Academic literature on the topic 'Anti-Tumoral immunity'
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Journal articles on the topic "Anti-Tumoral immunity"
Riachi, Mansour E., Carolina G. Alcantara Hirsch, Erica Ma, Beny Shapiro, Ammar Javed, Christopher L. Wolfgang, and Dafna Bar-Sagi. "Abstract A018: Exercise stimulates anti-tumoral immunity in metastatic PDAC." Cancer Research 84, no. 2_Supplement (January 16, 2024): A018. http://dx.doi.org/10.1158/1538-7445.panca2023-a018.
Full textBikorimana, Jean-Pierre, Natasha Salame, Simon Beaudoin, Mohammad Balood, Théo Crosson, Jamilah Abusarah, Sebastien Talbot, Raimar Löbenberg, Sebastien Plouffe, and Moutih Rafei. "Promoting antigen escape from dendritic cell endosomes potentiates anti-tumoral immunity." Cell Reports Medicine 3, no. 3 (March 2022): 100534. http://dx.doi.org/10.1016/j.xcrm.2022.100534.
Full textLeshem, 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 (November 14, 2018): 470. http://dx.doi.org/10.3390/toxins10110470.
Full textGiurini, 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 (June 14, 2022): 2923. http://dx.doi.org/10.3390/cancers14122923.
Full textRivera-Molina, Yisel, Juan Fueyo, Hong Jiang, Teresa Nguyen, Dong Ho Shin, Gilbert Youssef, Xuejun Fan, 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 (November 2019): vi87. http://dx.doi.org/10.1093/neuonc/noz175.359.
Full textCohen-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.
Full textMirlekar, 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 (November 15, 2021): PO—019—PO—019. http://dx.doi.org/10.1158/1538-7445.panca21-po-019.
Full textGeidel, 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 (May 2016): S115. http://dx.doi.org/10.1016/j.jid.2016.02.690.
Full textWu, 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 (March 2, 2022): 392. http://dx.doi.org/10.3390/biom12030392.
Full textRemsik, Jan, Xinran Tong, Min Jun Li, Ugur Sener, Jessica Wilcox, Kiana Chabot, Russell Kunes, et al. "LMD-16. Choroid plexus orchestrates anti-cancer immunity in leptomeninges." Neuro-Oncology Advances 3, Supplement_3 (August 1, 2021): iii10—iii11. http://dx.doi.org/10.1093/noajnl/vdab071.041.
Full textDissertations / Theses on the topic "Anti-Tumoral immunity"
They, Laetitia. "Renforcement des effets immunomodulateurs d’un anticorps monoclonal anti-tumoral : étude des effets potentialisateurs de thérapies combinées et analyse des mécanismes impliqués." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT076/document.
Full textMelanoma is the most aggressive form of skin cancer. Although early management is of good prognosis, the survival of patients decrease dramatically for metastatic stages. Despite the recent spectacular therapeutic advances, the major problem lies in resistance to treatment and relapse and the main challenge now is to develop an effective and sustainable control. Monoclonal antibodies (mAbs) have the ability to specifically target and eliminate tumor cells while recruiting cells from the immune system, to develop and / or enhance the immunity of the host with the development of a vaccinal immune response. In a solid tumor model of murine melanoma after subcutaneous transplantation of B16F10 cells, we investigated the immunomodulatory effect of TA99 mAb targeting a TYRP-1 surface antigen overexpressed in tumor melanocytes. Our results showed that about 30% of mice are protected in the long term and have an antitumoral humoral and cellular immune response. Moreover, the analysis of the immune infiltrate in mice that escape to the treatment with TA99 mAb and develop a tumor, shows an overexpression of PD-1 and Tim3 associated with a loss of effector cell functions within the tumor. This same phenotype has been observed in biopsies of patients with metastatic melanoma. Thus, blocking the PD-1 / PDL-1 axis by inoculation of an anti-PD1 mAb at the time of tumor escape potentiates the anti-tumor immune response and results in increased survival. However, the absence of complete regression suggests the establishment of other immunosuppressive pathways. Indeed we have observed an overexpression of CD39 and CD73 ectonucleotidases in the tumor microenvironment suggesting the involvement of adenosine in the resistance mechanisms observed and opening interesting perspectives for the concomitant blocking of this pathway and the PD1 / PDL-1 axis. Another strategy has been to improve the early immunomodulatory effects of TA99 mAb by combining it with oxaliplatin, a chemotherapy that promotes immunogenic death. Although the therapeutic combinations tested in this study showed encouraging in vivo effects with a significant delay in overall survival, no significant increase in the long-term anti-tumor response was observed, suggesting the establishment of other non-redundant immunosuppressive mechanisms or unsuitable combinations strategies. Both phenotypic and functional analysis of the different cellular actors of the tumor microenvironment will be a key step in the implementation of relevant combinations in association with the TA99 mAb. This work is highlighted by a phase I clinical trial (IMC-20D7S) using flanvotumab (human equivalent of mAb TA99) in 27 patients with metastatic melanoma that shows interesting clinical outcome without severe side effects, opening the way for the development of therapeutic combinations associated with this mAb
Prat, Mélissa. "Les macrophages au sein du microenvironnement tumoral : étude et modulation des mécanismes moléculaires et cellulaires de la réponse anti-tumorale au cours de carcinoses péritonéales." Thesis, Toulouse 3, 2019. http://www.theses.fr/2019TOU30116.
Full textMacrophages, which are crucial effectors of innate immune response, exhibit a remarkable phenotypic and functional plasticity that allows them to adapt to the different stimuli present in their microenvironment. Within the tumor microenvironment, macrophages or TAMs (Tumor-associated macrophages) represent the major leukocyte population. During tumor development, secreted mediators produced by transformed cells « educate » TAMs which acquire properties favorable to tumor growth. Thus, it is now widely accepted that TAMs, initially of anti-tumor M1 phenotype, differentiate towards an M2 phenotype able to promote tumor cell proliferation, angiogenesis, metastases, resistance to chemotherapy treatments and suppression of the adaptive anti-tumor immune response. However, this functional M1/M2 dichotomy, while facilitating the description TAMs phenotype and their associated functions, is an oversimplification of the macrophage biology within tumor tissues which is actually more complex. Thus, in the first part of this work, we showed that treatment with IL-13, a Th2 cytokine well described to be involved in macrophage M2 polarization, inhibits tumor growth in two murine models of T-cell lymphoma and ovarian adenocarcinoma via the promotion of macrophage cytotoxic activity. Interestingly, we demonstrated the key role of Mannose (RM) and Dectin-1 C-type Lectin receptors, strongly expressed on IL-13-activated macrophages, in tumor cell recognition. We specifically identified the sialic acid expressed on transformed cell surface as a critical epitope for their recognition by IL-13-activated macrophages. Moreover, we showed that, following this recognition, RM and Dectin-1 trigger cytotoxic signaling pathways leading to the production of radical oxygen species and the amplification of arginase activity. We finally demonstrated that these two mediators produced by IL-13-activated macrophages induce tumor cell necrosis. In the second part of this work, we studied the impact of 15(S)-HETE, a natural ligand of the PPAR-γ nuclear receptor involved macrophage M2 polarization, on tumor development. We showed that this lipid inhibits tumor growth in an experimental murine model of ovarian adenocarcinoma. Interestingly, we demonstrated that 15(S)-HETE anti-tumor effect depends on the activation of PPAR-γ in macrophages. We showed that 15(S)-HETE modifies peritoneal macrophage population balance, likely by promoting the differentiation of Small Peritoneal Macrophages (SPM) into Large Peritoneal Macrophages (LPMs). These LPMs display a phenotype which contributes to the increase of effector/regulatory T lymphocyte ratio in tumor ascites, and thus counteracts tumor-induced immunosuppression. Finally, in the third part of our work, the analysis of circulating blood monocytes in ovarian adenocarcinoma patients revealed a strong increase in the proportion of the « intermediate » subset (CD14high CD16+), usually poorly represented in healthy subjects. Interestingly, we demonstrated a positive correlation between a high proportion of intermediate blood monocytes and the presence of an immunosuppressive microenvironment in the tumor ascites of these patients (↗ Tregs, TAMS CD163high CD206high CCR2high CD86low and ↘ NK and CD8 + cytotoxic). In addition, we showed a positive correlation between the expansion of these intermediate monocytes and tumor development within the peritoneum. Together, these data highlight the role of blood monocytes as a predictive signature of immune status and tumor development within the peritoneum in patients with ovarian cancer
Conforti, Rosa. "Traitement anti tumoral par ciblage de TLR3 et découplage des effets opposés des chimiokines pour améliorer l’efficacité des agonistes de TLR3." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T067.
Full textThe rationale for the use of Toll –Like Receptor (TLR) agonists in cancer therapy relies upon their “beneficial” effects on immune cells leading to enhanced innate and adaptive immune responses. However, a variety of cancer epithelia express TLRs which, upon triggering, may mediate “deleterious” effects such as tumorigenesis. To further dissect the direct versus indirect biological effects of the TLR3 agonist polyadenylic-polyuridylic acid (poly(A:U)), we took advantage of two murine tumor models expressing TLR3 that failed to respond to chemotherapy but did produce large amounts of CCL5 and CXCL10 in response to the poly(A:U) and type I IFN. In vivo, the combination of chemotherapy and poly(A:U) mediated low tumoricidal activity unless a vaccination against tumor antigens was included in the regimen and the CCR5 receptor was blocked (CCR5 loss-of-function mice or WT animals treated with MetRANTES). The antitumor efficacy of the combination therapy was associated with the elicitation of CD8+CXCR3+IFN+ T cells and abrogated in nu/nu, Trif-/- and Cxcr3-/- mice. The source of CCR5L is the TLR3-activated tumor cells in that stable inhibition of the chemokine production by specific shRNA CCL5 ameliorated the efficacy of the combination therapy. These results support the notion that poly(A:U) can directly act on tumor epithelia to promote the release of beneficial CXCL10 for the recruitment of intratumoral CTLs but also the release of deleterious CCL5 acting on host immunosuppressors. Uncoupling chemokine release and prior vaccination may enable the CXCR3L-dependent CTLs to overrule the CCR5-dependent suppression and may be integrated in future trials using TLR3 agonists
Bouakka, Ibrahim. "Ciblage thérapeutique de l’Hepatic Leukemia Factor (HLF) dans les cancers du sein triple négatifs." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL017.
Full textThe intricate interplay between the immune response and tumor progression, particularly in the context of triple-negative breast cancer (TNBC), has been a focal point of oncological research over the last decade. Our preceding investigation highlighted the role of the HLF gene within a quartet gene signature, identifying its inverse association with the infiltration of immune cells within the tumor milieu. During my thesis, we investigated more precisely its implication in the immune response and TNBC tumor development. The bioinformatic analysis of clinical data from patients with TNBC demonstrated that low levels of HLF expression were associated with an overexpression of genes related to the mechanisms of attraction and activation of the immune system. The implication of neutrophils in cancer is contentious, as they can function either as active anti-tumoral partners or as pro-tumoral agents promoting immunosuppression and tumor growth. The duality of the immune system’s role in cancer, oscillating between antitumor action and support for tumor growth, reflects its great complexity within the tumor microenvironment. In this study, we employed CRISPR/Cas9 technology to inactivate the HLF gene in TNBC cell lines, enabling us to explore the repercussions on the chemokine network regulating the presence and activity of different immune populations in the tumor microenvironment. Finally, in vivo experiments conducted on immunodeficient mouse models demonstrated that reducing HLF in certain TNBC subtypes hindered tumor progression. Altogether, our results suggest that a reduction of HLF expression can lead in the early steps of tumor development to the awakening of the anti-tumoral function of the immune system to enforce the necessary immunological tone to tumor elimination. Thus, HLF emerges as a promising therapeutic target to promote the engagement and effectiveness of a competent immune response against aggressive subtypes of TNBC
Montégut, Léa. "Role of acyl-coenzyme A binding protein in age-related diseases and cancer." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL073.
Full textAcyl-coenzyme A binding protein (ACBP), also known as diazepam binding inhibitor (DBI), is a ubiquitous and highly conserved protein in eukaryota. In mammals, it plays a dual role: intracellular ACBP binds to activated fatty acids (acyl-CoAs) and, when secreted, ACBP acts as a peptide hormone regulating metabolism and obesity. The analysis of publicly available datasets demonstrates a tendency for increased ACBP in physio-pathological contexts, such as hepatic steatosis, severe forms of HIV or COVID-19, and certain cancers. Additionally, plasma ACBP concentrations are positively correlated with chronological age.Recent studies in mice have shown that modulation of circulating ACBP levels can also control metabolic parameters in animals. Obesity and metabolic syndrome are among the primary environmental risk factors for the development of age-related diseases, such as cardiovascular diseases and cancer, therefore our research aimed to determine if these diseases could be preceded by a modification in circulating ACBP levels.In cohorts of apparently healthy of individuals, we detected an elevation of ACBP in patients who would imminently develop cardiovascular events or cancer. The utility of this aging biomarker was further explored in different preclinical contexts. On one hand, neutralization of the protein extends the lifespan of yeast and, in mice, it protects against accelerated aging of the heart caused by anthracyclines (a class of chemotherapies commonly used and known for their cardiotoxic effects). In the context of cancer, modulation of this metabolic checkpoint has a positive impact on tumor immunosurveillance and improves the response to chemotherapy-immunotherapy treatments in mice. Thus, our study reveals that ACBP could be a biomarker of patients' "biological age,", with its elevation indicating the imminent onset of age-related diseases. Beyond its predictive value, initial preclinical trials demonstrate that neutralization of ACBP is a promising option for improving metabolic health in patients, which could be exploited to prevent or enhance the response to treatments for cardiovascular diseases and cancer
Chraa, Dounia. "Analyse du rôle de l’IL-17 dans la progression du cancer du sein chez différents sous-groupes moléculaires de patientes : effet sur l’expression de PD-L1, sur la prolifération des cellules cancéreuses et sur la survie des patientes." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0629.
Full textIn breast cancer, numerous types of immune cells are found within the tumor microenvironment. Both pro- and anti-tumor immune-based effects have been reported. Here, we show that IL-17, a pro-inflammatory cytokine, which is produced mainly by the Th17 T cell sub-population, was strongly associated to poor prognostic markers in breast cancer patients. When analyzed at both transcript and protein levels, IL-17 was highly expressed in ER- including TNBC patients. Furthermore, IL-17 expression in tumor tissues tightly correlated with the expression of the immune checkpoint regulator, PD-L1. Interestingly, IL-17 was found to significantly induce PD-L1 expression, in breast cancer cells in vitro, at both transcript and protein levels. IL-17 also specifically triggered proliferation of distinct breast cancer cell lines in vitro, in a dose-dependent manner, which could be abolished using neutralizing antibodies directed against IL-17 receptor or IL-17. Finally, increased IL-17 levels were associated to lower survival probability in breast cancer patients, especially when combined to the ER negative status. Altogether our data strongly suggest that IL-17 is associated to poor prognosis in breast cancer patients and could be considered as a potential therapeutic target
Book chapters on the topic "Anti-Tumoral immunity"
Brix, Nikko, and Kirsten Lauber. "Immune Checkpoint Inhibition and Radiotherapy in Head and Neck Squamous Cell Carcinoma: Synergisms and Resistance Mechanisms." In Critical Issues in Head and Neck Oncology, 11–21. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_2.
Full textConference papers on the topic "Anti-Tumoral immunity"
MacBeth, Morgan, Richard Tobin, Robert Van Gulick, Martin D. McCarter, William A. Robinson, and Kasey L. Couts. "Abstract PO048: Loss of intra-tumoral RIG-I immune signaling is a potential microbiome-mediated mechanism underlying poor anti-tumor immunity and immunotherapy resistance in mucosal melanoma." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-po048.
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