Relevant bibliographies by topics / Mesothelin targeted cancer immunotherapy

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Mesothelin targeted cancer immunotherapy'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Mesothelin targeted cancer immunotherapy"

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Hassan, Raffit, and Mitchell Ho. "Mesothelin targeted cancer immunotherapy." European Journal of Cancer 44, no. 1 (January 2008): 46–53. http://dx.doi.org/10.1016/j.ejca.2007.08.028.

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Yeo, Dannel, Laura Castelletti, Nico van Zandwijk, and John E. J. Rasko. "Hitting the Bull’s-Eye: Mesothelin’s Role as a Biomarker and Therapeutic Target for Malignant Pleural Mesothelioma." Cancers 13, no. 16 (August 4, 2021): 3932. http://dx.doi.org/10.3390/cancers13163932.

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Malignant pleural mesothelioma (MPM) is an aggressive cancer with limited treatment options and poor prognosis. MPM originates from the mesothelial lining of the pleura. Mesothelin (MSLN) is a glycoprotein expressed at low levels in normal tissues and at high levels in MPM. Many other solid cancers overexpress MSLN, and this is associated with worse survival rates. However, this association has not been found in MPM, and the exact biological role of MSLN in MPM requires further exploration. Here, we discuss the current research on the diagnostic and prognostic value of MSLN in MPM patients. Furthermore, MSLN has become an attractive immunotherapy target in MPM, where better treatment strategies are urgently needed. Several MSLN-targeted monoclonal antibodies, antibody–drug conjugates, immunotoxins, cancer vaccines, and cellular therapies have been tested in the clinical setting. The biological rationale underpinning MSLN-targeted immunotherapies and their potential to improve MPM patient outcomes are reviewed.
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Hassan, R., E. Alley, H. Kindler, S. Antonia, T. Jahan, J. Grous, S. Honarmand, et al. "87 Mesothelin-targeted immunotherapy CRS-207 plus chemotherapy as treatment for malignant pleural mesothelioma (MPM)." Lung Cancer 91 (January 2016): S31—S32. http://dx.doi.org/10.1016/s0169-5002(16)30104-0.

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Borgeaud, Maxime, Floryane Kim, Alex Friedlaender, Filippo Lococo, Alfredo Addeo, and Fabrizio Minervini. "The Evolving Role of Immune-Checkpoint Inhibitors in Malignant Pleural Mesothelioma." Journal of Clinical Medicine 12, no. 5 (February 22, 2023): 1757. http://dx.doi.org/10.3390/jcm12051757.

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Malignant pleural mesothelioma (MPM) is a rare cancer usually caused by asbestos exposure and associated with a very poor prognosis. After more than a decade without new therapeutic options, immune checkpoint inhibitors (ICIs) demonstrated superiority over standard chemotherapy, with improved overall survival in the first and later-line settings. However, a significant proportion of patients still do not derive benefit from ICIs, highlighting the need for new treatment strategies and predictive biomarkers of response. Combinations with chemo-immunotherapy or ICIs and anti-VEGF are currently being evaluated in clinical trials and might change the standard of care in the near future. Alternatively, some non-ICI immunotherapeutic approaches, such as mesothelin targeted CAR-T cells or denditric-cells vaccines, have shown promising results in early phases of trials and are still in development. Finally, immunotherapy with ICIs is also being evaluated in the peri-operative setting, in the minority of patients presenting with resectable disease. The goal of this review is to discuss the current role of immunotherapy in the management of malignant pleural mesothelioma, as well as promising future therapeutic directions.
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Luke, Jason J., Fabrice Barlesi, Ki Chung, Anthony W. Tolcher, Karen Kelly, Antoine Hollebecque, Christophe Le Tourneau, et al. "Phase I study of ABBV-428, a mesothelin-CD40 bispecific, in patients with advanced solid tumors." Journal for ImmunoTherapy of Cancer 9, no. 2 (February 2021): e002015. http://dx.doi.org/10.1136/jitc-2020-002015.

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BackgroundCD40 agonist immunotherapy can potentially license antigen-presenting cells to promote antitumor T-cell activation and re-educate macrophages to destroy tumor stroma. Systemic administration of CD40 agonists has historically been associated with considerable toxicity, providing the rationale for development of tumor-targeted immunomodulators to improve clinical safety and efficacy. This phase I study assessed the safety, tolerability, preliminary antitumor activity, and preliminary biomarkers of ABBV-428, a first-in-class, mesothelin-targeted, bispecific antibody designed for tumor microenvironment-dependent CD40 activation with limited systemic toxicity.MethodsABBV-428 was administered intravenously every 2 weeks to patients with advanced solid tumors. An accelerated titration (starting at a 0.01 mg/kg dose) and a 3+3 dose escalation scheme were used, followed by recommended phase II dose cohort expansions in ovarian cancer and mesothelioma, tumor types associated with high mesothelin expression.ResultsFifty-nine patients were treated at doses between 0.01 and 3.6 mg/kg. The maximum tolerated dose was not reached, and 3.6 mg/kg was selected as the recommended phase II dose. Seven patients (12%) reported infusion-related reactions. Treatment-related grade ≥3 treatment-emergent adverse events were pericardial effusion, colitis, infusion-related reaction, and pleural effusion (n=1 each, 2%), with no cytokine release syndrome reported. The pharmacokinetic profile demonstrated roughly dose-proportional increases in exposure from 0.4 to 3.6 mg/kg. Best response was stable disease in 9/25 patients (36%) treated at the recommended phase II dose. CD40 receptor occupancy >90% was observed on peripheral B-cells starting from 0.8 mg/kg; however, no consistent changes from baseline in intratumoral CD8+ T-cells, programmed death ligand-1 (PD-L1+) cells, or immune-related gene expression were detected post-ABBV-428 treatment (cycle 2, day 1). Mesothelin membrane staining showed greater correlation with progression-free survival in ovarian cancer and mesothelioma than in the broader dose escalation population.ConclusionsABBV-428 monotherapy exhibited dose-proportional pharmacokinetics and an acceptable safety profile, particularly for toxicities characteristic of CD40 agonism, illustrating that utilization of a tumor-targeted, bispecific antibody can improve the safety of CD40 agonism as a therapeutic approach. ABBV-428 monotherapy had minimal clinical activity in dose escalation and in a small expansion cohort of patients with advanced mesothelioma or ovarian cancer.Trial registration numberNCT02955251.
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Hassan, R., S. J. Antonia, E. W. Alley, H. L. Kindler, T. Jahan, J. J. Grous, S. Honarmand, et al. "515 CRS-207, a mesothelin-targeted immunotherapy, in combination with standard of care chemotherapy as treatment for malignant pleural mesothelioma (MPM)." European Journal of Cancer 51 (September 2015): S108. http://dx.doi.org/10.1016/s0959-8049(16)30316-1.

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Xiao, Zebin, Leslie A. Hopper, Meghan C. Kopp, Emily McMillan, Yue Li, Richard L. Barrett, and Ellen Puré. "Abstract C009: Disruption of tumor-promoting desmoplasia by adoptive transfer of fibroblast activation protein targeted chimeric antigen receptor (CAR) T cells enhances anti-tumor immunity and immunotherapy." Cancer Research 82, no. 22_Supplement (November 15, 2022): C009. http://dx.doi.org/10.1158/1538-7445.panca22-c009.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal disease due to the poor response to current therapeutic treatments. A major barrier to effective treatment of PDAC is the extensive remodeling of tumor stroma characterized by accumulation of cancer associated fibroblasts (CAFs) and extracellular matrix which forms a physical barrier that limits access of the drugs to the cancer cells, suppresses the immune system, and attenuates efficacy of immunotherapies. Fibroblast activation protein (FAP) is highly expressed in a pro-tumorigenic subset of CAFs in PDAC. We hypothesized that depletion of FAP+-CAFs would deplete extracellular matrix (ECM) and reduce the immune suppressive function of the stroma and thereby enhance the efficacy of tumor antigen targeted CAR T cell therapy in PDAC. Using real-time tumor fragment-based 2-photon microscopy, multiparametric flow cytometry and multiplexed immunofluorescence staining, we showed that FAP targeted CAR T cells (FAP-CAR T) efficiently traffic into tumors compared with tumor-antigen (mesothelin) targeted CAR (Meso-CAR) T cells which were trapped in the stroma-rich or matrix-dense areas and led to depletion of immunosuppressive FAP+ cells and reprogrammed the fibrillar collagen network surrounding tumor nests, advancing the infiltration of FAP-CAR T cells into tumor nests. Strikingly, FAP-CAR T cell-mediated depletion for FAP+ cells also rendered the tumor microenvironment permissive to the infiltration and anti-tumor activity of tumor antigen meso-CAR T cells. Moreover, ablation of FAP+ cells markedly enhanced endogenous T cell infiltration which further enhanced anti-tumor immunity and immunotherapy in PDAC models. Thus, our findings established that FAP-CAR T cell-mediated ablation of immunosuppressive FAP+-CAFs and disruption of the desmoplastic stroma they generate, can enhance accumulation and functionality of endogenous anti-tumor immunity and CAR-T cell therapy in the context of highly desmoplastic solid tumors. Citation Format: Zebin Xiao, Leslie A. Hopper, Meghan C. Kopp, Emily McMillan, Yue Li, Richard L Barrett, Ellen Puré. Disruption of tumor-promoting desmoplasia by adoptive transfer of fibroblast activation protein targeted chimeric antigen receptor (CAR) T cells enhances anti-tumor immunity and immunotherapy [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr C009.
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Adusumilli, Prasad S., Marjorie Glass Zauderer, Valerie W. Rusch, Roisin O'Cearbhaill, Amy Zhu, Daniel Ngai, Erin McGee, et al. "Regional delivery of mesothelin-targeted CAR T cells for pleural cancers: Safety and preliminary efficacy in combination with anti-PD-1 agent." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 2511. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.2511.

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2511 Background: We conducted a phase I dose escalation trial of first-in-human autologous chimeric antigen receptor (CAR) T-cell immunotherapy targeting mesothelin (MSLN), a cell-surface antigen that is highly expressed in pleural cancers- malignant pleural mesothelioma (MPM) and metastatic lung and breast cancers. Methods: A single dose of CD28-costimulated MSLN CAR T cells with the I-caspase-9 safety gene was administered intrapleurally in patients with MSLN-expressing pleural tumors. Following a 3+3 design, patients were treated in dose escalating cohorts (dose range 3E5 to 1E7 CAR T cells/kg) following IV cyclophosphamide lymphodepletion (first 3 patients did not receive cyclophosphamide). A subset of MPM patients received subsequent anti-PD-1 therapy, off-protocol, which we have shown to prolong CAR T-cell functional persistence in preclinical models. Results: Twenty patients (18 MPM, 1 lung cancer, 1 breast cancer) were treated (prior lines of therapy 1–8, 35% received ≥3 lines of therapy). No CAR T-cell–related toxicities higher than grade 1 were observed. Intense monitoring for on-target, off-tumor toxicity by clinical (chest or abdominal pain), radiological (CT/PET or echocardiogram for pericardial effusion, ascites), laboratory (troponin elevation), and EKG evaluation found no evidence of toxicity. Fourteen MPM patients received subsequent anti-PD1 therapy (1–21 cycles, pretreatment tumor PD-L1 < 10% in all patients except one), with 1 patient developing grade 3 pneumonitis that responded to steroid treatment. CAR T cells were detected in the peripheral blood of 13 of 14 patients (1-39 weeks). At data cut-off date (Jan 31, 2019), among 14 MPM patients that received combination therapy (follow-up 13-77 weeks, median 31 weeks), best responses included 2 patients with complete metabolic response on PET (62 and 39 weeks ongoing); 5 partial responses and 4 stable disease by investigator assessment. Conclusions: Intrapleurally administered MSLN-targeted CAR T cells were safe. Encouraging antitumor activity of MSLN-targeted CAR T-cell therapy was observed when combined with anti-PD1 therapy and shows promise for future development of this approach. Clinical trial information: NCT02414269.
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Hermanson, David L., Zhenya Ni, David A. Knorr, Laura Bendzick, Lee J. Pribyl, Melissa Geller, and Dan S. Kaufman. "Functional Chimeric Antigen Receptor-Expressing Natural Killer Cells Derived From Human Pluripotent Stem Cells." Blood 122, no. 21 (November 15, 2013): 896. http://dx.doi.org/10.1182/blood.v122.21.896.896.

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Abstract Natural killer (NK) cells are a key part in the innate immune system and have the ability to recognize diverse types of tumors and virally-infected targets. NK cells represent an attractive cell population for adoptive immunotherapy due to their ability to kill target cells in a human leukocyte antigen (HLA) non-restricted manner and without prior sensitization. Clinical studies using IL-2 activated NK cells demonstrate significant anti-tumor effects when adoptively transferred into patients with refractory leukemia (mainly AML). However, there has been a more limited response observed in clinical trials for the treatment of ovarian cancer and other solid malignancies. Chimeric antigen receptors (CARs) consist of an antigen-specific single chain antibody variable fragment fused to intracellular signaling domains derived from receptors involved in lymphocyte activation. CARs targeting various tumor-associated antigens have been developed and tested via expression in primary T cells with promising clinical results. However, engineering these T cells must be done on a patient-specific basis, thus limiting the number of patients who can be treated. In order to produce a potential targeted, “off-the-shelf” product suitable to treat patients with diverse tumors or chronic infections, we have generated human pluripotent stem cells with stable CAR expression. Previous studies by our group demonstrate that human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) provide an accessible, genetically tractable, and homogenous starting cell population to develop NK cells. We use a combined approach using “Spin-EB”- mediated differentiation of hESCs/iPSCs, followed by co-culture with artificial antigen presenting cells (aAPCs) that express mbIL-21. Using this strategy, we can generate 109 NK cells from a population of approximately 106 undifferentiated hESCs or iPSCs. This GMP compatible method is fully defined, without xenogeneic stromal cells or serum. Here, we have expressed both an anti-CD19 (targeting B cell malignancies) and an anti-mesothelin CAR (targeting ovarian cancer cells and other adenocarcinomas) in both hESCs and iPSCs. Using the Sleeping Beauty transposon system, both hESCs and iPSCs have been genetically engineered to express 3rd generation CARs, which express a single chain antibody fragment recognizing either CD19 or mesothelin, a CD8α hinge region, the transmembrane protein CD28, a co-stimulatory protein 4-1BB, and the activating domain CD3ζ. NK cells derived from hESCs/iPSCs with or without CAR expression are phenotypically similar to NK cells isolated from peripheral blood. These NK cells are CD56+, CD94+/CD117-, Nkp44+, Nkp46+, NKG2A+, NKG2D+, and KIR+. In 51Cr release assays against tumor targets expressing either CD19 or mesothelin, NK cells expressing the corresponding CAR show an enhanced killing ability. In cell lines lacking CD19 or mesothelin expression, the engineered cell lines exhibit equal activity compared to their non-engineered counterparts. Specifically, at a 10:1 effector:target ratio, anti-CD19 CAR+ iPSC-NK cells kill 58% of Lax7R cells (a CD19+ ALL cell line) compared to just 5% cell killing by CAR- iPSC-NK cells. Anti-CD19 CAR+ iPSC-NK cells also killed 2 other CD19+ ALL cell lines (018Z and Raji) better than CAR- iPSC-NK cells killing 63% vs 18% and 61% vs 8%, respectively. Similar results are seen against the mesothelin+ ovarian tumor line A1847. Here, anti-mesothelin CAR+ iPSC-NK cells kill 39% vs 14% for CAR- iPSC-NK cells. Currently, CAR-expressing NK cells derived from hESCs and iPSCs are being tested in vivo against both mesothelin+ ovarian tumor lines and CD19+ leukemia cells. Together, these studies demonstrate engineering hESCs and iPSCs with tumor-specific receptors provides a novel strategy to produce targeted NK cells suitable for immune therapies against refractory malignancies. Disclosures: No relevant conflicts of interest to declare.
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Glez-Vaz, Javier, Arantza Azpilikueta, Irene Olivera, Assunta Cirella, Alvaro Teijeira, Maria C. Ochoa, Maite Alvarez, et al. "Soluble CD137 as a dynamic biomarker to monitor agonist CD137 immunotherapies." Journal for ImmunoTherapy of Cancer 10, no. 3 (March 2022): e003532. http://dx.doi.org/10.1136/jitc-2021-003532.

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BackgroundOn the basis of efficacy in mouse tumor models, multiple CD137 (4-1BB) agonist agents are being preclinically and clinically developed. The costimulatory molecule CD137 is inducibly expressed as a transmembrane or as a soluble protein (sCD137). Moreover, the CD137 cytoplasmic signaling domain is a key part in approved chimeric antigen receptors (CARs). Reliable pharmacodynamic biomarkers for CD137 ligation and costimulation of T cells will facilitate clinical development of CD137 agonists in the clinic.MethodsWe used human and mouse CD8 T cells undergoing activation to measure CD137 transcription and protein expression levels determining both the membrane-bound and soluble forms. In tumor-bearing mice plasma sCD137 concentrations were monitored on treatment with agonist anti-CD137 monoclonal antibodies (mAbs). Human CD137 knock-in mice were treated with clinical-grade agonist anti-human CD137 mAb (Urelumab). Sequential plasma samples were collected from the first patients intratumorally treated with Urelumab in the INTRUST clinical trial. Anti-mesothelin CD137-encompassing CAR-transduced T cells were stimulated with mesothelin coated microbeads. sCD137 was measured by sandwich ELISA and Luminex. Flow cytometry was used to monitor CD137 surface expression.ResultsCD137 costimulation upregulates transcription and protein expression of CD137 itself including sCD137 in human and mouse CD8 T cells. Immunotherapy with anti-CD137 agonist mAb resulted in increased plasma sCD137 in mice bearing syngeneic tumors. sCD137 induction is also observed in human CD137 knock-in mice treated with Urelumab and in mice transiently humanized with T cells undergoing CD137 costimulation inside subcutaneously implanted Matrigel plugs. The CD137 signaling domain-containing CAR T cells readily released sCD137 and acquired CD137 surface expression on antigen recognition. Patients treated intratumorally with low dose Urelumab showed increased plasma concentrations of sCD137.ConclusionsCD137 in plasma and CD137 surface expression can be used as quantitative parameters dynamically reflecting therapeutic costimulatory activity elicited by agonist CD137-targeted agents.
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Dissertations / Theses on the topic "Mesothelin targeted cancer immunotherapy"

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Kwan, Byron H. (Byron Hua). "Integrin-targeted cancer immunotherapy." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104220.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, 2016.
Cataloged from PDF version of thesis.
Includes bibliographical references.
Integrins are a family of heterodimeric cell surface receptors that are functionally important for cell adhesion, migration and proliferation. Certain integrins, especially those that are known to recognize the arginine-glycine-aspartate (RGD) motif, are heavily overexpressed in many cancers relative to healthy tissue, making them attractive targets for therapeutic intervention. However, prior attempts to antagonize these integrins as a cancer therapy have all failed in the clinic. In this thesis, we instead exploit integrins as a target tumor antigen in the context of immunotherapy. The engineered cysteine knot peptide, 2.5F, is highly crossreactive and capable of recognizing multiple RGD-binding integrins. Our initial attempts to utilize this binder as a targeting moiety for delivering IL-2 as an immunocytokine failed. Mathematical modeling results indicated that immunocytokines, unless adhering to specific design criteria, are unlikely to benefit from targeting and may actually exhibit limited efficacy. Therefore, we "deconstructed" this immunocytokine into its functional parts: extended half-life IL-2 and 2.5F-Fc, the antibody-like construct directed against RGD-binding integrins. This combination immunotherapeutic approach was able to synergistically control tumor growth in three syngeneic murine models of cancer, including durable cures and development of immunological memory. Contrary to prior attempts at integrin-targeting, the mechanism of action was independent of functional integrin antagonism, including effects on angiogenesis and tumor proliferation. In fact, efficacy of this therapy depended solely upon the adaptive and innate arms of immunity, specifically CD8+ T cells, macrophages, and dendritic cells. Furthermore, checkpoint blockade, the gold standard for immunotherapy to date, can further enhance the efficacy of this therapeutic approach. This signifies that the combination of IL-2 and 2.5F-Fc exerts a distinct, yet complementary immune response that opens the door for clinical translation.
by Byron H. Kwan.
Ph. D.
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Beauregard, Caroline. "Type I Interferon-Mediated Killing of Cancer Cells with IAP-Targeted Combination Immunotherapy." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34201.

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SMAC mimetic compounds (SMCs) are small molecule antagonists of the Inhibitor of Apoptosis (IAP) family of proteins. Binding of SMCs to the IAPs results in the sensitization of cancer cells to apoptosis in the presence of death ligands, such as tumour necrosis factor alpha (TNFα). I hypothesize that type I interferon (IFN) stimulation in cancer cells and in immune cells leads to the production of TNFα, which can then synergize with SMCs to kill cancer cells. The combined treatment of SMC and IFNα induces tumour regression in mice, and this effect is completely abrogated upon treatment with TNFα-neutralizing antibody. The synergistic effects are mediated by tumour cells and by contribution of immune cells, particularly macrophages and dendritic cells, as the systemic depletion of phagocytic innate immune cells results in an increase in tumour volume following combination treatment. The characterization of immune cell contribution will aid in the translation of the SMC combination therapy into clinical applications for the treatment of cancer.
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Edes, Inan. "Targeted transduction of T cell subsets for immunotherapy of cancer and infectious disease." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2016. http://dx.doi.org/10.18452/17669.

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Das Ziel der vorliegenden Arbeit bestand darin, ein Vektorsystem zu entwickeln, dass den simultanen Transfer verschiedener Transgene in CD8+ und CD4+ T-Zellen und dadurch die Herstellung eines immunotherapeutischen T-Zell-Produkts ermöglicht, welches aus zwei unterschiedlich modifizierten T-Zell-Subtypen besteht. Im ersten Teil der Arbeit wurde die Targeting-Technologie von lentiviralen auf γ-retrovirale Vektoren übertragen. Anschließend wird die Herstellung von Vektoren beschrieben, die spezifisch für murines CD4 oder CD8 sind. Deren Spezifität wurde zum einen durch die exklusive Expression von GFP in CD4+ oder CD8+ Zellen und zum anderen durch den Dosis-abhängigen Verlust des GFP-Signals nach Inkubation dieser Zellen mit CD4- und CD8-blockierenden Antikörpern nachgewiesen. Im dritten Teil der Arbeit wird gezeigt, dass MVm8 und MVm4 primäre T-Zellen spezifisch transduzieren. MVm8-vermittelter Transfer des Ovalbumin (OVA)-reaktiven TZRs OT-I führte zu T-Zellen, die OVA+ Tumor-Zelllinien erkannten und Interferon-γ sezernierten. Der vierte Teil dieser Arbeit beschäftigt sich mit der in vivo Transduktion primärer T-Zellen mithilfe von MVm8, welches den OT-I-TZR und eine Luciferase transferiert (MVm8/OT-I-luc). Durch systemische Applikation von MVm8/OT-I-luc wurden T-Zellen in vivo transduziert. Durch Immunisierungen konnten antigen-spezifisches Homing, Expansion und eine anschließende Kontraktion in vivo transduzierter T-Zellen gezeigt werden. Mäuse mit starker OT-I-luc-Expression waren gegenüber einer Infektion durch OVA-transgene listeria monocytogenes geschützt. Zusammenfassend lässt sich sagen, dass das in dieser Arbeit entwickelte Vektorsystem in der Lage ist zwischen Subtypen von T-Zellen zu unterscheiden und sie simultan mit unterschiedlichen Transgenen auszustatten. Für MVm8 konnte gezeigt werden, dass es T-Zellen direkt in vivo transduzieren kann.
The aim of this thesis was to generate a vector system that allows the simultaneous transfer of different transgenes into CD8+ and CD4+ T cells, allowing the generation of a immunotherapeutic T cell product comprised of two differently engineered T cell subsets. The first part of the thesis describes the transfer of the measles virus (MV) envelope-based targeting technology from lentiviral (LV) to γ-retroviral (gRV) vectors. The second part reports the generation of two targeting vectors specific for murine CD4 or CD8. The exclusive specificity of MVm4 and MVm8 was proven by expression of GFP in CD4+ and CD8+ reporter cells, respectively, but not in CD4-CD8- cells after transduction, and by a dose-dependent loss of GFP signal after incubation of reporter cells with CD4 or CD8 blocking antibodies before transduction. The third part shows that MVm8 but not MVm4 transduced primary T cells. MVm8-mediated transfer of the ovalbumin (OVA)-reactive TCR OT-I resulted in T cells secreting interferon-γ (IFNγ) upon recognition of OVA+ tumor cell lines. The final part of this thesis describes the in vivo transduction of primary T cells using MVm8 transferring OT-I and a luciferase (MVm8/OT-I-luc). To this end, B6 mice deficient for Rag2 have been repopulated with either polyclonal (B6) or monoclonal T cells derived from P14-TCR transgenic mice (P14). One day later the transferred T cells were transduced in vivo by systemic application of MVm8/OT-I-luc. Upon immunization in vivo-transduced T cells homed, expanded and contracted repeatedly in an antigen-dependent manner. Finally, mice exhibiting strong luc-signals showed improved protection against infections by OVA-transgenic listeria monocytogenes (LM-OVA). In conclusion, the viral vector system developed within this thesis is able to discriminate between the two main T cell subsets and to equip them with distinct transgenes simultaneously.
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Kostova, Vesela. "Shiga toxin targeted strategy for chemotherapy and cancer immunotherapy application using copper-free « Click » chemistry." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB144.

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Pas de résumé
Recently targeted therapies appeared as attractive alternatives to classical antitumoral treatments. The approach, developed on the concept of targeting drug to cancer cells, aims to spear normal tissues and decrease the side effects. This doctoral dissertation focuses on developing new anticancer targeted treatments in the field of chemotherapy and cancer immunotherapy by exploiting an original targeting moiety, the B subunit of Shiga toxin (STxB). Its specific properties, such as, recognition with its receptor Gb3 overexpressed in cancer cells or in antigen-presenting cells, its unconventional intracellular trafficking, guided the choice of this protein as targeting carrier. This project is based in the use of copper-free Huisgen [3+2] cycloaddition as a coupling method, which led to successful preparation of various conjugates for their respective applications. The concept was first validated by STxB-biotin conjugate. The high yield of the reaction and the compatibility between the targeting carrier and the chemical ligation promoted the design of conjugates for chemotherapy and immunotherapy. Two therapeutical optimizations of previously developed strategy in STxB drug targeting delivery were investigated: synthesis of multivalent drug-conjugates and synthesis of conjugates containing a highly potent anticancer agent. Both approaches exploited three anticancer agents: SN38, Doxorubicin and Monomethyl auristatin F. The disulfide spacer, combined with various self-immolative systems, insured drug release. Two cytotoxic conjugates STxB–doxorubicin (STxB-Doxo) and STxB-monomethyl auristatin F (STxB-MMAF) were obtained in very high yield and demonstrated strong tumor inhibition activity in the nanomolar range on Gb3-positive cells. Based on the results the STxB-MMAF conjugate was investigated on a mouse model. The project aimed also to develop STxB bioconjugates for vaccine applications. Previous studies used B subunit as a targeting carrier coupled to an antigenic protein in order to induce a more potent immune response against cancer. The conjugates were prepared using a commercial linker, requiring modifying the antigen at first place, or by oxime ligation, where slightly acidic conditions promoted the coupling. Thus, the work presented herein proposed an alternative ligation via copper-free click chemistry especially for more sensitive antigenic proteins. Various types of conjugates were synthesised and investigated for their immune stimulation properties. The STxB targeting strategy was also applied to the development of a new vaccine based on coupling the targeting carrier to alpha-GalCer, one of the most potent immune stimulating agents known. The work focused on the synthesis of functionalised alpha-Galcer with an azide handle
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Hornig, Nora [Verfasser], and Roland [Akademischer Betreuer] Kontermann. "Combinations of costimulatory antibody-ligand fusion proteins for targeted cancer immunotherapy / Nora Hornig. Betreuer: Roland Kontermann." Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2013. http://d-nb.info/104519526X/34.

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Bento, Rui Pedro Garcia de Oliveira. "CAR-modified T cells targeted to CD19 antigen for lymphocytic leukemia." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/13445.

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Mestrado em Biomedicina Farmacêutica
Cellular immunotherapies, or Advanced Therapy Medicinal Products (ATMPs), are emerging as novel and specific therapeutic approaches to treat diseases, such as certain types of leukemias, which are difficult or impossible to treat with today’s biopharmaceutical products. Breakthroughs in basic, preclinical, and clinical science spanning cellular immunology, and cellprocessing technologies has allowed clinical applications of chimeric antigen receptor–based therapies. A recent example is CTL019, a lentivirus-based gene therapy for autologous T cells, acquired by Novartis in 2012 through a global alliance with the University of Pennsylvania. Although this technology is still in its infancy, clinical trials have already shown clinically significant antitumor activity in chronic lymphocytic leukemia and acute lymphocytic leukemia. Trials targeting a variety of other adult and pediatric malignancies are under way. The potential to target essentially any tumor-associated cell-surface antigen for which a monoclonal antibody can be made opens up an entirely new arena for targeted therapy of cancer. The regulatory environment for these Advanced Therapies Medicinal Products is complex and in constant evolution. Many challenges lie ahead in terms of manufacturing process, non-conventional supply chain logistics, business models, intellectual property, funding and patient access.
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Banaszek, Agnes [Verfasser], and Harald [Gutachter] Wajant. "Dual Antigen-Restricted Complementation of a Two-Part Trispecific Antibody for Targeted Immunotherapy of Blood Cancer / Agnes Banaszek. Gutachter: Harald Wajant." Würzburg : Universität Würzburg, 2013. http://d-nb.info/1110027168/34.

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Edes, Inan [Verfasser], Wolfgang [Gutachter] Uckert, Antonio [Gutachter] Pezzutto, and Christian [Gutachter] Buchholz. "Targeted transduction of T cell subsets for immunotherapy of cancer and infectious disease / Inan Edes ; Gutachter: Wolfgang Uckert, Antonio Pezzutto, Christian Buchholz." Berlin : Lebenswissenschaftliche Fakultät, 2016. http://d-nb.info/1124893423/34.

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Reul, Johanna [Verfasser], Beatrix [Akademischer Betreuer] Süß, Gerhard [Akademischer Betreuer] Thiel, and Christian [Akademischer Betreuer] Buchholz. "Viral gene transfer systems for cancer immunotherapy: semireplication-competent VSV and receptor-targeted AAV for the delivery of immunomodulatory proteins / Johanna Reul ; Beatrix Süß, Gerhard Thiel, Christian Buchholz." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2019. http://d-nb.info/1176107585/34.

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Lebdai, Souhil. "Potentialisation de la photothérapie dynamique à visée vasculaire par une modulation des cellules myéloïdes par le récepteur CSF-1R dans un modèle préclinique de cancer de la prostate Les traitements focaux : une alternative dans la prise en charge du cancer de la prostate de bas risque ? Potentiating vascular-targeted photodynamic therapy through CSF-1R modulation of myeloid cells in a preclinical model of prostate cancer." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS521.

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La photothérapie dynamique à visée vasculaire utilisant le WST11 (VTP) induit la destruction rapide des tissus ciblés et constitue un traitement prometteur pour le cancer de la prostate. Cependant, la réponse immunitaire qui en résulte, qui peut jouer un rôle important dans la potentialisation ou l’atténuation des effets de la VTP, n’a toujours pas été comprise. Les cellules myéloïdes, telles que les MDSC et les macrophages, sont souvent présentes dans les tumeurs et sont largement associées à l'angiogenèse, au remodelage tissulaire et à l'immunosuppression. On sait également que ces cellules jouent un rôle essentiel dans la cicatrisation des plaies, induite lors de la destruction rapide des tissus. Nous avons étudié les effets de la VTP sur le recrutement de cellules myéloïdes infiltrant la tumeur (TIM), en particulier les MDSC et les macrophages associés aux tumeurs (TAM), dans les modèles de cancer de la prostate murin Myc-Cap et TRAMP C2. Nous rapportons que la VTP augmentait à la fois l'infiltration de cellules myéloïdes dans les tumeurs, mais aussi l’expression de CSF1R ; CSF1R étant un récepteur nécessaire à la différenciation, à la prolifération et à la migration des cellules myéloïdes. Comme un traitement anti-CSF1R avait déjà été utilisé pour diminuer l’infiltration de cellules myéloïdes dans d'autres modèles murins de cancer de la prostate, nous avons émis l'hypothèse que l'association d'un anti-CSF1R à un traitement par VTP entraînerait une diminution de la repousse tumorale et une amélioration de la survie. Nous avons constaté que le ciblage des cellules myéloïdes en utilisant un anti-CSF1R en association avec la VTP diminuait le nombre de MDSC et de TAM, et en particulier les macrophages M2. De plus cette association induisait une infiltration accrue de cellules T CD8+, diminuait la croissance tumorale et prolongeait la survie globale. Ces résultats suggèrent que le ciblage des cellules myéloïdes via le récepteur CSF1R est une stratégie prometteuse pour potentialiser les effets anti-tumoraux de la VTP
Vascular-targeted photodynamic therapy (VTP) induces rapid destruction of targeted tissues and is a promising therapy for prostate cancer. However, the resulting immune response, which may play an important role in either potentiating or blunting the effects of VTP, is still incompletely understood. Myeloid cells such as myeloid-derived suppressor cells (MDSCs) and macrophages are often found in tumors and are widely reported to be associated with cancer angiogenesis, tissue remodelling and immunosuppression. These cells are also known to play a critical role in wound-healing, which is induced by rapid tissue destruction. In this study, we investigated the effects of VTP on the recruitment of tumor infiltrating myeloid cells, specifically MDSCs and tumor-associated macrophages (TAMs), in the Myc-Cap and TRAMP C2 murine prostate cancer models. We report that VTP increased the infiltration of myeloid cells into the tumors, as well as their expression of CSF1R, a receptor required for myeloid differentiation, proliferation and tumor migration. As anti-CSF1R treatment has previously been used to deplete these cells types in other murine models of prostate cancer, we hypothesized that combining anti-CSF1R with VTP therapy would lead to decreased tumor regrowth and improved survival. Importantly, we found that targeting myeloid cells using anti-CSF1R in combination with VTP therapy decreased the number of tumor MDSCs and TAMs, especially M2 macrophages, as well as increased CD8+ T cell infiltration, decreased tumor growth and improved overall survival. These results suggest that targeting myeloid cells via CSF1R targeting is a promising strategy to potentiate the anti-tumor effects of VTP
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Books on the topic "Mesothelin targeted cancer immunotherapy"

1

Yan, Cui, Li Shulin, and SpringerLink (Online service), eds. Targeted Cancer Immune Therapy. New York, NY: Springer-Verlag New York, 2009.

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N, Syrigos Konstantinos, and Harrington Kevin J. 1958-, eds. Targeted therapy for cancer. Oxford: Oxford University Press, 2003.

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Anderson, Kenneth C., Razelle Kurzrock, and Apostolia-Maria Tsimberidou. Targeted therapy in translational cancer research. Hoboken, New Jersey: John Wiley & Sons, Inc., 2016.

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Alharbi, Yousef, Manish S. Patankar, and Rebecca J. Whelan. Antibody-Based Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0006.

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With their role in connecting disease-associated antigens to the cellular immune response, antibodies hold considerable promise as therapeutic agents. This chapter discusses three classes of therapeutic antibodies that have been developed for use in ovarian cancer therapy. The first includes antibodies selected against tumor-associated antigens such as MUC16/CA125, mesothelin, epithelial cell adhesion molecule, and folate receptor α‎. Antibodies in the second class target proteins such as CTLA-4 and PD1 that act as immune response checkpoint receptors. The third class of antibodies target secreted factors that promote tumor growth: targets in this class include vascular endothelial growth factor, cytokines, and chemokines. The development of each of these is described. The chapter also discusses the complications presented by soluble antigens, which serve to limit the applicability of antigens (such as MUC16/CA125) that are both cell-surface associated and circulating and the prospects for the combination of antibody-based immunotherapy and chemotherapy.
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Williams, William Valentine, Karen Anderson, David B. Weiner, and Cara Haymaker, eds. Targeted Immunotherapy for Cancer. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-074-9.

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Li, Shulin, Yan Cui, and Joseph Lustgarten. Targeted Cancer Immune Therapy. Springer New York, 2016.

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Treating Cancer with Immunotherapy and Targeted Therapy. Mercury Learning & Information, 2019.

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Olle, David A. Treating Cancer with Immunotherapy and Targeted Therapy. Mercury Learning & Information, 2022.

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Olle, David A. Treating Cancer with Immunotherapy and Targeted Therapy. Mercury Learning & Information, 2022.

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Karp, Daniel D., Gerald S. Falchook MD MS, and Joann Lim. Handbook of Targeted Cancer Therapy and Immunotherapy. LWW, 2018.

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Book chapters on the topic "Mesothelin targeted cancer immunotherapy"

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Mahalingam, Devalingam, Michael J. Brumlik, Reinhard Waehler, David T. Curiel, and Tyler J. Curiel. "Targeted Toxins in Cancer Immunotherapy." In Cancer Immunotherapy, 377–96. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4732-0_12.

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Ebata, Takahiro. "Immunotherapy." In Molecular Targeted Therapy of Lung Cancer, 227–37. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2002-5_14.

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Baumeister, Susanne H. C., and Glenn Dranoff. "Principles of Targeted Immunotherapy." In Targeted Therapy in Translational Cancer Research, 27–38. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118468678.ch3.

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Cerbone, Linda, and Cora N. Sternberg. "Adjuvant Systemic Therapy, Immunotherapy, and Targeted Treatment." In Renal Cancer, 335–47. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7236-0_20.

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Burnside, Wesley, and Yan Cui. "Engineering Adult Stem Cells for Cancer Immunotherapy." In Targeted Cancer Immune Therapy, 191–206. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0170-5_11.

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Prieto, Peter A., Miles C. Andrews, Alexandria P. Cogdill, and Jennifer A. Wargo. "Interaction between Targeted Therapy and Immunotherapy." In Immunotherapy in Translational Cancer Research, 268–85. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781118684535.ch19.

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Farhangnia, Pooya, Ali-Akbar Delbandi, Maryam Sadri, and Mahzad Akbarpour. "Bispecific Antibodies in Targeted Cancer Immunotherapy." In Handbook of Cancer and Immunology, 1–46. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-030-80962-1_189-1.

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Mukaida, Naofumi, So-ichiro Sasaki, and Tomohisa Baba. "Tumor Immunotherapy by Utilizing a Double-Edged Sword, Chemokines." In Cancer Targeted Drug Delivery, 97–118. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7876-8_4.

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Friedmann-Morvinski, Dinorah, and Zelig Eshhar. "Adoptive Transfer of T-Bodies: Toward an Effective Cancer Immunotherapy." In Targeted Cancer Immune Therapy, 285–99. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0170-5_16.

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Vujanovic, Lazar, and Lisa H. Butterfield. "Dendritic Cell Vaccines for Immunotherapy of Cancer: Challenges in Clinical Trials." In Targeted Cancer Immune Therapy, 159–72. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0170-5_9.

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Conference papers on the topic "Mesothelin targeted cancer immunotherapy"

1

Ries, Carola. "Abstract SY06-02: Macrophage-targeted cancer immunotherapy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-sy06-02.

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Gottschalk, Stephen, Sunitha Karkala, LaTerrica Williams, and Xiao-Tong Song. "Abstract IA26: Stroma-targeted immunotherapy." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-ia26.

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Alewine, Christine, Emily Maon-Osann, and Ira Pastan. "Abstract 5440: Activity of mesothelin-targeted immunotoxin RG7787 against triple-negative breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5440.

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Zhao, Jean. "Abstract IA22: Integrating immunotherapy and targeted therapy in breast cancer." In Abstracts: AACR Special Conference: Advances in Breast Cancer Research; October 7-10, 2017; Hollywood, CA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3125.advbc17-ia22.

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Min, Jung-Joon, Jin Hai Zheng, Yeongjin Hong, Hyon E. Choy, and Joon Haeng Rhee. "Abstract 1610: Targeted cancer immunotherapy with engineeredSalmonella typhimuriumsecreting heterologous bacterial flagellin." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1610.

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Chou, Jeffrey, Lilien N. Voong, Xiaoji Chen, Cassian Yee, and Edus H. Warren. "Abstract 4778: Epigenetic modulation of colorectal cancer cells for cancer-testis antigen-targeted immunotherapy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4778.

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Valton, Julien, Anne-Sophie Gautron, Alexandre Juillerat, Philippe Duchateau, and Laurent Poirot. "Abstract A080: Targeted genome modifications for improved adoptive immunotherapy." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a080.

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Wittrup, Karl Dane. "Abstract IA25: Synergistic innate and adaptive integrin-targeted immunotherapy." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-ia25.

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Alewine, Christine Campo, Emily Kolyvas, Klaus Boslett, and Ira Pastan. "Abstract 2566: Combination of taxanes with mesothelin-targeted immunotoxin RG7787 induces synergistic killing of pancreatic cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2566.

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Phillips, Mariana, Constantine Bitsaktsis, and David Sabatino. "B7H6: A Bio-Marker for the Development of Cancer-Targeted Immunotherapy Applications." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.117.

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Reports on the topic "Mesothelin targeted cancer immunotherapy"

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Song, Xiao-Tong. Cancer and Stroma-Targeted Immunotherapy with a Genetically Modified DC Vaccine. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada591280.

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Song, Xiao-Tong. Cancer and Stroma-Targeted Immunotherapy with a Genetically Modified DC Vaccine. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada547382.

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Marenco-Hillembrand, Lina, Michael A. Bamimore, Julio Rosado-Philippi, Blake Perdikis, David N. Abarbanel, Alfredo Quinones-Hinojosa, Kaisorn L. Chaichana, and Wendy J. Sherman. The Evolving Landscape of Leptomeningeal Cancer from Solid Tumors: A Systematic Review of Clinical Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0112.

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Review question / Objective: Among adult patients with leptomeningeal carcinomatosis from solid tumors (population) treated with chemotherapy, targeted therapy, or immunotherapy (intervention and comparator) what are the differences in overall survival (OS) and progression-free survival (PFS) and treatment response based on clinical trial outcomes? Eligibility criteria: Included articles reported 1) human subjects ≥ 18 years 2) diagnosis of leptomeningeal carcinomatosis from solid tumors confirmed by imaging or cerebrospinal fluid (CSF) cytology and clinical or neurological symptoms 3) clinical trials 4) with either PFS or MOS outcomes listed. Book chapters, case reports, review articles, observational studies, ed-itorials, and publications of leptomeningeal cancer from hematological tumors and studies consisting solely of pediatric patients were excluded from the analysis.
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