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At the molecular level, the activation of growth factor receptors (GFRs) induces a mitogenic response and maintains cancer cell growth. The majority of malignant diseases are related to aberrant intra- and intercellular communication, associated with the GFR-mediated pathways. Moreover, the evasion of apoptotic signals and the requirement of angiogenesis were also found to be of fundamental importance for tumor progression and metastasis. In this context, a high expression of GFRs aids blood vessel formation, cell migration, and the inhibition of apoptosis. GFR-directed therapy that would theoretically selectively kill malignant cells and reduce the toxicity associated with nonselective conventional chemotherapy may be a promising treatment for cancer. Many intracellular proteins involved in GFR signal transduction can also function as oncogenes. Mutations affecting key proteins in the RAS/MAPK and PI3K/AKT pathways are known to be crucial in maintaining the malignancy of different types of cancers. This information has guided the development of compounds designed to target one or more of these pathways in cancer cells. Even though there have been important advances in our understanding of GFRs and their signaling, certain essential information is still lacking, and these membrane receptors are still being laboriously studied by several research groups, to find therapeutic solutions to unmet medical needs.

Cancer cells --- Growth. --- Cancer cell growth

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This book, part contributed volume, part proceedings, discusses state-of-the-art advances on human cell transformation in cell models for the study of cancer and aging. Several of the chapters are from the Human Cell Transformation: Advances in Cell Models for the Study of Cancer and Aging conference that was held in June 2018 at McGill University. The authors represent international expertise on a wide variety of topics ranging from different types of cancer (prostate, bone, breast, etc.) to tumor microenvironment, tumor progression, homogeneity, and possible therapies and treatments.

Cell biology. --- Cancer research. --- Oncology  . --- Cell Biology. --- Cancer Research. --- Oncology. --- Tumors --- Cancer research --- Cell biology --- Cellular biology --- Biology --- Cells --- Cytologists --- Cancer cells --- Growth. --- Cancer cell growth

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The extracellular matrix (ECM) scaffold, which surrounds and supports the cells in tissues, consists of fibrillar proteins, proteoglycans, glycosaminoglycans, signaling molecules, and enzymes involved in its remodeling. The stages of cancer progression, e.g., local invasion, intravasation, extravasation, distant invasion and immunosuppression, are obligatorily perpetrated through interactions of these tumor cells with the ECM. Cancer-related ECM changes can be exploited for the evaluation of disease progression, anticancer therapy development, and monitoring of therapy response. Thus, in breast cancer, hyaluronan-mediated wound repair mechanisms are hijacked to promote tumor development. Altered mechanical properties of the pancreatic cancer ECM are immunosuppressive and prevent the penetration of cytotoxic chemotherapy agents. The expression of the proteoglycan syndecan-4 is modulated by anticancer drugs, suggesting its potential druggabilty capacity. Another proteoglycan, lumican, is proposed as a cancer prognosis marker, chemoresistance regulator, and cancer therapy target. Due to their remodeling properties, the MMPs are vital mediators and important therapeutic targets. Treatment of breast cancer cells with sulfated hyaluronan has been shown to attenuate tumor cell growth, migration, and invasion. Extracellular vesicles (EVs), comprising exosomes, microvesicles, and apoptotic bodies, are released by all cells into the ECM and body fluids and can be utilized as diagnostic markers in malignant pleural mesothelioma. These exciting developments encourage tumor biology scientists for further creative research.

Research & information: general --- elastin --- ribosomal protein SA --- tongue carcinoma --- MMP-2 --- EGCG --- pancreatic ductal adenocarcinoma --- syndecans --- proteoglycans --- tumor progression --- angiogenesis --- syndecan-4 --- heparan sulfate --- cancer --- prognosis --- biomarker --- signal transduction --- proteoglycan --- metastasis --- extracellular matrix --- fibrosis --- immune cell modulation --- neutrophils --- neutrophil extracellular trap --- macrophages --- BCC --- MMP --- TIMP --- invasion --- lumican --- cancer cell growth --- motility --- hyaluronan --- RHAMM --- CD44 --- wound repair --- breast cancer --- malignant pleural mesothelioma --- pleural effusion --- extracellular vesicles --- biomarkers --- sulfated hyaluronan --- estrogen receptors --- epithelial-to-mesenchymal transition --- matrix metalloproteinases --- elastin --- ribosomal protein SA --- tongue carcinoma --- MMP-2 --- EGCG --- pancreatic ductal adenocarcinoma --- syndecans --- proteoglycans --- tumor progression --- angiogenesis --- syndecan-4 --- heparan sulfate --- cancer --- prognosis --- biomarker --- signal transduction --- proteoglycan --- metastasis --- extracellular matrix --- fibrosis --- immune cell modulation --- neutrophils --- neutrophil extracellular trap --- macrophages --- BCC --- MMP --- TIMP --- invasion --- lumican --- cancer cell growth --- motility --- hyaluronan --- RHAMM --- CD44 --- wound repair --- breast cancer --- malignant pleural mesothelioma --- pleural effusion --- extracellular vesicles --- biomarkers --- sulfated hyaluronan --- estrogen receptors --- epithelial-to-mesenchymal transition --- matrix metalloproteinases

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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.

Mathematics --- Biomathematics. Biometry. Biostatistics --- General biophysics --- Biology --- Oncology. Neoplasms --- Pathological biochemistry --- Human medicine --- Computer science --- medische biochemie --- biofysica --- biomathematica --- biochemie --- biologie --- biomedische wetenschappen --- informatica --- oncologie --- biometrie --- wiskunde --- Cancer research. --- Biomathematics. --- Biophysics. --- Biological physics. --- Cancer Research. --- Mathematical and Computational Biology. --- Biological and Medical Physics, Biophysics. --- Biological physics --- Medical sciences --- Physics --- Cancer research --- Carcinogenesis. --- Tumors --- Cancer cells --- Metabolism. --- Growth. --- Pathophysiology. --- Neoplasms --- Tumours --- Pathology --- Cysts (Pathology) --- Oncology --- Cancer cell growth --- Cancer --- Oncogenesis --- Pathogenesis of cancer --- Tumorigenesis --- Genetic toxicology --- Pathogenesis

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The extracellular matrix (ECM) scaffold, which surrounds and supports the cells in tissues, consists of fibrillar proteins, proteoglycans, glycosaminoglycans, signaling molecules, and enzymes involved in its remodeling. The stages of cancer progression, e.g., local invasion, intravasation, extravasation, distant invasion and immunosuppression, are obligatorily perpetrated through interactions of these tumor cells with the ECM. Cancer-related ECM changes can be exploited for the evaluation of disease progression, anticancer therapy development, and monitoring of therapy response. Thus, in breast cancer, hyaluronan-mediated wound repair mechanisms are hijacked to promote tumor development. Altered mechanical properties of the pancreatic cancer ECM are immunosuppressive and prevent the penetration of cytotoxic chemotherapy agents. The expression of the proteoglycan syndecan-4 is modulated by anticancer drugs, suggesting its potential druggabilty capacity. Another proteoglycan, lumican, is proposed as a cancer prognosis marker, chemoresistance regulator, and cancer therapy target. Due to their remodeling properties, the MMPs are vital mediators and important therapeutic targets. Treatment of breast cancer cells with sulfated hyaluronan has been shown to attenuate tumor cell growth, migration, and invasion. Extracellular vesicles (EVs), comprising exosomes, microvesicles, and apoptotic bodies, are released by all cells into the ECM and body fluids and can be utilized as diagnostic markers in malignant pleural mesothelioma. These exciting developments encourage tumor biology scientists for further creative research.

elastin --- ribosomal protein SA --- tongue carcinoma --- MMP-2 --- EGCG --- pancreatic ductal adenocarcinoma --- syndecans --- proteoglycans --- tumor progression --- angiogenesis --- syndecan-4 --- heparan sulfate --- cancer --- prognosis --- biomarker --- signal transduction --- proteoglycan --- metastasis --- extracellular matrix --- fibrosis --- immune cell modulation --- neutrophils --- neutrophil extracellular trap --- macrophages --- BCC --- MMP --- TIMP --- invasion --- lumican --- cancer cell growth --- motility --- hyaluronan --- RHAMM --- CD44 --- wound repair --- breast cancer --- malignant pleural mesothelioma --- pleural effusion --- extracellular vesicles --- biomarkers --- sulfated hyaluronan --- estrogen receptors --- epithelial-to-mesenchymal transition --- matrix metalloproteinases --- n/a