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Pick and Choose. Literature Updates. For Members. For Librarians. RSS Feeds. Chemistry World. Education in Chemistry. The role of the immune system in tumor progression has been subject to discussion for many decades.
- Systems Biology of Tumor Microenvironment : Quantitative Modeling and Simulations.
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- Systems Biology of Tumor Microenvironment.
Numerous studies suggest that a low immune response might be beneficial, if not necessary, for tumor growth, and only a strong immune response can counter tumor growth and thus inhibit progression. Without an immune response, a heterogeneous tumor population comprised of cancer stem cells and non-stem progenitors grows as conglomerates of self-metastases [ Enderling et al. This morphological phenomenon results from the interplay of cell proliferation, cell migration and cell death. With increasing cell death intra-tumoral spatial inhibitions are loosened, which in turn enable cancer stem cell cycling and thus, counter-intuitively, tumor progression [ Enderling et al.
By overlaying on this model the diffusion of immune reactants into the tumor from a peripheral source to target cells, we simulate the process of immune-system-induced cell kill on tumor progression. A low cytotoxic immune reaction continuously kills cancer cells and, although at a low rate, thereby causes the liberation of space-constrained cancer stem cells to drive self-metastatic progression and continued tumor growth. With increasing immune system strength, however, tumor growth peaks, and then eventually falls below the intrinsic tumor sizes observed without an immune response.
Focusing only on the cytotoxic function of the immune system, we were able to observe all immunoediting roles of the immune system: immune promotion at weak immune responses, immunoinhibition at strong immune responses, and immunoselection at all levels. Simulations of our model support a hypothesis previously put forward by Prehn [ Prehn, ] that comparable tumor sizes can be observed for weak and strong immune reactions.
With this increasing immune response the number and proportion of cancer stem cells monotonically increases, implicating an additional unexpected consequence, that of cancer stem cell selection, to the immune response. We propose more generally that a stem-cell-expansive influence may take the form of anything that encourages morphological fingering. Beyond immune response, this could include cell death, or even growth within restricted thin channels, as might be expected e. Tumor-host signaling interaction reveals a systemic, age-dependent splenic immune influence on tumor development.
Proton irradiation impacts age-driven modulations of cancer progression influenced by immune system transcriptome modifications from splenic tissue. J Radiat Res.
Quantitative Modeling and Simulations
Epub Aug 7. In: d'Onofrio A, Gandolfi A eds. Mathematical Oncology Wilkie KP , Hahnfeldt P. Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion. Interface Focus. Epub Jun J Hematol Oncol. Tumor—immune dynamics regulated in the microenvironment inform the transient nature of immune-induced tumor dormancy. Cancer Res. Further, the Stephen Hart.
Terrestrial microbial and ecosystem ecology, plant-soil interactions. Aaron Hernday. Epigenetic and transcriptional networks and metabolic engineering of yeasts. Linda Hirst. Experimental soft matter physics and biophysics. Katrina Hoyer. Immunological tolerance and auto-immune disease, regulatory T cells.
Kirk Jensen. Parasite pathogenesis and immunology, toxoplasma and host-immune responses. Shilpa Khatri. Changqing Li. Cancer imaging, cancer therapy, fluorescence molecular tomography, x-ray imaging, biomedical imaging system and algorithm. Bin Liu. Transport of microorganisms in complex environments, mechanics of biological media and mechanical metamaterials. Andy LiWang. NMR spectroscopy, structural biology, biochemistry, molecular mechanisms of biological clocks. Patricia LiWang.
The P. Gabriella Loots. Adjunct Associate Professor. Limb and skeletal development, genetics of bone metabolism, transcriptomics.
Jennifer Manilay. Developmental immunology, cell fate regulation, hematopoiesis. Kara McCloskey. Stem cell and tissue engineering for regenerative medicine applications. Emily Jane McTavish. Computational approaches to big trees and big data: phylogenetics, genomics, and the Open Tree of Life. Emily Moran. Evolutionary ecology of plant responses to environmental change. Within this broad area we investigate the conformational and functional behavior of proteins how they fold, bind, and function with the combined goals of deciphering their mechanisms of operation and understanding their general design principles towards developing exciting engineering applications in the emerging field of bionanotechnology.
Chih-Wen Ni. Gene regulation in vascular development and genetic engineering.
Clarissa Nobile. Research in the Nobile lab is directed towards understanding the molecular and mechanistic bases of microbial communities. We are interested in Molecular development of microbial communities, biofilm formation. Rudy Ortiz. Insulin resistance; cardiorenal and metabolic disorders; comparative physiology of Northern Elephant Seals. Stem cell regulation, cancer and regeneration in planarians.
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Scott Roy. Assistant Adjunct Professor. Ramen Saha. Jason Sexton. Plant adaptation, species range limits biological invasions and evolutionary conservation science. Suzanne Sindi. Mathematical biology, dynamical systems and computational biology and bioinformatics.
Systems Biology of Tumor Microenvironment
Mark Sistrom. We study evolutionary hypotheses in bacterial and viral systems using a combination of computational and laboratory genomic approaches. Paul Smaldino. Population dynamics, social and cultural evolution, self-organization, mathematical and computational modeling. Anand Subramaniam. Susannah Tringe.