Escape Phase Research Articles

Local weather routing in avoidance of adverse sea conditions based on reachability theory

In this paper, we put forward a local weather routing framework based on reachability theory to plan a time-optimal risk avoidance path in face of sudden changes in sea conditions. Our framework comprises of two phases, where the escape phase directs the vessel to withdraw from risky heading-speed combinations dictated by MSC.1/Circ. 1228. Subsequently, in the return phase, the algorithm guides the vessel back to its original global route while staying outside dangerous zones. Notably, our application of a four-dimensional state space for the description of a vessel’s configuration can accommodate both the safety and kinematic constraints. In the proposed state space, the path-finding algorithm based on reachability theory can figure out the optimal heading and speed of vessel simultaneously, providing a formal assurance of safety and global time-optimality for returning. To achieve this objective, we formulate and solve a new variational-inequality (VI) governing the forward propagation of the reachable set with both angular and acceleration rate treated as control inputs. Last but not least, we provide a rigorous proof for the proposed VI in the framework of viscosity solution and demonstrate the validity of our approach in two test scenarios including one integrated with a realistic control architecture.

Cooperative metaheuristic algorithm for global optimization and engineering problems inspired by heterosis theory

Swarm Intelligence-based metaheuristic algorithms are widely applied to global optimization and engineering design problems. However, these algorithms often suffer from two main drawbacks: susceptibility to the local optima in large search space and slow convergence rate. To address these issues, this paper develops a novel cooperative metaheuristic algorithm (CMA), which is inspired by heterosis theory. Firstly, simulating hybrid rice optimization algorithm (HRO) constucted based on heterosis theory, the population is sorted by fitness and divided into three subpopulations, corresponding to the maintainer, restorer, and sterile line in HRO, respectively, which engage in cooperative evolution. Subsequently, in each subpopulation, a novel three-phase local optima avoidance technique-Search-Escape-Synchronize (SES) is introduced. In the search phase, the well-established Particle Swarm Optimization algorithm (PSO) is used for global exploration. During the escape phase, escape energy is dynamically calculated for each agent. If it exceeds a threshold, a large-scale Lévy flight jump is performed; otherwise, PSO continues to conduct the local search. In the synchronize phase, the best solutions from subpopulations are shared through an elite-based strategy, while the classical Ant Colony Optimization algorithm is employed to perform fine-tuned local optimization near the shared optimal solutions. This process accelerates convergence, maintains population diversity, and ensures a balanced transition between global exploration and local exploitation. To validate the effectiveness of CMA, this study evaluates the algorithm using 26 well-known benchmark functions and 5 real-world engineering problems. Experimental results demonstrate that CMA outperforms the 10 state-of-the-art algorithms evaluated in the study, which is a very promising for engineering optimization problem solving.

Favourable Prognosis of Patients With Untreated HBeAg-Negative Chronic Hepatitis B Virus Infection With HBsAg < 100 IU/mL.

Serum hepatitis B surface antigen (HBsAg) < 100 IU/mL has been recently proposed as one of the key criteria of 'partial cure' in patients with chronic hepatitis B virus (HBV) infection. We analysed the clinical prognosis of hepatitis B e antigen (HBeAg)-negative untreated patients with HBsAg < 100 IU/mL and normal alanine aminotransferase (ALT) levels. Five hundred and twenty-one untreated patients with HBeAg negativity, HBsAg < 100 IU/mL and normal ALT levels were included from three hospitals. Spontaneous HBsAg seroclearance, phase transition, liver fibrosis progression and hepatocellular carcinoma (HCC) development were analysed. The median age was 43.0 years, and 62.2% of the patients were male. After a median follow-up of 25.0 months, 52 (10.0%) patients achieved spontaneous HBsAg seroclearance. The annual HBsAg seroclearance rate is 4.2%. Patients with baseline HBsAg ≤ 10 IU/mL (adjusted hazard ratio [aHR] = 3.490, p < 0.001) and male sex (aHR = 1.980, p = 0.041) were more likely to achieve HBsAg seroclearance. Only 4 (0.8%) and 23 (4.8%) patients transitioned to the immune escape phase and HBeAg-negative indeterminate phase, respectively. Baseline serum HBsAg > 10 IU/mL (aHR = 3.846, p = 0.034) and detectable HBV DNA (aHR = 2.672, p = 0.023) were associated with transition to the HBeAg-negative indeterminate phase. No patient developed HCC or had fatal outcomes. HBeAg-negative patients with serum HBsAg < 100 IU/mL and normal ALT levels had a favourable prognosis. HBsAg ≤ 10 IU/mL and male sex were associated with a higher rate of HBsAg seroclearance, while HBsAg > 10 IU/mL and detectable HBV DNA were associated with a higher risk of transition to the indeterminate phase.

Multi-phase trajectory optimization of space-based kinetic impactors for asteroid defense with multi-constraint

This paper presents a multi-phase nonlinear trajectory optimization model for space-based launch kinetic impactors, focusing on near-Earth asteroid defense. The model serves the purpose of analyzing space-based launch windows and obtaining optimal trajectories for achieving maximum deflection effectiveness. It comprises three phases: Earth-centered escape phase, heliocentric continuous low-thrust phase, and Keplerian flight phase. In the first phase, the impactor is considered to instantaneously acquire a significant velocity increment from space-based platform because of the extremely short duration of the space-based launch compared with the overall mission. By introducing the true anomaly of the impactor on the designated orbit, the launch velocity increment and launch window are obtained. In the second phase, by optimizing the direction of the low-thrust and the semi-latus rectum of the Keplerian orbit, the optimal shutdown time and state are obtained. In the last phase, the bilateral Keplerian motion between the impactor and the asteroid is considered, incorporating the true anomaly of the predicted impact point and the number of orbital revolutions to establish stringent temporal and spatial beneficial impact constraints. Subsequently, the parameterizable Lambert interception problem with multiple constraints is optimized using the Radau pseudospectral method. Results show that the proposed model has excellent adaptability for different deflection scenarios. Compared with the traditional ground-based continuous low-thrust flight scheme, the proposed method offers a larger launch window that is insensitive to the launch timing and can achieve a greater deflection distance while requiring lower launch capabilities.

Extracellular vesicles originating from melanoma cells promote dysregulation in haematopoiesis as a component of cancer immunoediting.

Haematopoiesis dysregulation with the presence of immature myeloid and erythroid immunosuppressive cells are key characteristics of the immune escape phase of tumour development. Here, the role of in vitro generated B16F10 tumour cell-derived extracellular vesicles (tEVs) as indirect cellular communicators, participating in tumour-induced dysregulation of haematopoiesis, was explored. The isolated tEVs displayed features of small EVs with a size range of 100-200nm, expressed the common EV markers CD63, CD9, and Alix, and had a spherical shape with a lipid bilayer membrane. Proteomic profiling revealed significant levels of angiogenic factors, particularly vascular endothelial growth factor (VEGF), osteopontin, and tissue factor, associated with the tEVs. Systemic administration of these tEVs in syngeneic mice induced splenomegaly and disrupted haematopoiesis, leading to extramedullary haematopoiesis, expansion of splenic immature erythroid progenitors, reduced bone marrow cellularity, medullary expansion of granulocytic myeloid suppressor cells, and the development of anaemia. These effects closely mirrored those observed in tumour-bearing mice and were not seen after heat inactivating the tEVs. In vitro studies demonstrated that tEVs independently induced the expansion of bone marrow granulocytic myeloid suppressor cells and B cells while reducing the frequency of cells in the erythropoietic lineage. These effects of tEVs were significantly abrogated by the blockade of VEGF or heat inactivation. Our findings underscore the important role of tEVs in dysregulating haematopoiesis during the immune escape phase of cancer immunoediting, suggesting their potential as targets for addressing immune evasion and reinstating normal hematopoietic processes.

Invoking Interfacial Engineering Boosts Structural Stability Empowering Exceptional Cyclability of Ni-Rich Cathode.

The cycling stability of LiNi0.8Co0.1Mn0.1O2 under high voltages is hindered by the occurrence of hybrid anion- and cation-redox processes, leading to oxygen escape and uncontrolled phase collapse. In this study, an interfacial engineering strategy involving a straightforward mechanical ball milling and low-temperature calcination, employing a Se-doped and FeSe2&Fe2O3-modified approach is proposed to design a stable Ni-rich cathode. Se2- are selectively adsorbed within oxygen vacancies to form O─TM─Se bond, effectively stabilizing lattice oxygen, and preventing structural distortion. Simultaneously, the Se-NCM811//FeSe2//Fe2O3 self-assembled electric field is activated, improving interfacial charge transfer and coupling. Furthermore, FeSe2 accelerates Li+ diffusion and reacts with oxygen to form Fe2O3 and SeO2. The Fe2O3 coating mitigates hydrofluoric acid erosion and acts as an electrostatic shield layer, limiting the outward migration of oxygen anions. Impressively, the modified materials exhibit significantly improved electrochemical performance, with a capacity retention of 79.7% after 500 cycles at 1C under 4.5V. Furthermore, it provides an extraordinary capacity retention of 94.6% in 3-4.25V after 550 cycles in pouch-type full battery. This dual-modification approach demonstrates its feasibility and opens new perspective for the development of stable lithium-ion batteries operating at high voltages.

Quantification of Neoantigen-Mediated Immunoediting in Cancer Evolution—Letter

Quantification of Neoantigen-Mediated Immunoediting in Cancer Evolution—Letter

Tumor-Derived Extracellular Vesicles in Cancer Immunoediting and Their Potential as Oncoimmunotherapeutics

The tumor microenvironment (TME) within and around a tumor is a complex interacting mixture of tumor cells with various stromal cells, including endothelial cells, fibroblasts, and immune cells. In the early steps of tumor formation, the local microenvironment tends to oppose carcinogenesis, while with cancer progression, the microenvironment skews into a protumoral TME and the tumor influences stromal cells to provide tumor-supporting functions. The creation and development of cancer are dependent on escape from immune recognition predominantly by influencing stromal cells, particularly immune cells, to suppress antitumor immunity. This overall process is generally called immunoediting and has been categorized into three phases; elimination, equilibrium, and escape. Interaction of tumor cells with stromal cells in the TME is mediated generally by cell-to-cell contact, cytokines, growth factors, and extracellular vesicles (EVs). The least well studied are EVs (especially exosomes), which are nanoparticle-sized bilayer membrane vesicles released by many cell types that participate in cell/cell communication. EVs carry various proteins, nucleic acids, lipids, and small molecules that influence cells that ingest the EVs. Tumor-derived extracellular vesicles (TEVs) play a significant role in every stage of immunoediting, and their cargoes change from immune-activating in the early stages of immunoediting into immunosuppressing in the escape phase. In addition, their cargos change with different treatments or stress conditions and can be influenced to be more immune stimulatory against cancer. This review focuses on the emerging understanding of how TEVs affect the differentiation and effector functions of stromal cells and their role in immunoediting, from the early stages of immunoediting to immune escape. Consideration of how TEVs can be therapeutically utilized includes different treatments that can modify TEV to support cancer immunotherapy.

Propagation of Type II spicules into the solar corona II. A Thermomechanical toy model (Plasma escape and descent phase)

This paper studies Phases 2 and 3 of jets’ propagation with some Type II spicules characteristics into the solar corona using a thermomechanical (TM) approximation. Embedding two plasmas with different densities (one representing the chromospheric plasma and the other the coronal plasma) in cylindrical sections, we use iterative processes to calculate the final temperatures due to the mixture between both plasmas. The heating process produced by phase 2 of descent and phase 3, which corresponds to plasma not trapped, could represent a source that maintains the current temperature of the low corona.

Consideration of possible effects of vitamin D on established cancer, with reference to malignant melanoma.

Epidemiological studies indicate that Vitamin D has a beneficial, inhibitory effect on cancer development and subsequent progression, including melanoma (MM), and favourable MM outcome has been reported as directly related to vitamin D3 status, assessed by serum 25‐hydroxyvitamin D3 (25[OH]D3 ) levels taken at diagnosis. It has been recommended that MM patients with deficient levels of 25(OH)D3 be given vitamin D3 . We examine possible beneficial or detrimental effects of treating established cancer with vitamin D3. We consider the likely biological determinants of cancer outcome, the reported effects of vitamin D3 on these in both cancerous and non‐cancerous settings, and how the effect of vitamin D3 might change depending on the integrity of tumour vitamin D receptor (VDR) signalling. We would argue that the effect of defective tumour VDR signalling could result in loss of suppression of growth, reduction of anti‐tumour immunity, with potential antagonism of the elimination phase and enhancement of the escape phase of tumour immunoediting, possibly increased angiogenesis but continued suppression of inflammation. In animal models, having defective VDR signalling, vitamin D3 administration decreased survival and increased metastases. Comparable studies in man are lacking but in advanced disease, a likely marker of defective VDR signalling, studies have shown modest or no improvement in outcome with some evidence of worsening. Work is needed in assessing the integrity of tumour VDR signalling and the safety of vitamin D3 supplementation when defective.

Survival Advantage Following TAG-72 Antigen-Directed Cancer Surgery in Patients With Colorectal Carcinoma: Proposed Mechanisms of Action.

Patients with colorectal carcinoma (CRC) continue to have variable clinical outcomes despite undergoing the same surgical procedure with curative intent and having the same pathologic and clinical stage. This problem suggests the need for better techniques to assess the extent of disease during surgery. We began to address this problem 35 years ago by injecting patients with either primary or recurrent CRC with 125I-labeled murine monoclonal antibodies against the tumor-associated glycoprotein-72 (TAG-72) and using a handheld gamma-detecting probe (HGDP) for intraoperative detection and removal of radioactive, i.e., TAG-72-positive, tissue. Data from these studies demonstrated a significant difference in overall survival data (p < 0.005 or better) when no TAG-72-positive tissue remained compared to when TAG-72-positive tissue remained at the completion of surgery. Recent publications indicate that aberrant glycosylation of mucins and their critical role in suppressing tumor-associated immune response help to explain the cellular mechanisms underlying our results. We propose that monoclonal antibodies to TAG-72 recognize and bind to antigenic epitopes on mucins that suppress the tumor-associated immune response in both the tumor and tumor-draining lymph nodes. Complete surgical removal of all TAG-72-positive tissue serves to reverse the escape phase of immunoediting, allowing a resetting of this response that leads to improved overall survival of the patients with either primary or recurrent CRC. Thus, the status of TAG-72 positivity after resection has a significant impact on patient survival.

Shape-Based Approach for Low-Thrust Earth–Moon Trajectories Initial Design

A robust finite Fourier series (R-FFS) approach is developed for fast generation of Earth–moon trajectories using continuous low thrust. Each component of the position vector is approximated using a finite Fourier series as a function of time; these approximations are then used to design a trajectory that satisfies the equations of motion and the constraints, at discrete points, as well as the problem boundary conditions. The R-FFS method leverages the three-body problem characteristics to achieve all the required plane change without the use of propulsion. The trajectory is divided into phases: escape, intermediate, and capture. The escape phase is further divided into segments. The phase of the trajectory near the L1 Lagrange point is designed first and is always a thrust-free phase. This thrust-free phase is optimized to achieve the required plane change, enabling planar trajectories in the other phases. The initial guess needed by the solver, in the escape and capture phases, is generated using an analytic approximation developed in this paper. The numerical results show that the R-FFS can generate three-dimensional transfers to high lunar orbits, low lunar orbits, and halo orbits, while meeting constraints on the maximum thrust level of the engine.

Mathematical modeling approach of cancer immunoediting reveals new insights in targeted-therapy and timing plan of cancer treatment

Mathematical modeling was shown to be a powerful tool to describe immune system-cancer dynamics and specifically immunoediting. Here, we used a system of two ordinary differential equations to investigate the fate of the tumor through the three main phases of cancer immunoediting: elimination phase (elimination of cancer cells by the immune system), dormancy phase (equilibrium between tumor growth and immune system response), and escape phase (escape of cancer cells and growth of tumor). The role of the tumor growth rate, tumor immunogenic properties (immunogenicity or immunosuppressive effects), and tumor accessibility for the immune system were evaluated. The results show that decreasing the growth rate and increasing accessibility of the tumor for the immune system may help immunogenic tumors to survive elimination and become dormant; dormant tumors may wake up later on, causing tumor escape and growth. The model also indicated that the synchronization of immune response and tumor growth is a key factor for successful tumor elimination. Simulation results for the fate of the residual tumor cells after surgical tumor resection, revealed the importance of timing in adjuvant targeted-therapy: a too late or a too early start of targeted therapy may result in tumor escape or tumor dormancy, respectively, while start at an intermediate timing results in the elimination of the tumor. Results of this simulation are corroborated with experimental and clinical observations.

NKG2D defines tumor-reacting effector CD8+ T cells within tumor microenvironment.

For successful immunotherapy for cancer, it is important to understand the immunological status of tumor antigen‐specific CD8+ T cells in the tumor microenvironment during tumor progression. In this study, we monitored the behavior of B16OVA‐Luc cells in mice immunized with a model tumor antigen ovalbumin (OVA). Using bioluminescence imaging, we identified the time series of OVA‐specific CD8+ T‐cell responses during tumor progression: initial progression, immune control, and the escape phase. As a result of analyzing the status of tumor antigen‐specific CD8+ cells in those 3 different phases, we found that the expression of NKG2D defines tumor‐reacting effector CD8+ T cells. NKG2D may control the fate and TOX expression of tumor‐reacting CD8+ T cells, considering that NKG2D blockade in OVA‐vaccinated mice delayed the growth of the B16OVA‐Luc2 tumor and increased the presence of tumor‐infiltrating OVA‐specific CD8+ T cells.

Abstract 2774: Establishment of in vitro human T cell exhaustion model to enable high throughput target validation for T cell phenotype restoring

Abstract Immune surveillance was defined as three phases during tumorigenesis: elimination, equilibrium and escape. During the escape phase, cancer cell acquire a series of mechanism to evade the recognition by immune system, including reduce the function of antigen presenting cells, recruitment of suppressive cells, induce T cell exhaustion etc. The exhaustion phenotype of T cells were frequently observed in various cancer types and exhibit as reduced effector cytokine production, decrease in proliferation and cytolytic activity and overexpression of inhibitory receptors. Restoring T cell exhaustion phenotype become the inspiring filed for cancer therapy and PD1 blocking antibody further encouraging the concept of intervention on T cell exhausted phenotype in tumor microenvironment. In this study, we utilize human primary T cell to establish the in vitro model of T cell exhaustion. Subsequent functional study reveal that the induced exhausted T cell (Tex) display significantly weak response towards dendritic cell activation compare to normal T cell (Tnorm). We take advantage of the model to validate the function of PD1 antibody and demonstrate that blocking of PD1 could partially restore the function of Tex, which suggesting there are still other regulators involved in mediating T cell exhaustion beyond PD1. Citation Format: Tienan Wang, Jie Zhang, Zhijun Wang, Yingnian Li, Linghong Shi, Qing Lin. Establishment of in vitro human T cell exhaustion model to enable high throughput target validation for T cell phenotype restoring [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2774.

Thermoelectric materials with crystal-amorphicity duality induced by large atomic size mismatch

Summary Discovering novel materials and attaining higher performance are the eternal pursuit of thermoelectric materials research. Here, we report a material series, (Cu1−xAgx)2(Te1−ySy) (0.16 ≤ x ≤ 0.24, 0.16 ≤ y ≤ 0.24), which adopts a complex orthorhombic structure differing from any known crystal structure of (Cu/Ag)2(S/Te). This material series is featured by the crystal-amorphicity duality induced by the large anionic size mismatch: a crystalline sublattice of highly size-mismatched anions Te/S coexists with an amorphous-like sublattice of cations Cu/Ag. In the context of structure-property correlation, the crystal-amorphicity duality gave rise to not only interesting electrical properties but also exceptionally low lattice thermal conductivities from 300 to 1,000 K. A state-of-the-art figure of merit zT of 2.0 is obtained in the x = y = 0.22 sample at 1,000 K. These results give insights into crystal-amorphicity duality as a paradigm-shifting materials design approach to develop high-performance thermoelectric materials.

Correction to 'Uncovering the underlying mechanism of cancer tumorigenesis and development under an immune microenvironment from global quantification of the landscape'.

You have accessMoreSectionsView PDF ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InRedditEmail Cite this article Li Wenbo and Wang Jin 2021Correction to ‘Uncovering the underlying mechanism of cancer tumorigenesis and development under an immune microenvironment from global quantification of the landscape’J. R. Soc. Interface.182021024720210247http://doi.org/10.1098/rsif.2021.0247SectionYou have accessCorrectionsCorrection to ‘Uncovering the underlying mechanism of cancer tumorigenesis and development under an immune microenvironment from global quantification of the landscape’ Wenbo Li Wenbo Li Google Scholar Find this author on PubMed Search for more papers by this author and Jin Wang Jin Wang Google Scholar Find this author on PubMed Search for more papers by this author Wenbo Li Wenbo Li Google Scholar Find this author on PubMed Search for more papers by this author and Jin Wang Jin Wang Google Scholar Find this author on PubMed Search for more papers by this author Published:14 April 2021https://doi.org/10.1098/rsif.2021.0247See original article.Uncovering the underlying mechanism of cancer tumorigenesis and development under an immune microenvironment from global quantification of the landscapeJ. R. Soc. Interface14, 20170105. (Published 28 June 2017) (doi:10.1098/rsif.2017.0105)On 2.1. Cancer-immune system network modelling, Paragraph 6, Th1 is mainly activated by IL-2 should be revised to: Th1 is mainly activated by IL-12.andNK cells and MDSCs are mainly activated by IL-17 should be revised to:TAN is mainly activated by IL-17.On 2.2. Landscape of cancer innate and adaptive immunity, paragraph 4, The dominant paths are shown on the landscape (figure 3b,d) should be revised to:The dominant paths are shown on the landscape (figure 3).On 2.5. Dynamic landscape of immunity along cancer development under an immune microenvironment, paragraph 3, The final stage of the escape phase emerges when a = 1.4, because the immune system starts to lose control of the cancer cells should be revised to:The final stage of the equilibrium phase emerges when a = 1.4, because the immune system starts to lose the control over the cancer cells.The authors apologize for these errors and state that this does not change the scientific conclusions of the article in any way. Previous Article FiguresRelatedReferencesDetailsRelated articlesUncovering the underlying mechanism of cancer tumorigenesis and development under an immune microenvironment from global quantification of the landscapeJun 28, 2017, 12:00:00 AMJournal of The Royal Society Interface This IssueApril 2021Volume 18Issue 177 Article InformationDOI:https://doi.org/10.1098/rsif.2021.0247PubMed:33849328Published by:Royal SocietyOnline ISSN:1742-5662History: Published online14/04/2021 License:© 2021 The Author(s)Published by the Royal Society. All rights reserved. Citations and impact Subjectsbiophysics

Longitudinal Immune Profiling Reveals Unique Myeloid and T-cell Phenotypes Associated with Spontaneous Immunoediting in a Prostate Tumor Model.

The theory of cancer immunoediting, which describes the dynamic interactions between tumors and host immune cells that shape the character of each compartment, is foundational for understanding cancer immunotherapy. Few models exist that facilitate in-depth study of each of the three canonical phases of immunoediting: elimination, equilibrium, and escape. Here, we utilized NPK-C1, a transplantable prostate tumor model that we found recapitulated the three phases of immunoediting spontaneously in immunocompetent animals. Given that a significant portion of NPK-C1 tumors reliably progressed to the escape phase, we were able to delineate cell types and mechanisms differentially prevalent in equilibrium versus escape phases. Using high-dimensional flow cytometry, we found that activated CD4+ effector T cells were enriched in regressing tumors, highlighting a role for CD4+ T cells in antitumor immunity. CD8+ T cells were also important for NPK-C1 control, specifically, central memory-like cytotoxic CD8+ T cells. Regulatory T cells (Treg), as a whole, were counterintuitively enriched in regressing tumors; however, high-dimensional analysis revealed their significant phenotypic diversity, with a number of Treg subpopulations enriched in progressing tumors. In the myeloid compartment, we found that iNOS+ dendritic cell (DC)-like cells are enriched in regressing tumors, whereas CD103+ DCs were associated with late-stage tumor progression. In total, these analyses of the NPK-C1 model provide novel insights into the roles of lymphoid and myeloid populations throughout the cancer immunoediting process and highlight a role for multidimensional, flow-based analyses to more deeply understand immune cell dynamics in the tumor microenvironment.

Comprehensive Phenotyping of Dendritic Cells in Cancer Patients by Flow Cytometry.

Dendritic cells (DCs) play a crucial role in the complex interplay between tumor cells and the immune system. During the elimination phase of cancer immunoediting, immunostimulatory DCs are critical for the control of tumor growth. During the escape phase, regulatory DCs sustain tumor tolerance and contribute to the development of the immunosuppressive tumor microenvironment that characterizes this phase. Moreover, increasing evidence indicates that DCs are also critical for the success of cancer immunotherapy. Hence, there is increasing need to fully characterize DC subsets and their activatory/inhibitory profile in cancer patients. In this review, we describe the role played by different DC subsets in the different phases of cancer immunoediting, the function exerted by different activatory and inhibitory molecules expressed on DC surface, and the cytokines produced by distinct DC subsets, in order to provide an overview on the DC features that may be useful to be assessed when dealing with the flow cytometric characterization of DCs in cancer patients. © 2020 International Society for Advancement of Cytometry.

Cancer immunoediting: A game theoretical approach.

The role of the immune system in tumor development increasingly includes the idea of cancer immunoediting. It comprises three phases: elimination, equilibrium, and escape. In the first phase, elimination, transformed cells are recognized and destroyed by immune system. The rare tumor cells that are not destroyed in this phase may then enter the equilibrium phase, where their growth is prevented by immunity mechanisms. The escape phase represents the final phase of this process, where cancer cells begin to grow unconstrained by the immune system. In this study, we describe and analyze an evolutionary game theoretical model of proliferating, quiescent, and immune cells interactions for the first time. The proposed model is evaluated with constant and dynamic approaches. Population dynamics and interactions between the immune system and cancer cells are investigated. Stability of equilibria or critical points are analyzed by applying algebraic analysis. This model allows us to understand the process of cancer development and might help us design better treatment strategies to account for immunoediting.