scholarly journals Cancer immunoediting: A game theoretical approach

2020 ◽  
pp. 1-12
Author(s):  
Fatemeh Tavakoli ◽  
Javad Salimi Sartakhti ◽  
Mohammad Hossein Manshaei ◽  
David Basanta
Keyword(s):  
Immune System ◽  
Cancer Cells ◽  
Evolutionary Game ◽  
Equilibrium Phase ◽  
Tumor Development ◽  
Treatment Strategies ◽  
Cancer Immunoediting ◽  
Proposed Model ◽  
Game Theoretical Approach ◽  
First Time

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.

scholarly journals Understanding Checkpoint Inhibitors in Cancer Therapy, Mechanisms of Action, Resistance and Future Challenges

2020 ◽  
pp. 1-13
Author(s):  
Harman Saman ◽  
Harman Saman ◽  
Shahab Uddin ◽  
Syed Raza ◽  
Raj Shrimali ◽  
...  
Keyword(s):  
Immune System ◽  
Cancer Cells ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Immune Surveillance ◽  
Tumor Development ◽  
Mechanisms Of Action ◽  
Programmed Death ◽  
Future Challenges

The immune system is the human body’s natural defence against mutated cells produced as the result of DNA replicative error or by the effect of carcinogens, a process rereferred to as immune surveillance. ‘Escaping’ of cancer cells from immune surveillance leads to tumor development, metastasis and progression. Avoiding detection and destruction by the immune system are the result of cancer cells evolution, caused primarily by cancer cells’ genomic instability. On the other hand, scientists attempted for decades to exploit the anticancer effect of the immune system with limited success. However, better understanding of the mechanisms behind the cancer cells’ ability to avoid detection and suppression by the immune system resulted in the development of immune checkpoint inhibitors, a form of immunotherapy, first approved by the Food and Drug Administration (FDA) in 2011. This article reviews the pathways involved in anticancer immune response, evading and supressing of the immune system by cancer cells mechanisms of action and successes of immune checkpoint inhibitors (ICI), particularly programmed death1 (PD-1) and programmed death-ligand (PD-L1) inhibitors as well as mechanisms that result in resistance of cancer cells to ICI.

scholarly journals Helicobacter hepaticus Infection Promotes Colon Tumorigenesis in the BALB/c-Rag2−/−ApcMin/+ Mouse

2008 ◽  
Vol 76 (6) ◽  
pp. 2758-2766 ◽  
Author(s):  
Claude M. Nagamine ◽  
Jane J. Sohn ◽  
Barry H. Rickman ◽  
Arlin B. Rogers ◽  
James G. Fox ◽  
...  
Keyword(s):  
Small Intestine ◽  
Immune System ◽  
Equilibrium Phase ◽  
Bacterial Pathogen ◽  
Adaptive Immune System ◽  
Helicobacter Hepaticus ◽  
Cancer Immunoediting ◽  
Tumor Multiplicity ◽  
Adaptive Immune ◽  
Colon Tumorigenesis

ABSTRACT Adenomatous polyposis coli (APC) mutations are linked to human and mouse colorectal cancers. The Apc multiple intestinal neoplasia (Min) mouse mutation causes adenomas to develop throughout the small and large intestines. The BALB-Min (C.B6-Apc Min/+) congenic strain was generated by backcrossing into BALB/c the Apc Min allele from C57BL/6J-Apc Min/+ mice. BALB-Min mice have a low tumor multiplicity (27.4 small intestine tumors/mouse) and a relatively long life span (>1 year) that makes them amenable to long-term studies. To investigate the interplay of the adaptive immune system and intestinal tumorigenesis, the immunodeficient compound mutant strain BALB-RagMin (C.Cg-Rag2 −/− Apc Min/+) was generated. BALB-RagMin mice had a significant increase in tumors in the small, but not large, intestine relative to their BALB-Min counterparts (43.0 versus 24.0 tumors/mouse, respectively). The results suggest that the adaptive immune system plays a role in either the elimination or the equilibrium phase of cancer immunoediting in the small intestine in this model. We investigated the effect of the enterohepatic bacterial pathogen Helicobacter hepaticus on liver and intestine tumorigenesis in BALB-RagMin mice. H. hepaticus-infected BALB-RagMin mice developed moderate hepatitis, moderate typhlitis, and mild colitis. There were no differences in small intestine and cecal tumor multiplicity, regionality, or size relative to that in uninfected mice. However, H. hepaticus-infected BALB-RagMin mice had a significant increase in colon tumor incidence relative to uninfected BALB-RagMin mice (23.5% versus 1.7%, respectively). The data suggest that H. hepaticus, which is present in many research colonies, promotes colon tumorigenesis in the BALB-RagMin mouse and that it has the potential to confound colon tumorigenesis studies.

scholarly journals Implications for Treatment Strategies in Cancer and Infectious Diseases

2021 ◽  
pp. 121-159
Author(s):  
Elena Locci ◽  
Silvia Raymond
Keyword(s):  
T Cells ◽  
Immune System ◽  
Infectious Diseases ◽  
Cancer Cells ◽  
Viral Infections ◽  
Treatment Strategies ◽  
Treatment Management ◽  
New Therapies ◽  
Long Time ◽  
Keywords Cancer

It is widely known that severe viral infections and cancer disrupt the immune system, including T cells, a process called "immune fatigue." Overcoming immune depletion is the main goal of developing new therapies for cancer or severe viral infections. Called Tpex cells, they can maintain their function for a long time. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management

scholarly journals Breast Cancer Cell Re-Dissemination from Lung Metastases—A Mechanism for Enhancing Metastatic Burden

2021 ◽  
Vol 10 (11) ◽  
pp. 2340
Author(s):  
Lucia Borriello ◽  
John Condeelis ◽  
David Entenberg ◽  
Maja H. Oktay
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Metastatic Disease ◽  
Breast Cancer Cells ◽  
Lung Metastases ◽  
Primary Tumors ◽  
Metastatic Burden ◽  
First Time ◽  
Do So

Although metastatic disease is the primary cause of mortality in cancer patients, the mechanisms leading to overwhelming metastatic burden are still incompletely understood. Metastases are the endpoint of a series of multi-step events involving cancer cell intravasation, dissemination to distant organs, and outgrowth to metastatic colonies. Here we show, for the first-time, that breast cancer cells do not solely disseminate to distant organs from primary tumors and metastatic nodules in the lymph nodes, but also do so from lung metastases. Thus, our findings indicate that metastatic dissemination could continue even after the removal of the primary tumor. Provided that the re-disseminated cancer cells initiate growth upon arrival to distant sites, cancer cell re-dissemination from metastatic foci could be one of the crucial mechanisms leading to overt metastases and patient demise. Therefore, the development of new therapeutic strategies to block cancer cell re-dissemination would be crucial to improving survival of patients with metastatic disease.

scholarly journals The Equilibrium Phase Formation and Thermodynamic Properties of Functional Tellurides in the Ag–Fe–Ge–Te System

Energies ◽  
2021 ◽  
Vol 14 (5) ◽  
pp. 1314
Author(s):  
Mykola Moroz ◽  
Fiseha Tesfaye ◽  
Pavlo Demchenko ◽  
Myroslava Prokhorenko ◽  
Nataliya Yarema ◽  
...  
Keyword(s):  
Electromotive Force ◽  
Equilibrium Phase ◽  
Stoichiometric Composition ◽  
Negative Electrode ◽  
Electrochemical Cells ◽  
Thermodynamic Quantities ◽  
Positive Electrodes ◽  
Gibbs Energies ◽  
Buffer Region ◽  
First Time

Equilibrium phase formations below 600 K in the parts Ag2Te–FeTe2–F1.12Te–Ag2Te and Ag8GeTe6–GeTe–FeTe2–AgFeTe2–Ag8GeTe6 of the Fe–Ag–Ge–Te system were established by the electromotive force (EMF) method. The positions of 3- and 4-phase regions relative to the composition of silver were applied to express the potential reactions involving the AgFeTe2, Ag2FeTe2, and Ag2FeGeTe4 compounds. The equilibrium synthesis of the set of phases was performed inside positive electrodes (PE) of the electrochemical cells: (−)Graphite ‖LE‖ Fast Ag+ conducting solid-electrolyte ‖R[Ag+]‖PE‖ Graphite(+), where LE is the left (negative) electrode, and R[Ag+] is the buffer region for the diffusion of Ag+ ions into the PE. From the observed results, thermodynamic quantities of AgFeTe2, Ag2FeTe2, and Ag2FeGeTe4 were experimentally determined for the first time. The reliability of the division of the Ag2Te–FeTe2–F1.12Te–Ag2Te and Ag8GeTe6–GeTe–FeTe2–AgFeTe2–Ag8GeTe6 phase regions was confirmed by the calculated thermodynamic quantities of AgFeTe2, Ag2FeTe2, and Ag2FeGeTe4 in equilibrium with phases in the adjacent phase regions. Particularly, the calculated Gibbs energies of Ag2FeGeTe4 in two different adjacent 4-phase regions are consistent, which also indicates that it has stoichiometric composition.

scholarly journals Current Trends in Non-Invasive Imaging of Interactions in the Liver Tumor Microenvironment Mediated by Tumor Metabolism

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3645
Author(s):  
Isabel Theresa Schobert ◽  
Lynn Jeanette Savic
Keyword(s):  
Tumor Microenvironment ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Imaging Techniques ◽  
Treatment Strategies ◽  
Tumor Metabolism ◽  
Resistance Mechanisms ◽  
Metabolic Reprogramming ◽  
Non Invasive

With the increasing understanding of resistance mechanisms mediated by the metabolic reprogramming in cancer cells, there is a growing clinical interest in imaging technologies that allow for the non-invasive characterization of tumor metabolism and the interactions of cancer cells with the tumor microenvironment (TME) mediated through tumor metabolism. Specifically, tumor glycolysis and subsequent tissue acidosis in the realms of the Warburg effect may promote an immunosuppressive TME, causing a substantial barrier to the clinical efficacy of numerous immuno-oncologic treatments. Thus, imaging the varying individual compositions of the TME may provide a more accurate characterization of the individual tumor. This approach can help to identify the most suitable therapy for each individual patient and design new targeted treatment strategies that disable resistance mechanisms in liver cancer. This review article focuses on non-invasive positron-emission tomography (PET)- and MR-based imaging techniques that aim to visualize the crosstalk between tumor cells and their microenvironment in liver cancer mediated by tumor metabolism.

scholarly journals Transcriptional landscape of cellular networks reveal interactions driving the dormancy mechanisms in cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dilara Uzuner ◽  
Yunus Akkoç ◽  
Nesibe Peker ◽  
Pınar Pir ◽  
Devrim Gözüaçık ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Regulatory Networks ◽  
Metastatic Cancer ◽  
Interaction Network ◽  
Current Treatment ◽  
Cellular Mechanisms ◽  
Protein Protein Interaction ◽  
Cancer Dormancy ◽  
Protein Protein Interaction Networks ◽  
First Time

AbstractPrimary cancer cells exert unique capacity to disseminate and nestle in distant organs. Once seeded in secondary sites, cancer cells may enter a dormant state, becoming resistant to current treatment approaches, and they remain silent until they reactivate and cause overt metastases. To illuminate the complex mechanisms of cancer dormancy, 10 transcriptomic datasets from the literature enabling 21 dormancy–cancer comparisons were mapped on protein–protein interaction networks and gene-regulatory networks to extract subnetworks that are enriched in significantly deregulated genes. The genes appearing in the subnetworks and significantly upregulated in dormancy with respect to proliferative state were scored and filtered across all comparisons, leading to a dormancy–interaction network for the first time in the literature, which includes 139 genes and 1974 interactions. The dormancy interaction network will contribute to the elucidation of cellular mechanisms orchestrating cancer dormancy, paving the way for improvements in the diagnosis and treatment of metastatic cancer.

scholarly journals Personalized Immunotherapy Treatment Strategies for a Dynamical System of Chronic Myelogenous Leukemia

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2030
Author(s):  
Paul A. Valle ◽  
Luis N. Coria ◽  
Corina Plata
Keyword(s):  
Dynamical System ◽  
Cancer Cells ◽  
Chronic Myelogenous Leukemia ◽  
Sufficient Conditions ◽  
Treatment Strategies ◽  
Myelogenous Leukemia ◽  
Invariant Sets ◽  
Cellular Immunotherapy ◽  
Complete Eradication ◽  
Treatment Parameter

This paper is devoted to exploring personalized applications of cellular immunotherapy as a control strategy for the treatment of chronic myelogenous leukemia described by a dynamical system of three first-order ordinary differential equations. The latter was achieved by applying both the Localization of Compact Invariant Sets and Lyapunov’s stability theory. Combination of these two approaches allows us to establish sufficient conditions on the immunotherapy treatment parameter to ensure the complete eradication of the leukemia cancer cells. These conditions are given in terms of the system parameters and by performing several in silico experimentations, we formulated a protocol for the therapy application that completely eradicates the leukemia cancer cells population for different initial tumour concentrations. The formulated protocol does not dangerously increase the effector T cells population. Further, complete eradication is considered when solutions go below a finite critical value below which cancer cells cannot longer persist; i.e., one cancer cell. Numerical simulations are consistent with our analytical results.

scholarly journals Spontaneous Fusion of MSC with Breast Cancer Cells Can Generate Tumor Dormancy

2021 ◽  
Vol 22 (11) ◽  
pp. 5930
Author(s):  
Catharina Melzer ◽  
Juliane von der Ohe ◽  
Tianjiao Luo ◽  
Ralf Hass
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumor Development ◽  
Cellular Interactions ◽  
Hybrid Cells ◽  
Induced Tumors ◽  
Culture Model ◽  
Gene Expression Levels

Direct cellular interactions of MDA-MB-231cherry breast cancer cells with GFP-transduced human mesenchymal stroma/stem-like cells (MSCGFP) in a co-culture model resulted in spontaneous cell fusion by the generation of MDA-MSC-hyb5cherry GFP breast cancer hybrid cells. The proliferative capacity of MDA-MSC-hyb5 cells was enhanced about 1.8-fold when compared to the parental MDA-MB-231cherry breast cancer cells. In contrast to a spontaneous MDA-MB-231cherry induced tumor development in vivo within 18.8 days, the MDA-MSC-hyb5 cells initially remained quiescent in a dormancy-like state. At distinct time points after injection, NODscid mice started to develop MDA-MSC-hyb5 cell-induced tumors up to about a half year later. Following tumor initiation, however, tumor growth and formation of metastases in various different organs occurred rapidly within about 10.5 days. Changes in gene expression levels were evaluated by RNA-microarray analysis and revealed certain increase in dormancy-associated transcripts in MDA-MSC-hyb5. Chemotherapeutic responsiveness of MDA-MSC-hyb5 cells was partially enhanced when compared to MDA-MB-231 cells. However, some resistance, e.g., for taxol was detectable in cancer hybrid cells. Moreover, drug response partially changed during the tumor development of MDA-MSC-hyb5 cells; this suggests the presence of unstable in vivo phenotypes of MDA-hyb5 cells with increased tumor heterogeneity.

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