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Delivery of Immune Checkpoint Inhibitors Using Nanoparticles
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Abdullah Shaito, Houssein Hajj Hassan
Currently, immunotherapy is one of the most promising cancer treatments [2] and the development of new immunotherapies has become a necessity [3, 4]. In recent years, immunotherapy has become widespread and has been used to treat both hematological and solid cancers [2]. Immunotherapy is a biological therapy that involves activation of the immune system to target and kill cancer cells through different approaches. Promising immunotherapy approaches include adoptive cell transfer, therapeutic monoclonal antibodies (mAbs), treatment vaccines, cytokine treatment using interferons and interleukins, Bacillus Calmette Guérin (BCG), which is a weakened bacterium used in the treatment of bladder cancer, and immune checkpoint inhibitors. Chimeric antigen receptor therapy also known as CAR T-cell therapy has stood out as a clinically effective type of adoptive cell transfer therapy. Immune checkpoint inhibitors, in particular, have shown potential in the treatment of several cancers and have been FDA approved for the treatment of melanoma (recurrent and/or metastatic), non-small cell lung cancers (NSCLCs), genitourinary cancers (GUCs), head and neck cancers (HNCs), renal cell carcinomas, urothelial carcinomas, non-Hodgkin lymphomas and other cancers [5].
In Vitro Models for Preclinical Drug Development
Published in Hyun Jung Kim, Biomimetic Microengineering, 2020
Jason Ekert, Sunish Mohanan, Julianna Deakyne, Philippa Pribul Allen, Nikki Marshall, Claire Jeong, Spiro Getsios
Immunocompetent animal models for preclinical development of immuno-oncology (I-O) drugs have either not been available or have been of limited effectiveness, as in vivo models do not closely resemble the immune system of cancer patients who enroll in immunotherapy trials. This is a major problem and requires the generation of I-O model systems that can be used to increase clinical relevance to perform preclinical drug screening, toxicity, and efficacy prediction. For agents targeting different immune effector cells, there has been an increase in the likelihood of cytokine-release syndrome (CRS) that has occurred with anti-CD20 (Coiffier et al. 2008, Goede et al. 2014) or anti-CD19 (Buie et al. 2015, Topp et al. 2015) antibodies and chimeric antigen receptor (CAR)-T therapy (Brudno and Kochenderfer 2016). While immune checkpoint inhibitors such as anti-PD-1 and anti-CTLA-4 can stimulate cellular immune effectors by blocking inhibitory signals, they can reduce tolerance and may lead to inflammation, tissue damage, and autoimmunity which have been reported as immune-related adverse events (IRAEs) in a percentage of patients (Michot et al. 2016). PD that is associated with the biochemical and physiological effect of an administered drug on a patient are still being developed for many I-O agents (Marshall and Djamgoz 2018).
Mechanistic Model of Tumor Response to Immunotherapy
Published in Vittorio Cristini, Eugene J. Koay, Zhihui Wang, An Introduction to Physical Oncology, 2017
Geoffrey V. Martin, Eman Simbawa
In this section, we extend our prior work on modeling chemotherapy to the realm of immunotherapies. We focus on modeling immune checkpoint inhibitor antibodies due to their success in recent clinical trials, although they can be extended to exogenous molecular immunotherapies in general. Briefly, immune checkpoint inhibitors attempt to block the interaction between immune-inhibiting ligands expressed on tumor cells and their binding counterparts on immune cells. Once the tumor ligands are bound to these proteins expressed on the immune cells, they begin a cascade of intracellular events that renders the immune cells ineffective at killing tumor cells. Tumors have a multitude of ways that they can inhibit immune cell killing, but these immune checkpoint pathways represent a prominent mode in some types of cancers. Two of the most clinically relevant immune checkpoint pathways are those associated with cytotoxic T lymphocyte–associated protein-4 (CTLA-4) and PD-1 [343,344]. Blocking the interaction between the tumor ligands specific for CTLA-4 or PD-1 (cluster of differentiation [CD] 80/86 or programmed death ligand-1 [PD-L1], respectively) on immune cells with anti-CTLA4 or anti-PD-1 antibodies has shown clinical responses in colorectal, lung, melanoma, urothelial, and renal cell cancers [293,330,345–347].
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
With the advances in cancer treatment using immunotherapies, research focus has shifted from TAMs and become slanted towards suppressing the functions of Treg, T cell inhibitory receptors (immune checkpoints) and chimeric antigen T cell receptors (CAR-T). Reduction in cancer burden and success with these immune checkpoint therapies relies largely on their ability to induce the activation and recruitment of tumour reactive-cytotoxic T cells (Wei et al. 2018). However, not every patient will benefit from immune checkpoint therapy, particularly those who have shown resistance to immunotherapies. Current research has shown that resistance to immune checkpoint can be overcome with increased tumour-associated myeloid cells such a macrophages, granulocytes and monocytes (De Henau et al. 2016; Pathria et al. 2019). Therapies that induce the recruitment of tumour-associated myeloid cells such as TLR agonists and signal transducer and activator of transcription (STAT)-3 inhibitors are currently being investigated for potential clinical use (Pathria et al. 2019).
Tumor growth suppression by implantation of an anti-CD25 antibody-immobilized material near the tumor via regulatory T cell capture
Published in Science and Technology of Advanced Materials, 2021
Tsuyoshi Kimura, Rino Tokunaga, Yoshihide Hashimoto, Naoko Nakamura, Akio Kishida
Cancer treatment can be classified into surgical treatment, chemotherapy, radiotherapy, and immunotherapy. Cancer immunotherapy is a method for treating cancer using the immune system. To date, various cancer immunotherapies have been proposed, including vaccine therapy using autologous cancer vaccines [1], dendritic cell vaccines [2], and adoptive immunotherapy using natural killer (NK) cells and cytotoxic T cells [3]. Among these approaches, cancer immunotherapy related to regulatory T cells (Tregs) has recently become a major research focus. Tregs, i.e., CD4-, CD25-, and FoxP3-positive T cells, are key players in immune suppression [4] and function by controlling the activation of antigen-presenting cells via cytotoxic T lymphocyte antigen (CTLA)-4 and immunosuppressive cytokines (e.g., interleukin-10). In addition, Tregs play roles in suppressing the attack of T cells and other immune cells by modulating the production of transforming growth factor-β [5]. Furthermore, in the tumor microenvironment, which is formed by various components, including cancer cells, immune cells, and the extracellular matrix, Treg accumulation is induced by secretion of the chemokine C-C motif chemokine ligand 22 (CCL22) from cancer cells and tumor-infiltrating macrophages, resulting in an antitumor immune response [6,7]. Several treatments that inhibit immunosuppressive signal transduction by immune checkpoint inhibitors (e.g., anti-CTLA-4 and anti-programmed death-1 antibodies) and depletion of Tregs by administration of anti-C-C motif chemokine receptor 4 antibodies have been proposed as Treg-related cancer immunotherapies [8,9]. The development of selective Treg removal methods is also proposed [10,11]. Although the efficacies of these treatments have been demonstrated, treatment with immune checkpoint inhibitors can induce serious side effects owing to activation of T cells [12]. In addition, because Tregs are strongly related to autoimmunity, Treg-removing treatments may cause systemic autoimmune diseases. Therefore, the development of a method for local Treg removal at the tumor is essential.