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Добірка наукової літератури з теми "Anti-Tumoral immunity"

Автор: Grafiati

Опубліковано: 7 жовтня 2023

Оновлено: 7 липня 2024

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Статті в журналах з теми "Anti-Tumoral immunity"

1

Riachi, Mansour E., Carolina G. Alcantara Hirsch, Erica Ma, et al. "Abstract A018: Exercise stimulates anti-tumoral immunity in metastatic PDAC." Cancer Research 84, no. 2_Supplement (2024): A018. http://dx.doi.org/10.1158/1538-7445.panca2023-a018.

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Abstract The majority of pancreatic ductal adenocarcinoma (PDAC) patients are metastatic at presentation with limited treatment options and a poor overall 5-year survival of 3%. The liver is the predominant site of distant metastasis in PDAC. Our group has previously shown that aerobic exercise can inhibit tumorigenesis in a primary PDAC mouse model by promoting anti-tumor immunity, however, the effects of exercise in the metastatic setting have not been explored. As such, we developed a model of PDAC liver metastasis by isolating primary pancreatic and liver metastatic cell lines from 18–20-w

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2

Bikorimana, Jean-Pierre, Natasha Salame, Simon Beaudoin, et al. "Promoting antigen escape from dendritic cell endosomes potentiates anti-tumoral immunity." Cell Reports Medicine 3, no. 3 (2022): 100534. http://dx.doi.org/10.1016/j.xcrm.2022.100534.

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3

Leshem, Yasmin, Emily King, Ronit Mazor, Yoram Reiter, and Ira Pastan. "SS1P Immunotoxin Induces Markers of Immunogenic Cell Death and Enhances the Effect of the CTLA-4 Blockade in AE17M Mouse Mesothelioma Tumors." Toxins 10, no. 11 (2018): 470. http://dx.doi.org/10.3390/toxins10110470.

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SS1P is an anti-mesothelin immunotoxin composed of a targeting antibody fragment genetically fused to a truncated fragment of Pseudomonas exotoxin A. Delayed responses reported in mesothelioma patients receiving SS1P suggest that anti-tumor immunity is induced. The goal of this study is to evaluate if SS1P therapy renders mesothelioma tumors more sensitive to cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) immune checkpoint blockade. We evaluated the ability of SS1P to induce adenosine triphosphate (ATP) secretion and calreticulin expression on the surface of AE17M mouse mesothelioma cell

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4

Giurini, Eileena F., Mary Beth Madonna, Andrew Zloza, and Kajal H. Gupta. "Microbial-Derived Toll-like Receptor Agonism in Cancer Treatment and Progression." Cancers 14, no. 12 (2022): 2923. http://dx.doi.org/10.3390/cancers14122923.

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Toll-like receptors (TLRs) are typical transmembrane proteins, which are essential pattern recognition receptors in mediating the effects of innate immunity. TLRs recognize structurally conserved molecules derived from microbes and damage-associated molecular pattern molecules that play an important role in inflammation. Since the first discovery of the Toll receptor by the team of J. Hoffmann in 1996, in Drosophila melanogaster, numerous TLRs have been identified across a wide range of invertebrate and vertebrate species. TLR stimulation leads to NF-κB activation and the subsequent production

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5

Rivera-Molina, Yisel, Juan Fueyo, Hong Jiang, et al. "EXTH-27. ACTIVATING THE IMMUNITY WITHIN THE TUMOR USING VIROIMMUNOTHERAPY: DELTA-24-RGD ONCOLYTIC ADENOVIRUS ARMED WITH THE IMMUNOPOSITIVE REGULATOR GITRL." Neuro-Oncology 21, Supplement_6 (2019): vi87. http://dx.doi.org/10.1093/neuonc/noz175.359.

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Abstract Based on promising results of recent clinical trials using oncolytic viruses, virotherapy is evolving as an alternative to treat patients with malignant glioma. Our group developed the oncolytic adenovirus Delta-24-RGD (DNX-2401) that is being tested, alone or in combination with anti-PD1, in clinical trials for recurrent glioblastoma (NCT00805376; NCT01956734; NCT02798406). The results suggest that, besides the expected oncolytic effect, the injection of the pathogen initiated, in a subset of patients, an anti-tumoral immunity that led to 20% of long-term survivors (3.5–5 years). To

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6

Cohen-Solal, Joel F. G., Lydie Cassard, Emilie M. Fournier, Shannon M. Loncar, Wolf Herman Fridman, and 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 dep

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7

Mirlekar, Bhalchandra, and Yuliya Pylayeva-Gupta. "Abstract PO-019: Reprogramming of naïve B cells in pancreatic cancer subverts humoral immunity." Cancer Research 81, no. 22_Supplement (2021): PO—019—PO—019. http://dx.doi.org/10.1158/1538-7445.panca21-po-019.

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Abstract B cells frequently infiltrate human tumors, and the intra-tumoral abundance of plasma cells can correlate with improved patient prognosis. However, many tumors are devoid of plasma B cells, and strategies to enhance anti-tumor B cell responses are needed. We report the existence of a negative regulatory signaling network that reprograms naïve B cells in pancreatic cancer to antagonize anti-tumor plasma B cells. This network is driven by IL-35-mediated STAT3 activation, which directly stimulates upregulation of the pioneer transcription factors Pax5 and Bcl6 in naïve B cells and impede

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8

Geidel, G., M. Maurer, T. Luger, and K. Loser. "649 OX40/OX40L and 4-1BB/4-1BBL signaling in cutaneous anti-tumoral immunity." Journal of Investigative Dermatology 136, no. 5 (2016): S115. http://dx.doi.org/10.1016/j.jid.2016.02.690.

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9

Wu, Deyang, Xiaowei Liu, Jingtian Mu, Jin Yang, Fanglong Wu, and Hongmei Zhou. "Therapeutic Approaches Targeting Proteins in Tumor-Associated Macrophages and Their Applications in Cancers." Biomolecules 12, no. 3 (2022): 392. http://dx.doi.org/10.3390/biom12030392.

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Tumor-associated macrophages (TAMs) promote tumor proliferation, invasion, angiogenesis, stemness, therapeutic resistance, and immune tolerance in a protein-dependent manner. Therefore, the traditional target paradigms are often insufficient to exterminate tumor cells. These pro-tumoral functions are mediated by the subsets of macrophages that exhibit canonical protein markers, while simultaneously having unique transcriptional features, which makes the proteins expressed on TAMs promising targets during anti-tumor therapy. Herein, TAM-associated protein-dependent target strategies were develo

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10

Remsik, Jan, Xinran Tong, Min Jun Li, et al. "LMD-16. Choroid plexus orchestrates anti-cancer immunity in leptomeninges." Neuro-Oncology Advances 3, Supplement_3 (2021): iii10—iii11. http://dx.doi.org/10.1093/noajnl/vdab071.041.

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Abstract Choroid plexus (CP) forms an anatomically functional barrier between the blood and cerebrospinal fluid (CSF) that dictates the cellular and humoral composition of the CSF. The immunological response of CP to inflammatory stimuli, such as cancer, remains unclear. Here, we find that CP orchestrates the immune composition of CSF in the steady state as well as in the presence of metastatic cancer. We show that the circulation-derived leptomeningeal monocyte-macrophages entering the CSF through CP promote the growth of leptomeningeal metastasis (LM) by perturbing the environment with a sto

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