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Spatiotemporal Noise Triggering Infiltrative Tumor Growth under Immune Surveillance  [PDF]
Wei-Rong Zhong,Yuan-Zhi Shao,Li Li,Feng-Hua Wang,Zhen-Hui He
Quantitative Biology , 2008, DOI: 10.1209/0295-5075/82/20003
Abstract: A spatiotemporal noise is assumed to reflect the environmental fluctuation in a spatially extended tumor system. We introduce firstly the structure factor to reveal the invasive tumor growth quantitatively. The homogenous environment can lead to an expansive growth of the tumor cells, while the inhomogenous environment underlies an infiltrative growth. The different responses of above two cases are separated by a characteristic critical intensity of the spatiotemporal noise. Theoretical and numerical results present a close annotation to the clinical images.
The role of the microenvironment in tumor immune surveillance  [cached]
Oluwadayo Oluwadara,Luca Giacomelli,Xenia Brant,Russell Christensen4
Bioinformation , 2011,
Abstract: The evidence appears compelling that the microenvironment, and associated biological cellular and molecular factors, may contribute to the progression of a variety of tumors. The effects of the microenvironment may directly influence the plasticity of T cell lineages, which was recently discussed (O’Shea & Paul, 2010 ). To review the putative role of the microenvironment in modulating the commitment of tumor immune surveillance, we use the model of oral premalignant lesions.
Tumor-Associated Glycans and Immune Surveillance  [PDF]
Behjatolah Monzavi-Karbassi,Anastas Pashov,Thomas Kieber-Emmons
Vaccines , 2013, DOI: 10.3390/vaccines1020174
Abstract: Changes in cell surface glycosylation are a hallmark of the transition from normal to inflamed and neoplastic tissue. Tumor-associated carbohydrate antigens (TACAs) challenge our understanding of immune tolerance, while functioning as immune targets that bridge innate immune surveillance and adaptive antitumor immunity in clinical applications. T-cells, being a part of the adaptive immune response, are the most popular component of the immune system considered for targeting tumor cells. However, for TACAs, T-cells take a back seat to antibodies and natural killer cells as first-line innate defense mechanisms. Here, we briefly highlight the rationale associated with the relative importance of the immune surveillance machinery that might be applicable for developing therapeutics.
The growth dynamics of tumor subject to both immune surveillance and external therapy intervention
YuanZhi Shao,WeiRong Zhong,FengHua Wang,ZhenHui He,ZhongJun Xia
Chinese Science Bulletin , 2007, DOI: 10.1007/s11434-007-0234-9
Abstract: Considering the growth of tumor cells modeled by an enzyme dynamic process under an immune surveillance, we studied in anti-tumor immunotherapy the single-variable growth dynamics of tumor cells subject to a multiplicative noise and an external therapy intervention simultaneously. The law of tumor growth of the above anti-tumor immunotherapy model was revealed through numerical simulations to the relevant stochastic dynamic differential equation. Two simulative parameters of therapy, i.e., therapy intensity and therapy duty-cycle, were introduced to characterize a treatment process similar to a tumor clinic therapy. There exists a critical therapy boundary which, in an exponent-decaying form, divides the parameter region of therapy into an invalid and a valid treatment zone, respectively. A greater critical therapy duty-cycle is necessary to achieve a valid treatment for a lower therapy intensity while the critical therapy intensity decreases accordingly with an enhancing immunity. A primary clinic observation of the patients with the typical non-hodgekin’s lymphoma was carried out, and there appears a basic agreement between clinic observations and dynamic simulations.
The growth dynamics of tumor subject to both immune surveillance and external therapy intervention
SHAO YuanZhi,ZHONG WeiRong,WANG FengHua,HE ZhenHui,XIA ZhongJun,
SHAO
,YuanZhi,ZHONG,WeiRong,WANG,FengHua,HE,ZhenHui,XIA,ZhongJun

科学通报(英文版) , 2007,
Abstract: Considering the growth of tumor cells modeled by an enzyme dynamic process under an immune surveillance, we studied in anti-tumor immunotherapy the single-variable growth dynamics of tumor cells subject to a multiplicative noise and an external therapy intervention simultaneously. The law of tumor growth of the above anti-tumor immunotherapy model was revealed through numerical simulations to the relevant stochastic dynamic differential equation. Two simulative parameters of therapy, i.e., therapy intensity and therapy duty-cycle, were introduced to characterize a treatment process similar to a tumor clinic therapy. There exists a critical therapy boundary which, in an exponent-decaying form, divides the parameter region of therapy into an invalid and a valid treatment zone, respectively. A greater critical therapy duty-cycle is necessary to achieve a valid treatment for a lower therapy intensity while the critical therapy intensity decreases accordingly with an enhancing immunity. A primary clinic observation of the patients with the typical non-hodgekin’s lymphoma was carried out, and there appears a basic agreement between clinic observations and dynamic simulations. Supported by the National Natural Science Foundation of China (Grant No. 60471023)
Tumor Evasion from T Cell Surveillance
Katrin T pfer,Stefanie Kempe,Nadja Müller,Marc Schmitz,Michael Bachmann,Marc Cartellieri,Gabriele Schackert,Achim Temme
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/918471
Abstract: An intact immune system is essential to prevent the development and progression of neoplastic cells in a process termed immune surveillance. During this process the innate and the adaptive immune systems closely cooperate and especially T cells play an important role to detect and eliminate tumor cells. Due to the mechanism of central tolerance the frequency of T cells displaying appropriate arranged tumor-peptide-specific-T-cell receptors is very low and their activation by professional antigen-presenting cells, such as dendritic cells, is frequently hampered by insufficient costimulation resulting in peripheral tolerance. In addition, inhibitory immune circuits can impair an efficient antitumoral response of reactive T cells. It also has been demonstrated that large tumor burden can promote a state of immunosuppression that in turn can facilitate neoplastic progression. Moreover, tumor cells, which mostly are genetically instable, can gain rescue mechanisms which further impair immune surveillance by T cells. Herein, we summarize the data on how tumor cells evade T-cell immune surveillance with the focus on solid tumors and describe approaches to improve anticancer capacity of T cells.
Immune Microenvironment in Tumor Progression: Characteristics and Challenges for Therapy  [PDF]
Valerie Chew,Han Chong Toh,Jean-Pierre Abastado
Journal of Oncology , 2012, DOI: 10.1155/2012/608406
Abstract: The tumor microenvironment plays a critical role in cancer development, progression, and control. The molecular and cellular nature of the tumor immune microenvironment influences disease outcome by altering the balance of suppressive versus cytotoxic responses in the vicinity of the tumor. Recent developments in systems biology have improved our understanding of the complex interactions between tumors and their immunological microenvironment in various human cancers. Effective tumor surveillance by the host immune system protects against disease, but chronic inflammation and tumor “immunoediting” have also been implicated in disease development and progression. Accordingly, reactivation and maintenance of appropriate antitumor responses within the tumor microenvironment correlate with a good prognosis in cancer patients. Improved understanding of the factors that shape the tumor microenvironment will be critical for the development of effective future strategies for disease management. The manipulation of these microenvironmental factors is already emerging as a promising tool for novel cancer treatments. In this paper, we summarize the various roles of the tumor microenvironment in cancer, focusing on immunological mediators of tumor progression and control, as well as the significant challenges for future therapies. 1. Introduction The tumor microenvironment consists of cancer cells, stromal tissue, and extracellular matrix. The immune system is an important determinant of the tumor microenvironment. Indeed, the complex interplay between cancer cells and the host immune response has been extensively investigated in the past few decades. Several immunological deficiencies have been linked with enhanced tumor development in mouse models as well as in humans [1, 2]. The higher incidence of cancers in transplant patients receiving long-term immunosuppressive treatment is well documented [3–5]. Similarly, mice with compromised immune functions due to genetic modifications develop more tumors [6–9]. It is now well recognized that effective tumor surveillance by the immune system is critical to maintain homeostasis in the host. Despite exerting a key role in host protection, tumor surveillance by the immune system may eventually fail. As described in the three “Es” of cancer immunoediting, tumor cells are initially eliminated by the immune system before becoming clinically detectable. This is then followed by an equilibrium phase, where a selection process for less immunogenic tumor variants take place until the tumors finally “escape” the immune
Semi-allogeneic vaccines and tumor-induced immune tolerance
Jin Yu, Mark S Kindy, Sebastiano Gattoni-Celli
Journal of Translational Medicine , 2009, DOI: 10.1186/1479-5876-7-3
Abstract: Almost a century has passed since Paul Erlich first proposed that the immune system has the potential to eradicate cancer even though tumor cells arise from normal cells. Fifty years later the immune surveillance theory put forth that lymphocytes have the capacity to survey and destroy newly arising tumor cells that continuously appear in the body [1]. The conviction that the immune system can be mobilized as well as manipulated to eradicate tumor cells has invigorated the field of tumor immunology, one of the most active fields in immunology. The parallel discoveries of histocompatibility antigens in humans and mice are a good example of how studies in animal models and humans may go hand in hand [2]. In fact, animal studies continue as a basis for important advances because they have allowed the evaluation of multiple parameters in tumor immunology that are not possible in clinical studies [3].Despite a reasonable understanding of anti-tumor effector mechanisms, clinical studies investigating spontaneous anti-tumor immune responses have yet to lead to reproducible or consistent tumor regression. Thus, the question of why tumors continue to grow and metastasize in immunological competent cancer patients remains unanswered. Several observations have demonstrated that tumors evade and actively suppress the immune system. Tumor evasion of the immune system, termed immune escape, may occur through several mechanisms, including (i) tolerance or anergy induction; (ii) the genetic instability of tumors; (iii) modulation of tumor antigens; and (iv) decreased major histocompatibility complex class I (MHC-I) expression [4]. In addition to evasion of the immune system, tumors actively suppress the immune system directly through production of immune suppressive cytokines and indirectly through the induction of immune inhibitory cells [5]. This secretion of soluble factors is thought to contribute to the Th2-skewed immune responses observed in cancer patients and to induce the
Effects of delayed immune-response in tumor immune-system interplay
Giulio Caravagna,Alex Graudenzi,Marco Antoniotti,Giancarlo Mauri
Electronic Proceedings in Theoretical Computer Science , 2012, DOI: 10.4204/eptcs.92.8
Abstract: Tumors constitute a wide family of diseases kinetically characterized by the co-presence of multiple spatio-temporal scales. So, tumor cells ecologically interplay with other kind of cells, e.g. endothelial cells or immune system effectors, producing and exchanging various chemical signals. As such, tumor growth is an ideal object of hybrid modeling where discrete stochastic processes model agents at low concentrations, and mean-field equations model chemical signals. In previous works we proposed a hybrid version of the well-known Panetta-Kirschner mean-field model of tumor cells, effector cells and Interleukin-2. Our hybrid model suggested -at variance of the inferences from its original formulation- that immune surveillance, i.e. tumor elimination by the immune system, may occur through a sort of side-effect of large stochastic oscillations. However, that model did not account that, due to both chemical transportation and cellular differentiation/division, the tumor-induced recruitment of immune effectors is not instantaneous but, instead, it exhibits a lag period. To capture this, we here integrate a mean-field equation for Interleukins-2 with a bi-dimensional delayed stochastic process describing such delayed interplay. An algorithm to realize trajectories of the underlying stochastic process is obtained by coupling the Piecewise Deterministic Markov process (for the hybrid part) with a Generalized Semi-Markovian clock structure (to account for delays). We (i) relate tumor mass growth with delays via simulations and via parametric sensitivity analysis techniques, (ii) we quantitatively determine probabilistic eradication times, and (iii) we prove, in the oscillatory regime, the existence of a heuristic stochastic bifurcation resulting in delay-induced tumor eradication, which is neither predicted by the mean-field nor by the hybrid non-delayed models.
The Initial Immune Reaction to a New Tumor Antigen Is Always Stimulatory and Probably Necessary for the Tumor's Growth  [PDF]
Richmond T. Prehn
Journal of Immunology Research , 2010, DOI: 10.1155/2010/851728
Abstract: All nascent neoplasms probably elicit at least a weak immune reaction. However, the initial effect of the weak immune reaction on a nascent tumor is always stimulatory rather than inhibitory to tumor growth, assuming only that exposure to the tumor antigens did not antedate the initiation of the neoplasm (as may occur in some virally induced tumors). This conclusion derives from the observation that the relationship between the magnitude of an adaptive immune reaction and tumor growth is not linear but varies such that while large quantities of antitumor immune reactants tend to inhibit tumor growth, smaller quantities of the same reactants are, for unknown reasons, stimulatory. Any immune reaction must presumably be small before it can become large; hence the initial reaction to the first presentation of a tumor antigen must always be small and in the stimulatory portion of this nonlinear relationship. In mouse-skin carcinogenesis experiments it was found that premalignant papillomas were variously immunogenic, but that the carcinomas that arose in them were, presumably because of induced immune tolerance, nonimmunogenic in the animal of origin. 1. Introduction The immune surveillance hypothesis, championed in the 60s by Burnet [1] to explain why many cancers, although part of the self, are nonetheless immunogenic, has had a disputatious history. One of the earliest arguments in favor of the surveillance hypothesis was the observation that immunodepression increased the incidence of certain human cancers, especially those of the skin and of the lymph system [2]. However, Stutman, in a comprehensive survey, could find no evidence that immunodepression affected carcinogenesis [3]. More recently, Schreiber and Podack have reopened the question by publishing an analysis of the validity of the immune surveillance hypothesis in the case of methylcholanthrene-induced carcinogenesis [4]. Their conclusion was, in essence, that immunodepression often increased tumor growth and/or incidence, thus supporting the existence of anticancer immune surveillance. 2. Two Illustrative Experiments The late Dr. Marc Lappé and I published a paper apparently showing the role of immune surveillance during chemically induced skin carcinogenesis [5]. We based these studies upon a system in which a suboncogenic dosage of 3-methylcholanthrene (MCA) was applied as an “initiator” to the backs of BALB/c mice. After a short interval, the initiated skin was “promoted” by orthotopic transplantation to syngeneic mice whose immune capacities had been modified by various means; the
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