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| Author | : Daniela F. Quail |
| Publisher | : Frontiers Media SA |
| Total Pages | : 229 |
| Release | : 2022-11-10 |
| Genre | : Medical |
| ISBN | : 2832504841 |
| Author | : Debabrata Banerjee |
| Publisher | : Springer Nature |
| Total Pages | : 171 |
| Release | : 2021-12-09 |
| Genre | : Medical |
| ISBN | : 3030832821 |
Over the past decade, the tumor microenvironment has become one of the most important research areas in cancer biology, as cells within the tumor microenvironment, despite being outnumbered by healthy cells, are able to evade surveillance and immune-mediated destruction. While researchers have learned a great deal about the cellular and structural makeup of the tumor microenvironment, there has been a growing understanding of the metabolic interplay between the tumor micronenvironment’s various cellular constituents and how each of them contributes to overall tumor growth and metastases. This new volume will guide researchers, students, oncologists and academics through a rapidly developing and changing field with a thorough understanding of tumor microenvironment biology from a cellular, structural, metabolic, and immunological perspective.
| Author | : Constantinos Koumenis |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 293 |
| Release | : 2013-11-23 |
| Genre | : Medical |
| ISBN | : 146145915X |
The collection of chapters in this proceeding volume reflects the latest research presented at the Aegean meeting on Tumor Microenvironment and Cellular Stress held in Crete in Fall of 2012. The book provides critical insight to how the tumor microenvironment affects tumor metabolism, cell stemness, cell viability, genomic instability and more. Additional topics include identifying common pathways that are potential candidates for therapeutic intervention, which will stimulate collaboration between groups that are more focused on elucidation of biochemical aspects of stress biology and groups that study the pathophysiological aspects of stress pathways or engaged in drug discovery.
| Author | : Anne Le |
| Publisher | : Springer |
| Total Pages | : 186 |
| Release | : 2018-06-26 |
| Genre | : Medical |
| ISBN | : 331977736X |
Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
| Author | : Satyendra Chandra Tripathi |
| Publisher | : Frontiers Media SA |
| Total Pages | : 336 |
| Release | : 2021-03-01 |
| Genre | : Science |
| ISBN | : 2889665232 |
| Author | : Katarzyna A. Rejniak |
| Publisher | : Springer |
| Total Pages | : 264 |
| Release | : 2016-10-13 |
| Genre | : Medical |
| ISBN | : 3319420232 |
This edited volume discusses the complexity of tumor microenvironments during cancer development, progression and treatment. Each chapter presents a different mathematical model designed to investigate the interactions between tumor cells and the surrounding stroma and stromal cells. The topics covered in this book include the quantitative image analysis of a tumor microenvironment, the microenvironmental barriers in oxygen and drug delivery to tumors, the development of tumor microenvironmental niches and sanctuaries, intravenous transport of the circulating tumor cells, the role of the tumor microenvironment in chemotherapeutic interventions, the interactions between tumor cells, the extracellular matrix, the interstitial fluid, and the immune and stromal cells. Mathematical models discussed here embrace both continuous and agent-based approaches, as well as mathematical frameworks of solid mechanics, fluid dynamics and optimal control theory. The topics in each chapter will be of interest to a biological community wishing to apply the mathematical methods to interpret their experimental data, and to a biomathematical audience interested in exploring how mathematical models can be used to address complex questions in cancer biology.
| Author | : Jianchen Yang (Ph. D. in biomedical engineering) |
| Publisher | : |
| Total Pages | : 254 |
| Release | : 2021 |
| Genre | : |
| ISBN | : |
The varying and extreme nutrient conditions found in the tumor microenvironment force reprogramming of metabolism in tumor cells. This metabolic reprogramming has been identified as a hallmark of cancer. This dissertation focuses on the development and validation of an experimental-mathematical approach that predicts how the dynamics of glucose and lactate influence tumor metabolism and development. Firstly, we developed a baseline model that predicts tumor cell growth as a function of glucose availability. We employed time-resolved microscopy to track the temporal change in the number of live and dead tumor cells under different initial conditions and seeding densities. A family of mathematical models that describes the overall tumor cell growth in response to the initial glucose and confluence was constructed. The most parsimonious model selected from the family using the Akaike Information Criteria was calibrated and validated in two breast cancer cell lines (BT-474 and MDA-MB-231) and demonstrated accuracy in predicting tumor growth. Secondly, we developed noninvasive imaging of nutrient dynamics with a stable transfection of two FRET reporters, one assaying glucose concentration and one assaying lactate concentration, in the MDA-MB-231 breast cancer cell line. The FRET ratio from both reporters was found to increase with increasing concentration of the corresponding ligand and decrease over time for high initial concentration of the ligand. Significant differences in the FRET ratio corresponding to metabolic inhibition were found when cells were treated with glucose/lactate transporter inhibitors. The FRET reporters enabled us to track intracellular glucose and lactate dynamics, providing insight into tumor metabolism and response to therapy over time. Finally, we compared mechanism-based and machine learning models for predicting tumor cells growth when we introduced an inhibitor of glucose uptake as a potential treatment. We extended the baseline model to account for glucose uptake inhibition, considering both the real glucose level in the system and the glucose level accessible to tumor cells. The random forest model provided the best prediction while the mechanism-based model presented a comparable predictive capability
| Author | : Z. Kmiec |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 154 |
| Release | : 2013-06-29 |
| Genre | : Science |
| ISBN | : 3642565530 |
It is only during the last decade that the functions of sinusoidal endothelial cells, Kupffer cells, hepatic stellate cells, pit cells and other intrahepatic lymphocytes have been better understood. The development of methods for isolation and co-culturing various types of liver cells has established that they communicate and cooperate via secretion of various intercellular mediators. This monograph summarizes multiple data that suggest the important role of cellular cross-talk for the functions of both normal and diseased liver. Special features of the book include concise presentation of the majority of detailed data in 19 tables. Original schemes allow for the clear illustration of complicated intercellular relationships. This is the first ever presentation of the newly emerging field of liver biology, which is important for hepatic function in health and disease and opens new avenues for therapeutic interventions.
| Author | : Rebecca G. Bagley |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 765 |
| Release | : 2010-09-02 |
| Genre | : Medical |
| ISBN | : 1441966153 |
The fact that tumors are composed of both tumor cells and host cells has long been known. These tumor-associated cells include vascular endothelial cells and pe- cytes, as well as inflammatory cells such as neutrophils, monocytes, macrophages, mast cells and eosinophils, and lymphocytes. The tumor cells also interact with stromal cells and with elements of the tissue extracellular matrix. What has been less appreciated is the role that these cells could have in modulating the growth, invasion, and metastasis of the tumor. Early on, the elements of what we now call the tumor microenvironment were considered to be more or less innocent bysta- ers to the role of the tumor cells as they grew and invaded local sites. Today, there is an increased understanding of the critical role of the tumor microenvironment as dramatically influencing the course of tumor development and dissemination. This volume represents a superb compilation of the latest thoughts and data regarding the role of each essential component of the tumor microenvironment in cancer development and progression. Perhaps, the earliest recognition of the role of nonmalignant cells as cancer re- lators was the recognition that lymphocytes can participate in what was termed “immune surveillance” in the 1960s. Our understanding of tumor immunity has improved markedly since then, and there are now successful clinical studies sh- ing the potential use of immune-based therapies in cancer treatment.
| Author | : Kaitlyn M. Dvorak |
| Publisher | : |
| Total Pages | : 143 |
| Release | : 2018 |
| Genre | : |
| ISBN | : |
The tumor microenvironment (TME) is a heterogeneous region that is comprised of tumor cells, stromal cells, and secreted factors and creates an environment favorable for tumor cell invasion and metastasis. An important step in the shift to a pro-cancerous microenvironment is the transformation of normal stromal fibroblasts to carcinoma-associated fibroblasts (CAFs). CAFs are present in a majority of solid tumors and can directly promote tumor cell motility via cytokine, chemokine and growth factor secretion into the TME, making them a critical TME component to understand. The exact effects that the TME has upon cytoskeletal regulation in motile tumor cells remain enigmatic. The conserved formin family of cytoskeleton regulating proteins plays essential roles in the assembly and/or bundling of unbranched actin filaments. Mammalian Diaphanous-related formin-2 (mDia2/DIAPH3/Drf3/Dia) assembles a dynamic F-actin cytoskeleton that underlies tumor cell migration and invasion. We previously showed that the chemokine CXCL12 can influence breast tumor cell migration and invasion through modification of the mDia2-directed actin cytoskeleton. The endogenous source of CXCL12 was unexplored. Therefore, the objective of this study was to understand whether CAF-derived chemokines from the TME impact breast tumor cell motility through modification of the formin-assembled F-actin cytoskeleton. In this study, we used CAF-derived conditioned media (CM) from WS19T fibroblasts, a transformed patient-derived tumor-adjacent breast CAF cell line, and studied its cell-autonomous impact upon tumor-cell motility. In triple-negative MDA-MB-231 human breast cancer cells, WS19T CAF-CM significantly and robustly increased wound closure and invasion relative to normal human mammary fibroblast (HMF)-CM. Unexpectedly, western blot analysis of WS19T-CM-treated MDA-MB-231 cells revealed a significant loss of mDia2 protein expression. WS19T-CM also promoted proteasome-mediated mDia2 degradation in MDA-MB-231s relative to control HMF-CM and WS21T CAF-CM, a breast CAF cell line that failed to reduced mDia2 expression, but significantly increased MDA-MB-231 migration. Cytokine array analysis of CM identified upregulated secreted factors in WS19T-CM relative to control WS21T CM, including the chemokine CXCL12 (SDF1a). As CXCL12 was identified as a factor secreted by fibroblasts and heavily involved in cancer cell migration and invasion, we hypothesized that CXCL12 is a CM factor influencing mDia2 protein loss, while increasing MDA-MB-231 cell invasion and migration. Exogenous CXCL12 treatment resulted in increased wound closure and loss of mDia2 protein expression. Blocking CXCL12 signaling with AMD3100, a specific inhibitor of CXCR4, augmented motility and rescued mDia2 protein expression in the presence of WS19T-CM. Our data suggest a mechanism whereby CAFs promote tumor cell migration and invasion through CXCL12 secretion to regulate the mDia2-directed cytoskeleton in breast tumor cells, and highlights a novel therapeutic approach of treating highly invasive primary lesions through targeting the TME.
