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ESTROGEN RECEPTORS --- MODULATORS --- PHARMACOLOGY --- ESTROGEN RECEPTORS --- MODULATORS --- PHARMACOLOGY
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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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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 --- n/a
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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
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Oxytocin secretion from the posterior pituitary gland is increased during parturition, stimulated by the uterine contractions that forcefully expel the fetuses. Since oxytocin stimulates further contractions of the uterus, which is exquisitely sensitive to oxytocin at the end of pregnancy, a positive feedback loop is activated. The neural pathway that drives oxytocin neurons via a brainstem relay has been partially characterised, and involves A2 noradrenergic cells in the brainstem. Until close to term the responsiveness of oxytocin neurons is restrained by neuroactive steroid metabolites of progesterone that potentiate GABA inhibitory mechanisms. As parturition approaches, and this inhibition fades as progesterone secretion collapses, a central opioid inhibitory mechanism is activated that restrains the excitation of oxytocin cells by brainstem inputs. This opioid restraint is the predominant damper of oxytocin cells before and during parturition, limiting stimulation by extraneous stimuli, and perhaps facilitating optimal spacing of births and economical use of the store of oxytocin accumulated during pregnancy. During parturition, oxytocin cells increase their basal activity, and hence oxytocin secretion increases. In addition, the oxytocin cells discharge a burst of action potentials as each fetus passes through the birth canal. Each burst causes the secretion of a pulse of oxytocin, which sharply increases uterine tone; these bursts depend upon auto-stimulation by oxytocin released from the dendrites of the magnocellular neurons in the supraoptic and paraventricular nuclei. With the exception of the opioid mechanism that emerges to restrain oxytocin cell responsiveness, the behavior of oxytocin cells and their inputs in pregnancy and parturition is explicable from the effects of hormones of pregnancy (relaxin, estrogen, progesterone) on pre-existing mechanisms, leading through relative quiescence at term inter alia to net increase in oxytocin storage, and re
Activation. --- Activity. --- Adaptation. --- Allopregnanolone. --- Behavior. --- Birth. --- Brainstem. --- C-fos expression. --- Dendrites. --- Dynorphin. --- Enkephalin. --- Estrogen receptors. --- Estrogen. --- Feedback. --- Fetuses. --- Firing. --- Gaba. --- Gamma-aminobutyric-acid. --- Gland. --- Hormone. --- Hormones. --- Hypothalamic paraventricular nucleus. --- Increase. --- Increases. --- Inhibition. --- Main olfactory-bulb. --- Mechanisms. --- Messenger-ribonucleic-acid. --- Milk-ejection reflex. --- Neurons in-vitro. --- Neurons. --- Nitric oxide synthase. --- Nitric-oxide synthase. --- Nucleus tractus solitarius. --- Opioid. --- Oxytocin mrna. --- Oxytocin. --- Parturition. --- Pattern. --- Patterns. --- Pituitary. --- Potentials. --- Pregnancy. --- Progesterone-receptor expression. --- Progesterone. --- Rat supraoptic nucleus. --- Response. --- Restraint. --- Review. --- Secretion. --- Steroid metabolites. --- Steroid. --- Stimulation. --- Stimuli. --- Supraoptic nucleus. --- System. --- Time. --- Uterus.
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