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"Dong, Haidong"
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The basics of cancer immunotherapy
\"This book provides patients and their physicians (especially \"non-oncologist\" health care providers) with a clear and concise introduction to cancer immunotherapy, which, unlike traditional forms of cancer therapy, acts by boosting the patient's own immune system to fight cancer. The unique features of cancer immunotherapy make its management, monitoring and side-effects different from those of traditional cancer therapy. Especially novel are the side effects of cancer immunotherapy, necessitating greater awareness for both patients and physicians in order to minimize complications of therapy. The patient-friendly, concise, easy-to-understand, and up-to-date knowledge presented in this book will inform patients about the benefits and risks of cancer immunotherapy, and help them and their care providers to understand how immunotherapy would control their unique disease. Researchers and academic professionals in the field of cancer immunotherapy will also find clear and useful information to help them communicate with patients or address unresolved problems. Some key features of the book are:Expertise. All editors and authors are scientists and oncologists specializing in cancer immunotherapy, and are involved in scientific discovery from the early stage of immune-checkpoint inhibitors to today's daily patient care. Their insights, expertise and experience guarantee the high quality and authority in the science, medicine and practice of cancer immunotherapy. Patient-friendly. This book is written for cancer patients in order to meet their needs when considering immunotherapy. As an educational tool, this book will help the reader balance the risks and benefits based on both science and clinical facts, and therefore to make the best choice in receiving or withdrawing from immunotherapy. Disease Specificity. Cancer is a complicated disease involving multiple stages and pathology. Its response to immunotherapy is individualized and varies depending on cancer types. The authors' expertise in treating different types of cancers, including melanoma, lung, kidney, bladder, and lymphoma, provides disease-specific insights in applying immunotherapy to each disease.\"-- Provided by publisher.
Book
Regulation of sister chromatid cohesion by nuclear PD-L1
Programmed death ligand-1 (PD-L1 or B7-H1) is well known for its role in immune checkpoint regulation, but its function inside the tumor cells has rarely been explored. Here we report that nuclear PD-L1 is important for cancer cell sister chromatid cohesion. We found that depletion of PD-L1 suppresses cancer cell proliferation, colony formation in vitro, and tumor growth in vivo in immune-deficient NSG mice independent of its role in immune checkpoint. Specifically, PD-L1 functions as a subunit of the cohesin complex, and its deficiency leads to formation of multinucleated cells and causes a defect in sister chromatid cohesion. Mechanistically, PD-L1 compensates for the loss of Sororin, whose expression is suppressed in cancer cells overexpressing PD-L1. PD-L1 competes with Wing Apart-Like (WAPL) for binding to PDS5B, and secures proper sister chromatid cohesion and segregation. Our findings suggest an important role for nuclear PD-L1 in cancer cells independent of its function in immune checkpoint.
Journal Article
Targeting tumor-associated macrophages and granulocytic myeloid-derived suppressor cells augments PD-1 blockade in cholangiocarcinoma
Immune checkpoint blockade (ICB) has revolutionized cancer therapeutics. Desmoplastic malignancies, such as cholangiocarcinoma (CCA), have an abundant tumor immune microenvironment (TIME). However, to date, ICB monotherapy in such malignancies has been ineffective. Herein, we identify tumor-associated macrophages (TAMs) as the primary source of programmed death-ligand 1 (PD-L1) in human and murine CCA. In a murine model of CCA, recruited PD-L1+ TAMs facilitated CCA progression. However, TAM blockade failed to decrease tumor progression due to a compensatory emergence of granulocytic myeloid-derived suppressor cells (G-MDSCs) that mediated immune escape by impairing T cell response. Single-cell RNA sequencing (scRNA-Seq) of murine tumor G-MDSCs highlighted a unique ApoE G-MDSC subset enriched with TAM blockade; further analysis of a human scRNA-Seq data set demonstrated the presence of a similar G-MDSC subset in human CCA. Finally, dual inhibition of TAMs and G-MDSCs potentiated ICB. In summary, our findings highlight the therapeutic potential of coupling ICB with immunotherapies targeting immunosuppressive myeloid cells in CCA.
Journal Article
Combining Immune Checkpoint Inhibitors With Conventional Cancer Therapy
Immune checkpoint inhibitors (ICIs) have recently revolutionized cancer treatment, providing unprecedented clinical benefits. However, primary or acquired therapy resistance can affect up to two-thirds of patients receiving ICIs, underscoring the urgency to elucidate the mechanisms of treatment resistance and to design more effective therapeutic strategies. Conventional cancer treatments, including cytotoxic chemotherapy, radiation therapy, and targeted therapy, have immunomodulatory effects in addition to direct cancer cell-killing activities. Their clinical utilities in combination with ICIs have been explored, aiming to achieve synergetic effects with improved and durable clinical response. Here, we will review the immunomodulatory effects of chemotherapy, targeted therapy, and radiation therapy, in the setting of ICI, and their clinical implications in reshaping modern cancer immunotherapy.
Journal Article
Targeting IFNα to tumor by anti-PD-L1 creates feedforward antitumor responses to overcome checkpoint blockade resistance
Many patients remain unresponsive to intensive PD-1/PD-L1 blockade therapy despite the presence of tumor-infiltrating lymphocytes. We propose that impaired innate sensing might limit the complete activation of tumor-specific T cells after PD-1/PD-L1 blockade. Local delivery of type I interferons (IFNs) restores antigen presentation, but upregulates PD-L1, dampening subsequent T-cell activation. Therefore, we armed anti-PD-L1 antibody with IFNα (IFNα-anti-PD-L1) to create feedforward responses. Here, we find that a synergistic effect is achieved to overcome both type I IFN and checkpoint blockade therapy resistance with the least side effects in advanced tumors. Intriguingly, PD-L1 expressed in either tumor cells or tumor-associated host cells is sufficient for fusion protein targeting. IFNα-anti-PD-L1 activates IFNAR signaling in host cells, but not in tumor cells to initiate T-cell reactivation. Our data suggest that a next-generation PD-L1 antibody armed with IFNα improves tumor targeting and antigen presentation, while countering innate or T-cell-driven PD-L1 upregulation within tumor.
Despite the presence of tumor-infiltrating lymphocytes, many patients do not respond to PD-L1/PD-1 blockade therapy. Here they show that PD-L1 antibody armed with interferon-α (IFNα) improves tumor targeting and antigen presentation while countering innate or T-cell-drive PD-L1 upregulation, and overcomes resistance to checkpoint blockade therapy.
Journal Article
Functional Expression of Programmed Death-Ligand 1 (B7-H1) by Immune Cells and Tumor Cells
The programmed death-1 (PD-1) and its ligand PD-L1 (B7-H1) signaling pathway has been the focus of much enthusiasm in the fields of tumor immunology and oncology with recent FDA approval of the anti-PD-1 antibodies pembrolizumab and nivolumab and the anti-PD-L1 antibodies durvalumab, atezolimuab, and avelumab. These therapies, referred to here as PD-L1/PD-1 checkpoint blockade therapies, are designed to block the interaction between PD-L1, expressed by tumor cells, and PD-1, expressed by tumor-infiltrating CD8
T cells, leading to enhanced antitumor CD8
T cell responses and tumor regression. The influence of PD-L1 expressed by tumor cells on antitumor CD8
T cell responses is well characterized, but the impact of PD-L1 expressed by immune cells has not been well defined for antitumor CD8
T cell responses. Although PD-L1 expression by tumor cells has been used as a biomarker in selection of patients for PD-L1/PD-1 checkpoint blockade therapies, patients whose tumor cells lack PD-L1 expression often respond positively to PD-L1/PD-1 checkpoint blockade therapies. This suggests that PD-L1 expressed by non-malignant cells may also contribute to antitumor immunity. Here, we review the functions of PD-L1 expressed by immune cells in the context of CD8
T cell priming, contraction, and differentiation into memory populations, as well as the role of PD-L1 expressed by tumor cells in regulating antitumor CD8
T cell responses.
Journal Article
Evaluating the Degree of Blending and Properties of Recycled Asphalt Mixtures Containing Fine Reclaimed Asphalt Pavement Particles Designed Across Different Methods
Owing to certain inherent deficiencies in their properties, fine reclaimed asphalt pavement (RAP) particles have not yet been widely reused worldwide, resulting in significant environmental pollution and economic waste. Currently, a diverse array of design methods for asphalt mixes has been proposed. These methods can exert a varying influence on the degree of blending (DoB) and the performance of recycled hot-mix asphalt containing fine RAP particles, and some methods may be better suited for recycling fine RAP particles. However, the specific effects and differences among these various methods have yet to be fully revealed. Therefore, this research comprehensively explored these behaviors. Four distinct mix design formulations were investigated: the dense-graded Asphalt Concrete Group (Group AC), the Stone Mastic Asphalt Group (Group SMA), the High-modulus Asphalt Concrete Group (Group HMAC), and the rejuvenator-modified Asphalt Concrete Group (Group AC+Re). It can be found that the DoB and performance varied across different groups. The DoB spanned from 69% to 82%, with Group SMA showing the highest and Group HMAC exhibiting the lowest. The tensile strength ratio (TSR) of Group AC performed only 73.7%, failing to meet the specification threshold; nevertheless, this shortfall can be compensated by employing alternative methods or adding rejuvenator. Group HMAC exhibited the highest splitting-tensile strength and fracture energy. In addition, the incorporation of rejuvenator can enhance most performance of mixes. Some findings may provide a new perspective for the application of fine RAP particles.
Journal Article
Bidirectional signals of PD-L1 in T cells that fraternize with cancer cells
PD-L1 expressed by T cells provides backward and forward signals to restrain both innate and adaptive immune responses in tumor tissues.
Journal Article