma Cell Apoptosis in the Liver Induced by Distant Murine Cytomegalovirus Infection". Journal of Virology 80, n.º 10 (15 de mayo de 2006): 4801–19. http://dx.doi.org/10.1128/jvi.80.10.4801-4819.2006.

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ABSTRACT Cytomegalovirus (CMV) poses a threat to the therapy of hematopoietic malignancies by hematopoietic stem cell transplantation, but efficient reconstitution of antiviral immunity prevents CMV organ disease. Tumor relapse originating from a minimal residual leukemia poses another threat. Although a combination of risk factors was supposed to enhance the incidence and severity of transplantation-associated disease, a murine model of a liver-adapted B-cell lymphoma has previously shown a survival benefit and tumor growth inhibition by nonlethal subcutaneous infection with murine CMV. Here we have investigated the underlying antitumoral mechanism. Virus replication proved to be required, since inactivated virions or the highly attenuated enhancerless mutant mCMV-ΔMIEenh did not impact the lymphoma in the liver. Surprisingly, the dissemination-deficient mutant mCMV-ΔM36 inhibited tumor growth, even though this virus fails to infect the liver. On the other hand, various strains of herpes simplex viruses consistently failed to control the lymphoma, even though they infect the liver. A quantitative analysis of the tumor growth kinetics identified a transient tumor remission by apoptosis as the antitumoral effector mechanism. Tumor cell colonies with cells surviving the CMV-induced “apoptotic crisis” lead to tumor relapse even in the presence of full-blown tissue infection. Serial transfer of surviving tumor cells did not indicate a selection of apoptosis-resistant genetic variants. NK cell activity of CD49b-expressing cells failed to control the lymphoma upon adoptive transfer. We propose the existence of an innate antitumoral mechanism that is triggered by CMV infection and involves an apoptotic signal effective at a distant site of tumor growth.
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30

Riva, Erika, Susanna Carboni, Wilma di Berardino-Besson, Mati Moyat, Elodie Belnoue, Laetitia Devy-Dimanche y Matteo Rossi. "Bimodal Effect of NKG2A Blockade on Intratumoral and Systemic CD8 T Cell Response Induced by Cancer Vaccine". Cancers 16, n.º 11 (27 de mayo de 2024): 2036. http://dx.doi.org/10.3390/cancers16112036.

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Immune check-point blockade (ICB) has revitalized cancer immunotherapy, showing unprecedented efficacy despite only a narrow number of indications and with limited long-term protection. Cancer vaccines are promising combination partners for ICB to widen the patient population profiting from these treatments. Therapeutic heterologous prime-boost vaccination with KISIMATM protein vaccine and VSV-GP-TAg oncolytic virus was shown to inflame the tumor microenvironment, promoting significant infiltration of antigen-specific CD8 T cells resulting in robust antitumoral efficacy in mouse tumor models, and clinical trials are currently ongoing. Here, we report the impact of NKG2A blockade on antitumoral CD8 T cell immune response elicited by KISIMA—VSV-GP-TAg vaccination in tumor mouse models. Combination therapy significantly reduced the amount of vaccine-induced exhausted CD8 T cells infiltrating the tumor, resulting in short-term improved tumor growth control and prolonged mouse survival, while it also influenced the establishment of systemic effector memory CD8 T cell response. Taken together, these data show a compartment-dependent effect of NKG2A blockade on cancer vaccine-induced T cell immunity, increasing intratumoral T cell efficacy and attenuating the development of peripheral effector memory CD8 T cell response.
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31

Ummarino, Aldo, Clément Anfray, Andrea Mariancini, Domenico Supino, Cecilia Garlanda, Fernando Torres Andòn, Alberto Mantovani y Paola Allavena. "Abstract 5140: Combined administration of poly(I:C) and resiquimod triggers effective antitumoral response in mouse models of pancreatic adenocarcinoma". Cancer Research 83, n.º 7_Supplement (4 de abril de 2023): 5140. http://dx.doi.org/10.1158/1538-7445.am2023-5140.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) represents one of the deadliest malignancies worldwide. The lack of clinical symptoms in the early stages of the disease and the poor immunogenicity of PDAC are two major causes of late diagnosis and inefficient therapies. The tumor microenvironment of PDAC is rich in stromal cells inducing desmoplasia, complicating the arrival of medical compounds, as well as in immune cells, that are suppressed by several mediators produced by cancer cells. In this setting, it has been shown that some medications can restore the antitumoral activity of innate immune cells that, in turn, re-activate also adaptive immune cells. In this study, we present the combination of the TLR agonists poly(I:C) (pIC - TLR3) and resiquimod (R848 - TLR7/8) as an immunotherapeutic tool in PDAC. In a subcutaneous model of PDAC (K8484 cells, isolated from KPC mice that spontaneously develop PDAC and recapitulate the features of human pancreatic cancer), the intratumoral administration of pIC+R848 for 5 times every 2-3 days led to the complete regression of the tumor in 100% of the treated mice. Moreover, all mice were protected from a second and a third rechallenge with the same cell line, performed months after the first treatments. Mechanistic studies performed on the tumors with flow cytometry demonstrated an increase of MHC-II positive cells in the monocytic (Ly6C+) compartment, as well as an increase in the number of mature CD8+ T cells and NK cells. Similar findings were demonstrated also in another heterotopic model obtained injecting Panc02 cells, another cell line with a sarcomatous phenotype. Consistently with the flow cytometry data, the depletion of CD4+ and CD8+ T cells abolished the antitumoral efficacy of pIC+R848, while the depletion of NK cells and CSF-1R+ cells was not sufficient to abolish the antitumoral response, suggesting a strong involvement of the adaptive immunity. In line with these findings, the intratumoral administration of pIC+R848 in mice unable to produce IFN-γ failed to reduce the tumor growth. In conclusion, our work clearly demonstrates that pIC+R848 are an effective treatment for PDAC when injected intratumorally and that this activity strongly relies on IFN-γ and adaptive immunity. Further investigations are ongoing to assess their potential in orthotopic models using different routes of administration, in a setting closer to the real clinical situation. Citation Format: Aldo Ummarino, Clément Anfray, Andrea Mariancini, Domenico Supino, Cecilia Garlanda, Fernando Torres Andòn, Alberto Mantovani, Paola Allavena. Combined administration of poly(I:C) and resiquimod triggers effective antitumoral response in mouse models of pancreatic adenocarcinoma. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5140.
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32

Kaymak, Deniz, Tala Shekarian, Marie-Françoise Ritz, Nicoletta Ferrari, Roland Kälin, Rainer Glass y Gregor Hutter. "TMIC-43. THE IMPACT OF MICROGLIA MODULATION ON THE IMMUNE TUMOR MICROENVIRONMENT IN SYNGENEIC GLIOBLASTOMA MOUSE MODELS". Neuro-Oncology 25, Supplement_5 (1 de noviembre de 2023): v287—v288. http://dx.doi.org/10.1093/neuonc/noad179.1109.

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Abstract BACKGROUND Glioblastoma is exceptionally resistant to immunotherapies for which the immunosuppressive myeloid compartment is held responsible. As influencer and instructor of T-cell-immunity this compartment mainly consists of Monocyte-derived Cells (MdCs) and tissue-resident (TR) macrophages called microglia (MG). Since the response to immunotherapies depends on antigen presenting cells, we investigate this compartment and its individual role in tumor progression by genetically depleting/activating the TR MG. METHODS We made use of two MG-specific and tamoxifen inducible knockout mouse models in which 1) we activate MG by excision of the activation-repressing transcription factor Sall1 and 2) deplete MG by deleting Csf1r on MG. To investigate the effect of MG activation/depletion on the immune tumor microenvironment (iTME), immunocompetent mice were engrafted with syngeneic glioma cells and the iTME subsequently characterized by scRNAseq, spectral flow cytometry and immunofluorescence imaging. RESULTS Upon Sall1-KO, MG demonstrate a morphologically reactive phenotype. The deletion of Csf1r depletes the brain parenchyma of MG which rapidly gets repopulated by a morphologically distinct microglia-(like) population. Genetic activation of MG leads to a survival benefit in Gl261-engrafted mice compared to Cre- littermates. In contrast, depletion of MG significantly reduces the survival in Gl261 and CT-2A engrafted mice. ScRNAseq confirms the effective depletion of MG and the subsequent emergence of a MG-like cell cluster that transcriptionally remains distinct. The iTME in MG-depleted mice is characterized by a decreased abundance of exhausted and naïve CD8-Tcells and an increased infiltration of MdCs. GSEA demonstrates a dampened inflammatory profile of infiltrating MdCs. CONCLUSION The presence of MG orchestrates the development towards a more antitumorigenic iTME by shaping the antitumoral response of incoming myeloid cells and furthermore directly or indirectly influencing T-cell immunity. Understanding this interplay of MG and MdCs and its impact on instruction of antitumoral T-cell immunity could help guiding the development of novel immunotherapeutic strategies.
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33

Cerullo, Vincenzo, Sari Pesonen, Iulia Diaconu, Sophie Escutenaire, Petteri T. Arstila, Matteo Ugolini, Petri Nokisalmi et al. "Oncolytic Adenovirus Coding for Granulocyte Macrophage Colony-Stimulating Factor Induces Antitumoral Immunity in Cancer Patients". Cancer Research 70, n.º 11 (18 de mayo de 2010): 4297–309. http://dx.doi.org/10.1158/0008-5472.can-09-3567.

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34

Fodale, Vincenzo, Maria G. D’Arrigo, Stefania Triolo, Stefania Mondello y Domenico La Torre. "Anesthetic Techniques and Cancer Recurrence after Surgery". Scientific World Journal 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/328513.

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Many of the most common anesthetics are used in surgical oncology, yet effects on cancer cells are still not known. Anesthesia technique could differentially affect cancer recurrence in oncologic patients undergoing surgery, due to immunosuppression, stimulation of angiogenesis, and dissemination of residual cancer cells. Data support the use of intravenous anesthetics, such as propofol anesthesia, thanks to antitumoral protective effects inhibiting cyclooxygenase 2 and prostaglandins E2 in cancer cells, and stimulation of immunity response; a restriction in the use of volatile anesthetics; restriction in the use of opioids as they suppress humoral and cellular immunity, and their chronic use favors angiogenesis and development of metastases; use of locoregional anesthesia compared with general anesthesia, as locoregional appears to reduce cancer recurrence after surgery. However, these findings must be interpreted cautiously as there is no evidence that simple changes in the practice of anesthesia can have a positive impact on postsurgical survival of cancer patients.
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35

Gajendran, Nithya, Manasa Suresh, David Quiceno, Xintang Li, Marie Durr, Karen Tan, Satish Kumar Reddy Noonepalle y Alejandro Villagra. "Abstract 4583: Development of selective HDAC6 inhibitors to improve cancer immunotherapy". Cancer Research 84, n.º 6_Supplement (22 de marzo de 2024): 4583. http://dx.doi.org/10.1158/1538-7445.am2024-4583.

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Abstract Histone Deacetylases (HDACs) are enzymes that modify histones and non-histone proteins. Our group has previously demonstrated that HDAC6 inhibitors (HDAC6is) modulate multiple immune pathways, including those that suppress the antitumoral M2 phenotype, leading to improved antitumor immunity. Despite the potential of HDAC6is, current inhibitors have poor selectivity and off-target effects and only work at micromolar concentrations. In this work, we designed a screening pipeline of HDAC6i, considering selectivity, potency, capacity to prevent the protumoral phenotype of macrophages, and low cytotoxicity on macrophages and other immune cells. This approach has not been tested before, as the standard screening method for antitumoral HDACis has focused on its cytotoxic effect on cancer cells. We initially designed in silico 980 compound derivatives from previously reported HDAC6i, such as SS208, Nexturastat A, and Suprastat. Twenty-four compounds with a high capacity to bind HDAC6 and chemical stability were screened by their ability to inhibit HDAC6 in cell-free conditions. Sixteen compounds demonstrated high potency and were further evaluated in murine macrophages by their cytotoxic effect using CellTox. The capacity to impede tubulin deacetylation was assessed by western blot and deacetylase activity by HDAC-Glo. The top six candidates were then evaluated by their selectivity compared to other HDAC members and by their effect on repressing the expression of protumoral M2 macrophages Arginase 1 and Fizz1, and activation of antitumoral markers TNFa and iNOS by western blot and qRT-PCR. The best three candidates were then evaluated at nanomolar concentrations to explore their immunomodulatory potential of M1 against M2 by performing antigen presentation (SIINFEKL presentation) and phagocytic capacity using microscopy. Two of these compounds, SM-06-09 and SM-05-947, will be further tested in syngeneic murine melanoma models for their ability in tumor regression and antitumor immunity. This study has yielded important insights into developing new and improved HDAC6is with minimal cytotoxicity, and we believe our work will help advance cancer research and ultimately lead to better patient outcomes. Citation Format: Nithya Gajendran, Manasa Suresh, David Quiceno, Xintang Li, Marie Durr, Karen Tan, Satish Kumar Reddy Noonepalle, Alejandro Villagra. Development of selective HDAC6 inhibitors to improve cancer immunotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4583.
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36

Geissler y Weth. "Immuntherapie: Neue Entwicklungen". Praxis 91, n.º 51 (1 de diciembre de 2002): 2236–46. http://dx.doi.org/10.1024/0369-8394.91.51.2236.

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Trotz enormer Fortschritte in den letzten Jahren beim Verständnis der Regulation und Aktivierung antiviraler und antitumoraler Immunität, befindet sich das Gebiet der Immuntherapie gegen Tumoren, chronische Virus- und Autoimmunerkrankungen noch in einem frühen Entwicklungsstadium. Aufgrund der ausserordentlichen Diversität dieses Forschungsgebietes fokussiert diese Übersicht auf neue Entwicklungen im Bereich der Tumor-Immuntherapie. Viele bisherige immuntherapeutische Strategien, obwohl vielversprechend in präklinischen Modellen, zeigten nur mässigen klinischen Erfolg. Durch die Identifizierung neuer Tumorantigene mittels molekularer Methoden und das verbesserte Verständnis grundlegender Funktionen des Immunsystems wurde aber in den letzten Jahren der Grundstein für zukünftige, erfolgreiche, immuntherapeutische Ansätze gegen Tumore gelegt. Die Verwendung dendritischer Zellen als zelluläres Adjuvans zur Tumorantigenvakzinierung ist ein potentiell sicherer und vielversprechender antitumoraler Therapieansatz. Die bisher durchgeführten klinischen Studien besassen aber ein Defizit bezüglich der Korrelation von klinischem Verlauf und Monitoring der Immuneffektoren nach Tumorvakzinierung. Diese wichtige Korrelierung kann nun aber mittels neuer immunologischer Techniken, die Immuneffektoren auf Einzelzellebene charakterisieren und in vivo verfolgen können, durchgeführt werden. Für zukünftige immuntherapeutische klinische Studien müssen standardisierte Kriterien für Qualitätskontrollen und Studienprotokolle geschaffen werden. Damit können prognostische Parameter für bestimmte Patientenuntergruppen, optimierte Vakzinierungsprotokolle und letztendlich auch neue immunologisch-molekulare Surrogatmarker für die Diagnostik von Tumoren und Tumormetastasen entwickelt werden.
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37

Keane, Colm, Frank Vari, Mark S. Hertzberg, Michael R. Green, Erica Han, John Francis Seymour, Rodney J. Hicks et al. "Net antitumoral immunity and the predictive power of conventional prognosticators in diffuse large B-cell lymphoma." Journal of Clinical Oncology 32, n.º 15_suppl (20 de mayo de 2014): 8542. http://dx.doi.org/10.1200/jco.2014.32.15_suppl.8542.

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Ma, Shoubao, Sai Xiao, Michael Caligiuri y Jianhua Yu. "YTHDF2 promotes tumor immune evasion by inhibiting CD8+ T cell-mediated anti-tumor immunity". Journal of Immunology 212, n.º 1_Supplement (1 de mayo de 2024): 1381_5293. http://dx.doi.org/10.4049/jimmunol.212.supp.1381.5293.

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Abstract YTHDF2 is a well-known m6A reader protein that binds and destabilizes m6A-modified mRNA. We have identified YTHDF2 as a novel regulator of antitumoral polarization in tumor-associated macrophages (TAMs). However, whether YTHDF2 regulates tumor immune evasion remains unknown. Here, we found that loss of YTHDF2 inhibited tumor growth and prolonged survival in syngeneic B16-OVA melanoma and MC38 colon cancer mouse models. Mechanistically, Ythdf2 deficiency-mediated immune remolding was multifactorial, involving promoting the recruitment and polarization of TAMs via chemoattractant CX3CL1, as well as impairing the tumor glycolysis metabolism and enhancing the mitochondrial respiration of tumor-infiltrating CD8+ T cells, thereby enhancing CD8+ T cell effector functions. We screened a small compound that can target YTHDF2 and promote its degradation. YTHDF2 degrader showed a potent anti-tumor effect and better efficacy when combined with anti-PD-L1 antibody therapy. Collectively, YTHDF2 is implicated as a regulator that orchestrates immune evasion and is a promising target to enhance cancer immunotherapy.
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39

Haddada, Hedi, Thierry Ragot, Laurence Cordier, Marie T. Duffour y Michel Perricaudet. "Adenoviral Interleukin-2 Gene Transfer into P815 Tumor Cells Abrogates Tumorigenicity and Induces Antitumoral Immunity in Mice". Human Gene Therapy 4, n.º 6 (diciembre de 1993): 703–11. http://dx.doi.org/10.1089/hum.1993.4.6-703.

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40

Gürlevik, Engin, Norman Woller, Nina Strüver, Peter Schache, Arnold Kloos, Michael P. Manns, Lars Zender, Florian Kühnel y Stefan Kubicka. "Selectivity of Oncolytic Viral Replication Prevents Antiviral Immune Response and Toxicity, but Does Not Improve Antitumoral Immunity". Molecular Therapy 18, n.º 11 (noviembre de 2010): 1972–82. http://dx.doi.org/10.1038/mt.2010.163.

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41

Azaïs, Henri, Nadira Delhem, Céline Frochot, Ludovic Colombeau, Anne Grabarz, Olivier Moralès, Serge Mordon y Pierre Collinet. "Photodynamic therapy of peritoneal metastases of ovarian cancer to improve microscopic cytoreduction and to enhance antitumoral immunity". European Journal of Obstetrics & Gynecology and Reproductive Biology 234 (marzo de 2019): e181. http://dx.doi.org/10.1016/j.ejogrb.2018.08.556.

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42

Cohen-Solal, Joel F. G., Lydie Cassard, Emilie M. Fournier, Shannon M. Loncar, Wolf Herman Fridman y Catherine Sautès-Fridman. "Metastatic Melanomas Express Inhibitory Low Affinity Fc Gamma Receptor and Escape Humoral Immunity". Dermatology Research and Practice 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/657406.

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Our research, inspired by the pioneering works of Isaac Witz in the 1980s, established that 40% of human metastatic melanomas express ectopically inhibitory Fc gamma receptors (FcRIIB), while they are detected on less than 5% of primary cutaneous melanoma and not on melanocytes. We demonstrated that these tumoral FcRIIB act as decoy receptors that bind the Fc portion of antimelanoma IgG, which may prevent Fc recognition by the effector cells of the immune system and allow the metastatic melanoma to escape the humoral/natural immune response. The FcRIIB is able to inhibit the ADCC (antibody dependent cell cytotoxicity) in vitro. Interestingly, the percentage of melanoma expressing the FcRIIB is high (70%) in organs like the liver, which is rich in patrolling NK (natural killer) cells that exercise their antitumoral activity by ADCC. We found that this tumoral FcRIIB is fully functional and that its inhibitory potential can be triggered depending on the specificity of the anti-tumor antibody with which it interacts. Together these observations elucidate how metastatic melanomas interact with and potentially evade humoral immunity and provide direction for the improvement of anti-melanoma monoclonal antibody therapy.
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43

Liu, Weilin, Hongqi Chen, Zhi Zhu, Zuqiang Liu, Congrong Ma, Yong J. Lee, David L. Bartlett y Zong-Sheng Guo. "Ferroptosis Inducer Improves the Efficacy of Oncolytic Virus-Mediated Cancer Immunotherapy". Biomedicines 10, n.º 6 (15 de junio de 2022): 1425. http://dx.doi.org/10.3390/biomedicines10061425.

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Ferroptosis is a type of programmed cell death dependent on iron and characterized by the accumulation of lipid peroxides. In this study, we explore the combination of a ferroptosis activator with an oncolytic vaccinia virus in tumor models. Erastin induced cell death in hepatoma, colon, and ovarian cancer cells, but not in melanoma cancer cells. Erastin, not the oncolytic vaccinia virus (OVV), induced the expression of key marker genes for ferroptosis in cancer cells. In hepatocellular carcinoma and colon cancer models, either erastin or OVV inhibited tumor growth, but a combination of the two yielded the best therapeutic effects, as indicated by inhibited tumor growth or regression and longer host survival. Immunological analyses indicate that erastin alone had little or no effect on systemic immunity or local immunity in the tumor. However, when combined with OV, erastin enhanced the number of activated dendritic cells and the activity of tumor-infiltrating T lymphocytes as indicated by an increase in IFN-γ+CD8+ and PD-1+CD8+ T cells. These results demonstrate that erastin can exert cytotoxicity on cancer cells via ferroptosis, but has little effect on immune activity by itself. However, when combined with an OVV, erastin promoted antitumoral immunity and efficacy by increasing the number of activated dendritic cells and promoting the activities of tumor specific CD8+ T cells in the tumor.
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44

Arrieta, Victor Andrés, Jasim K. Benotmane, Junfei Zhao, Silpol Dhiantravan, David Hou, Joshua L. Katz, Si Wang et al. "1228 Comprehensive T-cell Profiling in Chordomas: Single-cell RNA-Seq and TCR Profiling Analysis Uncover Antitumor and Exhaustion Phenotypes for Targeted Immunotherapies". Neurosurgery 70, Supplement_1 (abril de 2024): 190. http://dx.doi.org/10.1227/neu.0000000000002809_1228.

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INTRODUCTION: Chordomas, a rare type of tumor, originate from residual notochord tissue. These tumors present important challenges due to the limited treatment options. Investigating the intricacies of T-cell composition and function in chordoma immunity holds the potential to advance immunotherapy strategies for these patients. METHODS: We generated a comprehensive single-cell atlas of T cells of chordomas, incorporating paired single-cell transcriptomic samples from the tumor and blood of five patients and single-cell TCR sequencing data to assess T-cell clonality. Additionally, we analyzed T cells in 33 chordomas (22 newly diagnosed and 11 recurrent tumors) using multiplex immunofluorescence. RESULTS: Our results demonstrate that CD8+ T-cell antitumoral immunity originates in the periphery, marked by clonal expansion of cytotoxic and memory T cells in the blood. However, this immunity experiences progressive exhaustion upon tumor infiltration. Notably, a large percentage of CD8+ T-cells from the tumors and blood shared their TCRs with exhausted CD8+ T-cells known for tumor specificity, confirming the origin of a peripheral antitumor response. We identified specific antigen peptide sequences through TCR analysis that were enriched in exhausted T cell receptors' binding sites that uncovered shared motifs within the reactive tumor-infiltrating compartment. Moreover, we observed that CTLA-expressing central memory and Tregs made up most of the CD4 T-cell tumoral landscape. Interestingly, multiplex immunofluorescence showed a higher abundance of CD3+ T cells in newly diagnosed chordomas compared to recurrent cases. CONCLUSIONS: This study sheds light on the composition and function of T cells in chordomas, revealing the origin and exhaustion of CD8+ T-cell antitumor immunity. These findings contribute to our understanding of chordoma immunity to guide the development of targeted immunotherapies for both newly diagnosed and recurrent cases.
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Merindol, Natacha, Martine Caty, Sylvain Gimmig, Michel Duval, Martin A. Champagne y Hugo Soudeyns. "Diversity and fate of pre-immune anti-tumor T cells after umbilical cord blood transplantation (102.28)". Journal of Immunology 178, n.º 1_Supplement (1 de abril de 2007): S209—S210. http://dx.doi.org/10.4049/jimmunol.178.supp.102.28.

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Abstract Umbilical cord blood (UCB) has been used successfully as a source of progenitor cells to treat a variety of haematological and immune disorders in children. Donor-derived T cells play a key role in antitumoral and antiviral immunity and contribute to the survival of the graft recipient. Here we studied the diversity, persistence, fate and antitumoral function of UCB-derived T cells and characterized their persistence and function in the graft recipient. Naïve CD8+ T cells specific for the Melan-A26-35 peptide were isolated from UCB and UCB recipients at 1, 3, and 6 months post-transplant using Melan-A26-35-HLA-A2 tetramers and cell sorting, and were cultured in the presence of IL-2, IL-7, PHA and peptide. Melan-A-specific cytotoxicity was tested in 51Cr-release assays, and the clonal diversity of the pre-immune Melan-A-specific repertoire was determined by sequencing of the T cell receptor β chain CDR3 region. 14 UCB recipients were enrolled. Melan-A-specific CD8+ T cells were detected at a median frequency of 2.28% (range=0.0–8.18%) in 4 of 6 UCB samples initially analyzed. These cells proliferated in the presence of Melan-A peptide in 4 of 6 cases, and showed cognate cytotoxicity in 2 of 6 cases. Finally, tetramer-positive cells were detected in UCB recipients as early as 1 month post-transplant. This study will lead to a better understanding of the fate of the pre-immune T cell repertoire in UCB recipients.
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46

Van den Eynde, Benoit J., Nicolas van Baren y Jean-François Baurain. "Is There a Clinical Future for IDO1 Inhibitors After the Failure of Epacadostat in Melanoma?" Annual Review of Cancer Biology 4, n.º 1 (9 de marzo de 2020): 241–56. http://dx.doi.org/10.1146/annurev-cancerbio-030419-033635.

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Indoleamine-2,3 dioxygenase 1 (IDO1) contributes to tumor immunosuppression by enzymatically degrading tryptophan, which is required for T cell activity, and producing kynurenine. Small-molecule inhibitors, such as epacadostat, have been developed to block IDO1 activity. In preclinical models, they can restore antitumoral T cell immunity and synergize with immune checkpoint inhibitors or cancer vaccines. Based on encouraging clinical results in early phase trials, a randomized phase III study (ECHO-301/KN-252) was launched in metastatic melanoma to test the benefit of adding epacadostat to the reference pembrolizumab therapy. The result was negative. We briefly review the clinical trials that investigated epacadostat in cancer patients and discuss possible explanations for this negative result. We end by suggesting paths to resume clinical development of compounds targeting the IDO1 pathway, which in our view remains an attractive target for cancer immunotherapy.
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47

Félix-Piña, Pedro, Moisés Armides Franco Molina, Diana Ginette Zarate Triviño, Paola Leonor García Coronado, Pablo Zapata Benavides y Cristina Rodríguez Padilla. "Antitumoral and Immunogenic Capacity of β-D-Glucose—Reduced Silver Nanoparticles in Breast Cancer". International Journal of Molecular Sciences 24, n.º 10 (9 de mayo de 2023): 8485. http://dx.doi.org/10.3390/ijms24108485.

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Immunogenic cell death (ICD) is a type of cell death capable of stimulating immunity against cancer through danger signals that lead to an adaptive immune response. Silver nanoparticles (AgNPs) have been shown to have a cytotoxic effect on cancer cells; however, their mechanism of action is not fully understood. The present study synthesized, characterized, and evaluated the cytotoxic effect of beta-D-glucose-reduced AgNPs (AgNPs-G) against breast cancer (BC) cells in vitro; and assess the immunogenicity of cell death in vitro and in vivo. The results showed that AgNPs-G induce cell death in a dose-dependent manner on BC cell lines. In addition, AgNPs show antiproliferative effects by interfering with the cell cycle. Regarding the detection of damage-associated molecular patterns (DAMPs), it was found that treatment with AgNPs-G induces calreticulin exposure and the release of HSP70, HSP90, HMGB1, and ATP. In vivo, prophylactic vaccination did not prevent tumor establishment; however, tumor weight was significantly lower in AgNPs-G vaccinated mice, while the survival rate increased. In conclusion, we have developed a new method for the synthesis of AgNPs-G, with in vitro antitumor cytotoxic activity on BC cells, accompanied by the release of DAMPs. In vivo, immunization with AgNPs-G failed to induce a complete immune response in mice. Consequently, additional studies are needed to elucidate the mechanism of cell death that leads to the design of strategies and combinations with clinical efficacy.
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48

Puisieux, Isabelle, Laurence Odin, Dominique Poujol, Philippe Moingeon, James Tartaglia, William Cox y Marie Favrot. "Canarypox Virus-Mediated Interleukin 12 Gene Transfer into Murine Mammary Adenocarcinoma Induces Tumor Suppression and Long-Term Antitumoral Immunity". Human Gene Therapy 9, n.º 17 (20 de noviembre de 1998): 2481–92. http://dx.doi.org/10.1089/hum.1998.9.17-2481.

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49

Brisson, Lydie y Alice Carrier. "A novel actor in antitumoral immunity: The thymus-specific serine protease TSSP/PRSS16 involved in CD4+T-cell maturation". OncoImmunology 4, n.º 9 (2 de abril de 2015): e1026536. http://dx.doi.org/10.1080/2162402x.2015.1026536.

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Puisieux, Isabelle, Laurence Odin, Dominique Poujol, Philippe Moingeon, James Tartaglia, William Cox y Marie Favrot. "Canarypox Virus-Mediated Interleukin 12 Gene Transfer into Murine Mammary Adenocarcinoma Induces Tumor Suppression and Long-Term Antitumoral Immunity". Human Gene Therapy 9, n.º 17 (20 de noviembre de 1998): 2481–92. http://dx.doi.org/10.1089/10430349850019328.

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